Care plan III

June 3, 2024
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Care plan III

 

Shock, the whole-body response to poor tissue oxygenation, is a condition rather than a disease state. Any situation that impairs oxygen delivery to tissues and organs can start a syndrome of shock and lead to a life-threatening emergency. Clients in acute care settings are at high risk for conditions that lead to shock, but shock can occur in any setting. When compensation or interventions are ineffective and shock progresses, extensive hypoxiacan lead to the complication of multiple organ dysfunction syndrome (MODS) and death. Table 37-1 lists important concepts related to shock.

OVERVIEW Body organs, tissues, and cells need a continuous supply of oxygen for proper metabolism and function. The pulmonary system initially supplies oxygen to the body. The cardiovascular system delivers oxygen to all tissues and removes cellular wastes. The units of the cardiovascular system are the blood, blood vessels, and heart. When any component of the cardiovascular system does not function properly for any reason, shock can result.

Shock, a pathologic condition, is started by abnormal cellular metabolism that occurs when too little oxygen is delivered to the tissues (Guyton & Hall, 2000). Shock used to be classified as hypovolemic, cardiogenic, vasogenic, or septic, which indicated the origin of the problem causing the shock. Shock is now classified by the specific functional impairment caused: hypovolemic shock, cardiogenic shock, distributive shock, and obstructive shock (Effron & Chernow, 1992).

Table 37-2 compares the old and new classification systems and common conditions causing each category of shock. The functional classification is used by researchers and guides clinicians and therefore is used in this chapter.

Many clinical manifestations of shock are similar regardless of what starts the process or which tissues are affected first. These common clinical manifestations are due to physiologic compensatory mechanisms. Manifestations unique to any one type of shock result from specific tissue dysfunction. The common clinical features of shock are listed in Chart 37-1.

Physiology Review

Oxygenation of any organ or tissue depends on how much oxygenated arterial blood perfuses the organ or tissue. Organ perfusion is related to mean arterial pressure (MAP). Because the cardiovascular system is a closed but continuous circuit, the factors that influence MAP include the following:

• Total blood volume

• Cardiac output

• Size of the vascular bed

Total blood volume and cardiac output are directly related to MAP—increases in either total blood volume or cardiac output usually raise MAP. Decreases in either total blood volume or cardiac output eventually lower MAP. The size of the vascular bed is inversely (negatively) related to MAP—increases in the size of the vascular bed lower MAP, and decreases raise MAP (Figure 37-1). Blood vessels, especially small arteries and veins connected directly to cap- illaries, can increase in diameter by relaxing the smooth muscle in vessel walls (dilating) or decrease in diameter by contracting the muscle (vasoconstriction). When blood vessels dilate and total blood volume remains the same, blood pressure decreases and blood flow is slower. When blood vessels constrict and total blood volume remains the same, blood pressure increases and blood flow is faster.

Blood vessels contain nerves from the sympathetic division of the autonomic nervous system. Some nerves continuously stimulate vascular smooth muscle so that the blood vessels are normally partially constricted. This state of partial blood vessel constriction is called sympathetic tone. An increase in sympathetic stimulation causes the smooth muscle of the blood vessels to constrict further, raising MAP; a decrease in sympathetic stimulation causes the smooth muscle of the blood vessels to relax, dilating them and lowering MAP.

Blood flow to body organs varies and adjusts to changes in tissue oxygeeeds. The body can selectively increase blood flow to some areas while reducing blood flow to others. Some organs, such as the skin and skeletal muscles, can tolerate low levels of oxygen for hours without dying or being damaged. Other organs (e.g., heart, brain, and liver) tolerate hypoxic conditions (low levels of tissue oxygenation) poorly, and even just a few minutes without adequate oxygen results in serious or permanent damage.

Pathophysiology The underlying problems common to all types of shock, regardless of cause, are the effects of anaerobic cellular metabolism (metabolism without oxygen). These effects result from inadequate tissue oxygenation and cause adverse changes in tissue function. The body begins to compensate in an attempt to maintain or restore tissue perfusion and oxygenation—even while the causes of shock are still present.  

When the conditions that cause shock remain uncorrected, shock progresses through the following predictable stages:

1. Initial stage

2. Nonprogressive stage

3. Progressive stage

4. Refractory stage

The stages of shock are identified on the basis of the following:

• How well the client’s compensatory mechanisms are working

• The severity of the clinical manifestations

• Whether tissue damage is reversible

The main trigger leading to the recognizable picture of shock is a sustained decrease in mean arterial pressure (MAP) that results from decreased cardiac output, decreased circulating blood volume, or expansion of the vascular bed. A decrease in MAP of 5 to 10 mm Hg below the client’s baseline value is immediately detected by pressure-sensitive nerve receptors (baroreceptors) in the aortic arch and carotid sinus (Guyton & Hall, 2000). This information is transmitted to brain centers, which stimulates compensatory mechanisms. These mechanisms ensure continued blood flow and oxygen delivery to vital organs while limiting blood flow to less vital areas. Moving blood into selected areas while bypassing others (shunting) causes the physiologic changes and clinical manifestations of shock.

If the events that caused the initial decrease in MAP are halted at this point, the compensatory mechanisms can return the body to a normal perfused and oxygenated state, even without outside intervention. However, if the initiating events continue and MAP decreases further, some tissues function under anaerobic conditions. This condition creates an increase in lactic acid levels and other harmful metabolites (e.g., protein-destroying enzymes and oxygen radicals). These substances cause electrolyte and acid-base imbalances that have generalized, tissue-damaging effects and depress cardiac activity. Such effects are temporary and reversible if the cause of shock is corrected within 1 to 2 hours after onset. When such conditions continue for longer periods without help, the resulting acid-base imbalance, electrolyte imbalances, and increased levels of toxic metabolites cause so much cell damage in vital organs that multiple organ dysfunction syndrome (MODS) occurs and full recovery from shock is no longer possible. Table 37-3 summarizes the progression of shock.

INITIAL STAGE OF SHOCK (EARLY STAGE)

The initial (early) stage of shock is present when any condition causes MAP to decrease from the client’s baseline level by less than 10 mm Hg. During this stage, active compensatory mechanisms are so effective at returning MAP to normal levels that oxygenated blood flow to all vital organs is maintained. Cellular changes in this stage are decreased aerobic metabolism and increased anaerobic metabolism with a production of lactic acid; overall cellular metabolism is still aerobic. Compensation (vascular constriction and increased heart rate) is effective, and both cardiac output and MAP are maintained within the normal range. Because vital organ function is not disrupted, the signs and symptoms of shock are difficult to detect. An increase in heart rate from the client’s baseline level or a slight increase in diastolic blood pressure may be the only objective manifestation of this early stage of shock.

NONPROGRESSIVE STAGE OF SHOCK (COMPENSATORY STAGE)

The nonprogressive (compensatory) stage of shock occurs when conditions decrease MAP 10 to 15 mm Hg from baseline. Kidney and chemical compensatory mechanisms need to be activated because cardiovascular compensation alone is not enough to maintain MAP and supply needed oxygen to the vital organs. The kidneys and baroreceptors sense an ongoing decrease in MAP and cause the release of renin, antidiuretic hormone (ADH), aldosterone, epinephrine, and norepinephrine. Kidney compensation occurs through the actions of renin, aldosterone, and ADH. Renin, which is secreted by the kidney, starts the reactions that eventually cause decreased urine output, increased sodium reabsorption, and widespread vasoconstriction. ADH is secreted by the posterior pituitary gland. ADH increases water reabsorption in the kidney and causes blood vessel constriction in the skin and other less vital tissue areas. Together, these actions attempt to compensate for shock by maintaining the volume in the central blood vessels (Guyton & Hall, 2000). Tissue hypoxia is present ionvital organs and in the kidney but is not great enough to cause severe symptoms or permanent damage. Because some metabolism is anaerobic, acid-base and electrolyte changes occur in response to the buildup of metabolites. Changes include acidosis (low blood pH) and hyperkalemia (increased blood potassium level). If the client’s condition is stable and compensatory mechanisms are supported by medical and nursing interventions, he or she can remain in this stage for hours without experi encing permanent damage. Stopping the conditions that started the shock and providing supportive interventions can prevent the shock from progressing and reverse the effects of this stage.

PROGRESSIVE STAGE OF SHOCK (INTERMEDIATE STAGE) The progressive stage of shock results when there is a sustained decrease in MAP of more than 20 mm Hg from baseline. In this stage, compensatory mechanisms are functioning but are no longer able to deliver sufficient oxygen, even to vital organs. Compensatory mechanisms use large amounts of oxygen in certain tissues, which worsens the problem of general inadequate oxygenation. Vital organs develop hypoxia, and less vital organs experience anoxia (no oxygen) and ischemia (cell dysfunction or death from lack of oxygen). As a result of inadequate oxygenation and a buildup of toxic metabolites, some tissues experience extensive cell damage and ultimately die. The progressive stage of shock is a life-threatening emergency. Vital organs can tolerate this situation for only a short time before being permanently damaged. Immediate interventions are needed to reverse the effects of this stage of shock. Tolerance varies from person to person and depends greatly on pre-existing health. Usually the client’s life can be saved if the conditions causing shock are corrected within 1 hour of the onset of the progressive stage.

REFRACTORY STAGE OF SHOCK (IRREVERSIBLE STAGE) Formerly called the irreversible stage, the refractory stage of shock occurs when too much cell death and tissue damage results from too little oxygen reaching the tissues. As a result, the vital organs experience overwhelming changes. This stage is termed refractory because the body is unable to respond effectively to interventions, and the syndrome of shock continues. The remaining cells perform their metabolic functions anaerobically. Therapy is ineffective in saving the client’s life, even if the underlying cause of shock is corrected and MAP temporarily returns to normal. So much tissue damage has occurred, causing widespread release of toxic metabolites and destructive enzymes, that cell deterioration in vital organs continues

MULTIPLE ORGAN DYSFUNCTION SYNDROME The sequence of cell damage caused by the massive release of toxic metabolites and enzymes is termed multiple organ dysfunction syndrome (MODS). Once the damage has started, the sequence of events becomes a vicious cycle as more dead or dying cells break open and release more harmful metabolites. The metabolites cause the formation of small clots (microthrombi); this blocks tissue oxygenation and damages more cells, thus continuing the devastating cycle. MODS occurs first in the liver, heart, brain, and kidney. In sepsis-induced distributive shock, the lungs also are affected. The most profound change is deterioration of the heart muscle. One contributing factor is the release of myocardial depressant factor (MDF) from the ischemic pancreas.

Etiology Because shock is a manifestation of a pathologic condition rather than a disease state, its causes vary. Specific conditions leading to hypovolemic, cardiogenic, distributive, and obstructive shock are listed in Table 37-4. More than one type of shock can be present at the same time. For example, trauma caused by an automobile accident may trigger hemorrhage (leading to hypovolemic shock) and a myocardial infarction (leading to cardiogenic shock).

HYPOVOLEMIC SHOCK Hypovolemic shock occurs when too little circulating blood volume causes a MAP decrease so that the body’s total need for tissue oxygenation is not met. The most common conditions leading to hypovolemic shock are hemorrhage (external or internal) and dehydration. Hypovolemic shock caused by external hemorrhage is common after trauma, wounds, and surgery. Hypovolemic shock caused by internal hemorrhage occurs with blunt trauma, gastrointestinal (GI) ulcers, and poor control of surgical bleeding. External and internal hemorrhage can be caused by any health problem that reduces the levels of clotting factors (see Table 37-4). Hypovolemia as a result of dehydration can be caused by any condition that decreases fluid intake or increases fluid loss (see Table 37-4).

 CARDIOGENIC SHOCK Cardiogenic shock occurs when the actual heart muscle is unhealthy and contraction is directly impaired. Table 37-4 lists the common causes of direct pump failure. These conditions decrease cardiac output and afterload, thus reducing MAP. 

DISTRIBUTIVE SHOCK Distributive shock is caused by a loss of sympathetic tone, blood vessel dilation, pooling of blood in venous and capillary beds, and increased blood vessel permeability (leak). All of these factors can decrease mean arterial pressure (MAP) and may be induced either neurogenically or chemically.

NEURAL-INDUCED DISTRIBUTIVE SHOCK. Neural-induced loss of MAP occurs when sympathetic stimulation of the nerves controlling blood vessel smooth muscle is decreased and the smooth muscles of blood vessels relax, causing vasodilation. This blood vessel dilation can be a normal local response to injury, but shock results when the vasodilation is widespread or systemic. Common conditions that can cause a systemic loss of sympathetic tone are listed in Table 37-4.

CHEMICAL-INDUCED DISTRIBUTIVE SHOCK. Chemical-induced distributive shock has three common origins: anaphylaxis, sepsis, and capillary leak syndrome. Chemical-induced distributive shock occurs when certain chemicals or foreign substances within the blood and blood vessels start widespread changes in blood vessel walls. The chemicals are usually exogenous (originate outside the body), but this type of shock can be induced by substances normally found in the body (endogenous).

ANAPHYLAXIS. Anaphylaxis is one result of type I allergic reactions. It usually begins within seconds to minutes after exposure to a specific allergen. However, it is termed delayed because this type of reaction rarely occurs the first time a person encounters the allergen. It occurs on repeated exposure to the same allergen (Guyton & Hall, 2000). Table 23-2 lists common allergens that can cause anaphylaxis. Anaphylaxis is due to an antigen-antibody reaction that occurs in blood vessels throughout the body in response to contact with a substance to which the person has a severe allergy (hypersensitivity). This widespread reaction involves the interaction of the allergen, immunoglobulin E (IgE), basophils, and mast cells. It occurs within the walls of blood vessels, heart muscle cells, and bronchial tubes. Anaphylaxis damages cells and causes the release of large amounts of histamine and other inflammatory chemicals. These substances move rapidly throughout the circulatory system, causing massive blood vessel dilation and increased capillary permeability. These responses result in severe hypovolemia and vascular collapse. Decreased cardiac contractility and dysrhythmias occur during anaphylaxis. These symptoms may be the direct result of heart muscle changes induced by the antigen-antibody reaction, or they may result from the profound hypovolemia. Antigen-antibody reactions in the bronchial tissues cause severe edema and pulmonary obstruc- tion, which greatly reduce gas exchange. The pulmonary problems, together with inadequate circulation, cause extreme whole-body hypoxia. Without intervention, this condition results in death.

 SEPSIS. Sepsis leading to distributive shock occurs when microorganisms are present in the blood. This form of shock is most commonly called septic shock in clinical situations. Sepsis is often associated with disseminated intravascular coagulation (DIC). Distributive shock (septic shock) is more often associated with bacterial infection and has also been reported among clients with viral and yeast sepsis. Organisms often causing sepsis include gram-negative bacteria {Pseudomonas aeruginosa, Escherichia coli, and Klebsiella pneumoniae) and gram-positive bacteria (Staphylococcus and Streptococcus). Table 37-5 lists some of the conditions that put the client at risk for septic shock (sepsis-induced distributive shock). Septic shock results when large amounts of toxins and endotoxins produced by bacteria are secreted into the blood, causing a whole-body inflammatory reaction. These toxins and endotoxins react with blood vessels and cell membranes. Through the activity of white blood cells, the resulting reactions start inflammatory and immune events known as the systemic inflammatory response syndrome (SIRS). These toxin-host interactions activate complement, alter microcirculation within the vital organs (including selective coagulation and thrombus formation), increase capillary permeability (leakiness), cause cell injury, and increase cell metabolism (in combination with a decreased ability of some cells to take up needed oxygen). Metabolism becomes anaerobic because of decreased MAP, clot formation in capillaries, and poor cell uptake of oxygen.

CAPILLARY LEAK SYNDROME. Capillary leak syndrome leading to distributive shock occurs when there is a fluid shift from the blood to the interstitial space. Such shifts are caused by increased capillary permeability, loss of plasma osmolarity, and increased hydrostatic pressure in the blood. Specific conditions causing fluid shifts include severe burns, bullous skin disease, liver disorders, abdominal ascites, acute peritonitis, paralytic ileus, severe malnutrition, surgical wounds, hyperglycemia, kidney disease, hypoproteinemia, and trauma.

 OBSTRUCTIVE SHOCK Obstructive shock is caused by conditions that affect the ability of the normal heart muscle to pump effectively. The heart itself is normal, but conditions outside the heart prevent either adequate filling of the heart or adequate contraction of the healthy heart muscle. Common causes of obstructive shock are listed in Table 37-4.

Incidence/Prevalence The exact incidence of shock is not known because it is a response rather than a separate disease entity. Some degree of shock is a common complication among hospitalized clients. Hypovolemic shock is the most common type experienced by clients in emergency departments and after surgery or invasive procedures. Cardiogenic shock is the most common complication of myocardial infarction in clients who experience damage to 40% or more of the heart muscle. The frequency of distributive shock as a result of sepsis, which has a 40% to 85% mortality rate, is increasing among clients who are immunocompromised or have infections (Ackerman, 1994; Clochesy, 1996). This chapter presents the collaborative management of clients experiencing hypovolemic shock caused by hemorrhage and distributive shock caused by sepsis.

COLLABORATIVE MANAGEMENT: HYPOVOLEMIC SHOCK

The Concept Map addresses assessment and nursing care issues related to clients with hypovolemic shock.

Assessment

HISTORY The nurse collects data on risk factors and causative factors related to hypovolemic shock. Age is important because hypovolemic shock associated with trauma is more common in young adults, whereas sepsis is more common among older adults. Clients are asked specific questions about recent illness, trauma, procedures, or chronic conditions that may lead to shock. Such conditions include gastrointestinal ulcers, general surgery, hemophilia, liver disorders, prolonged vomiting, and prolonged diarrhea. Medications such as aspirin, diuretics, and antacids may cause changes leading to hypovolemic shock or may indicate the presence of a problem that can contribute to hypovolemic shock. The nurse asks about fluid intake and output during the previous 24 hours. Information about urine output is especially important because the first stages of shock are characterized by a reduced urine output, even when fluid intake is normal. The nurse assesses the client and the immediate environment for obvious signs of factors leading to shock. Areas to examine for signs of hemorrhage include the gums, wounds, and sites of dressings, drains, and vascular access. The nurse observes for any swelling, skin discoloration, or manifestations of pain that may indicate an internal hemorrhage.

PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS

Most of the visible signs of hypovolemic shock are caused by the changes resulting from compensatory efforts. Compensation or compensatory mechanisms are physiologic responses that try to keep an adequate blood flow to vital organs. Signs of shock are first evident as changes in cardiovascular function. As shock progresses, changes in the kidney, respiratory, integumentary, musculoskeletal, and central nervous systems become evident.

CARDIOVASCULAR MANIFESTATIONS. Shock involves a decrease of mean arterial pressure (MAP), and the resulting early compensation is cardiovascular. Therefore the earliest clinical signs of hypovolemic shock are also cardiovascular.

PULSE. The nurse or assistive nursing personnel assesses the central and peripheral pulses for rate and quality. In the initial stage of hypovolemic shock, the pulse rate increases to keep cardiac output and MAP at normal levels, even though the actual stroke volume (amount of blood pumped out from the heart) per beat is usually decreased. Because stroke volume is decreased, the peripheral pulses are more difficult to palpate and are easily blocked with light pressure. As hypovolemic shock progresses, superficial peripheral pulses may be absent.

BLOOD PRESSURE. Changes in systolic blood pressure are not always present in the initial stage of hypovolemic shock. When assessing the blood pressure of a client at risk for shock, the nurse considers the client’s normal baseline blood pressure level. Although a blood pressure of 90/50 may indicate severe shock in one person, it may be the normal blood pressure value for another healthy adult. When vasoconstriction is present, diastolic pressure increases but systolic pressure remains the same. As a result, the pulse pressure, or the difference between the systolic and diastolic pressures, is smaller. The blood pressure is monitored for changes from baseline levels and for changes from the previous measurement. For accuracy, the same equipment is used on the same extremity. When possible, the nurse measures blood pressure with the client in the lying, sitting, and standing positions. Systolic pressure decreases as shock progresses and cardiac output decreases; this reduces the pulse pressure even further. When shock continues and interventions are not adequate, compensation fails and systolic and diastolic pressures decrease. At this stage, blood pressure is difficult to hear. Palpation or a Doppler device may be needed to detect the systolic blood pressure.

OXYGEN SATURATION. Peripheral oxygen saturation is assessed through pulse oximetry. Hemoglobin oxygen saturation values between 90% and 95% are associated with the nonprogressive stage of shock, and values between 75% and 80% are associated with the progressive stage of shock. Any value below 70% is considered a life-threatening emergency and may signal the refractory stage of shock.

INTEGUMENTARY MANIFESTATIONS. Skin changes occur in shock because of decreased perfusion. An early compensatory mechanism for hypovolemic shock is vasoconstriction in the skin, which results in minimal perfusion. This allows more blood to circulate to the vital organs, which cannot tolerate low oxygen levels. The skin is assessed for temperature, color, and degree of moisture. It feels cool or cold to the touch, and the color is pale to cyanotic. Color changes are first evident in the mucous membranes and in the skin around the mouth. Pallor or cyanosis may be difficult to observe in many areas in darkskinned clients, and the nurse particularly assesses color changes in oral mucous membranes. As shock progresses, color changes in clients with lighter skin are noted first in the extremities and then in the central trunk area. The skin also feels clammy or moist to the touch, not because sweating increases but because the normal fluid lost through the skin does not evaporate quickly on cold skin. Capillary refill time is evaluated by pressing on the client’s fingernail until it blanches and then observing how fast the nail bed resumes color when pressure is released. Normally the nail bed capillaries resume color as soon as pressure is released. With shock, capillary refill is usually slow and is sometimes absent.

RESPIRATORY MANIFESTATIONS. The nurse assesses the rate, depth, and ease of respiration and also auscultates the lungs for abnormal breath sounds. Respiratory rate increases during hypovolemic shock. This increase is a compensatory mechanism to provide adequate oxygen to the critical tissues. When shock progresses to the stage at which lactic acidosis is present, the depth of respiration also increases.

KIDNEY/URINARY MANIFESTATIONS. The renal system compensates for decreased MAP by conserving body water through decreased filtration and increased water reabsorption. Urine is assessed for color, specific gravity, and the presence of blood or protein. The nurse or assistive nursing personnel measures urine output every hour. In severe shock, urine output is decreased (compared with fluid intake) or even absent. Of the four vital organs (heart, brain, liver, and kidney), only the kidney can tolerate hypoxia and anoxia for up to 1 hour without permanent damage. When hypoxic or anoxic conditions persist beyond this time, clients are at grave risk for acute tubular necrosis (ATN) and renal failure.

CENTRAL NERVOUS SYSTEM MANIFESTATIONS. Clients in hypovolemic shock are thirsty. This sensation is caused by stimulation of the osmoreceptors in the brain in response to decreased blood volume. The nurse assesses the client’s level of consciousness (LOC) and orientation to person, time, and place. Most causes of hypovolemic shock do not interfere with the transmission of nerve impulses. The central nervous system manifestations of hypovolemic shock are instead associated with cerebral hypoxia. In the initial and nonprogressive stages, clients may be restless or agitated and may be anxious or have a feeling of impending doom that has no obvious cause. As hypoxia progresses, clients become confused and lethargic. Lethargy progresses to somnolence and loss of consciousness as cerebral hypoxia worsens.

MUSCULOSKELETAL MANIFESTATIONS. Tissue hypoxia, anaerobic metabolism, and lactic acidosis cause weakness and pain in skeletal muscle. This weakness is generalized and has no specific pattern. The electrolyte disturbances in the progressive and refractory stages of shock worsen muscle weakness by interfering with action potentials. In this situation, deep tendon reflexes are decreased or absent. The nurse assesses muscle strength by having the client squeeze the nurse’s hand and try to keep the arms flexed while the nurse pulls downward on the lower arms. Deep tendon reflexes are assessed by lightly tapping the patellar tendons and Achilles tendons with a reflex hammer and observing the degree of reflexive movement.  

PSYCHOSOCIAL ASSESSMENT Changes in mental status and behavior may be early signs of hypovolemic shock. The nurse observes the client closely and documents behavior. The nurse assesses current mental status by evaluating LOC and noting whether the client is asleep or awake. If the client is asleep, the nurse attempts to awaken him or her and documents how easily he or she is aroused. If the client is awake, the nurse establishes whether he or she is oriented to person, time, and place.

Questions that can be answered with a “yes” or a “no” response are avoided. The following points are considered during evaluation:

• Is it necessary to repeat questions to obtain a response?

 • Does the response answer the question asked?

• Does the client have difficulty making word choices?

• Is the client irritated or upset by the questions?

• Can the client concentrate on a question long enough to answer appropriately, or is attention span limited?

If possible, the nurse questions family members or a significant other to determine whether the client’s behavior and mental status are typical.

LABORATORY ASSESSMENT Although no single laboratory finding confirms or rules out the presence of shock, changes in laboratory data may support the diagnosis of hypovolemic shock. (Chart 37-2 lists the common laboratory findings associated with hypovolemic shock.)

As shock progresses, arterial blood gas values become abnormal. The pH usually decreases, the partial pressure of arterial oxygen (Pao2) decreases, and the partial pressure of arterial carbon dioxide (Paco2) increases. Changes in other laboratory values may be associated with specific causes of hypovolemic shock. Hematocrit and hemoglobin concentrations decrease if hypovolemic shock is caused by hemorrhage. When hypovolemic shock is the result of dehydration or a fluid shift, hematocrit and hemoglobin values are elevated.

Interventions Interventions for clients in hypovolemic shock are focused on reversing the shock, restoring fluid volume, and preventing ischemic complications through supportive and drug therapies. Surgery may be necessary to correct the underlying problem leading to hypovolemic shock. Chart 37-3 summarizes best practices for clients in hypovolemic shock. Chart 37-4 lists selected interventions based on the Nursing Interventions Classification (NIC) for clients with hypovolemic shock.

 

NONSURGICAL MANAGEMENT. The goals of intervention are to maintain tissue oxygenation, increase body fluid compartment volumes to normal ranges, and support operating compensatory mechanisms. Oxygen therapy, intravenous (IV) therapy, fluid replacement therapy, and drug therapies are the management choices for this problem.

OXYGEN THERAPY. Oxygen therapy is useful whenever shock is present. Oxygen can be administered by mask, hood, nasal cannula, nasopharyngeal tube, endotracheal tube, and tracheostomy tube. Oxygen is administered in liters per minute (for administration via cannula) or concentration by percentage (for administration by mask), as specified by the health care provider’s order.

INTRAVENOUS THERAPY. Colloids and crystalloids are the two types of fluids commonly used for volume replacement during hemorrhagic hypovolemia. IV colloid solutions are used to restore plasma volume and colloidal osmotic pressure and contain large molecules (usually proteins or starches). IV crystalloid solutions are given for fluid and electrolyte replacement and contaionprotein substances (e.g., minerals, salts, and sugars). A current controversy involves the infusion rate of fluids when hypovolemia is a result of hemorrhage that has not yet been controlled. A consideration is that the rapid infusion of large-volume IV fluids can increase blood pressure and may actually increase the rate of blood loss (see the Evidence-Based Practice for Nursing box on p. 781).

Colloid Fluid Replacement. Protein-containing colloid fluids are good for restoring vascular osmotic pressure and fluid volume. Blood and blood products are often used for this purpose and are the treatment of choice for hypovolemia caused by blood loss. These products include whole blood, packed red blood cells, plasma, plasma fractions, and synthetic plasma expanders. Whole blood and packed red blood cells increase hematocrit and hemoglobin concentrations as well as vascular fluid volume. Whole blood is used to replace large volumes of blood loss because it provides increased intravascular volume while improving the oxygen-carrying capacity of the blood. Packed red cells are given for moderate blood loss because they replenish the red blood cell deficit and improve oxygencarrying capacity without adding excessive fluid volume. Chapter 40 discusses nursing care issues in blood and blood product administration. Human plasma, an acellular blood product containing some clotting factors, is given to correct plasma deficits and restore osmotic pressure when hematocrit and hemoglobin levels are withiormal ranges. Plasma protein fractions (e.g., Plasmanate) and synthetic plasma expanders (e.g., hetastarch [hydroxyethyl starch, Hespan]) increase plasma volume and are often used as early treatment for hypovolemic shock before a cause has been established.

Crystalloid Fluid Replacement. Crystalloid solutions are given to help establish and maintain an adequate fluid and electrolyte balance. Two common crystalloid solutions are Ringer’s lactate and normal saline. Ringer’s lactate contains physiologic concentrations of sodium, chloride, calcium, potassium, and lactate dissolved in water. This isotonic solution is a good volume expander, and the lactate is a buffer in the presence of acidosis. Normal saline (0.9% sodium chloride in water) is a fluid replacement used to increase plasma volume when there has beeo loss of red blood cells.

DRUG THERAPY. Medications may be necessary if the volume deficit is severe and the client does not respond sufficiently to the replacement of fluid volume and blood products. The actions of drugs for shock increase venous return, improve cardiac contractility, or ensure adequate cardiac perfusion through dilation of the coronary vessels. Chart 37-5 lists the drugs commonly used to treat hypovolemic shock.

Vasoconstricting Agents. Many drugs stimulate venous return by causing vasoconstriction and decreasing venous pooling of blood. These actions increase cardiac output and mean arterial pressure (MAP), which helps to improve tissue perfusion and oxygenation. Examples of such agents include dopamine (Intropin, Reviminc) and norepinephrine (Levophed). Most of these drugs produce serious side effects, and their dosages must be carefully calculated on the basis of the client’s size and degree of response (see Chart 37-5).

Agents Enhancing Myocardial Contractility. Some drugs directly stimulate adrenergic receptor sites on the heart muscle (especially beta, receptors) and increase the contraction of the cardiac muscle cells. Other agents enhance cardiac contractility—they slow heart rate by altering electrical conduction and allowing the left ventricle a longer filling time. When filling time is increased, more blood enters the left ventricle and stretches the muscle fibers. Thus greater recoil is achieved, and more blood leaves the left ventricle during contraction. Some of these drugs also stimulate the ventricles. Agents with these types of actions include digoxin (Lanoxin) and dobutamine (Dobutrex).

Agents Enhancing Myocardial Perfusion. The treatment of shock includes giving agents that cause systemic vasoconstriction to help enhance venous return and increase MAP. It is important to ensure that the heart is well perfused so that aerobic metabolism is maintained in the cardiac cells and maximum contractility can be achieved. Agents that dilate coronary blood vessels while causing minimal systemic vasodilation are used for this purpose. A common agent with this action is sodium nitroprusside (Nitropress, Nipride). Care is taken because higher dosages can cause some systemic vasodilation and increase shock.

MONITORING. A major nursing responsibility in caring for the client in hypovolemic shock is monitoring his or her vital signs and level of consciousness (LOC).

On the acute nursing unit, the nurse monitors the client’s:

Ø Pulse

Ø Blood pressure

Ø Pulse pressure

Ø Central venous pressure

Ø Respiratory rate

Ø Skin and mucosal color

Ø Oxygen saturation

These parameters are assessed at least every 15 minutes until the shock is under control and the client’s condition improves. More extensive monitoring of cardiac output (hemodynamic monitoring) occurs in critical care settings and includes intra-arterial monitoring, mixed venous oxygen saturation (Svo2), and pulmonary artery wedge pressures. Clients in shock are transported to a critical care unit if they require more invasive monitoring such as central venous pressure (CVP), pulmonary artery pressure (PAP), and pulmonary artery wedge pressure (PAWP). Table 37-6 compares the changes in hemodynamic patterns seen with different types of shock.

Insertion of a CVP catheter allows pressure to be monitored in the client’s right atrium or superior vena cava while providing venous access. Changes in CVP reflect hypovolemic shock. As circulating volume decreases, the amount of blood returning to the right atrium also decreases, causing the CVP to decrease from baseline levels. Intra-arterial catheter placement provides a means of monitoring blood pressure continuously and serves as an access for arterial blood sampling. Intra-arterial catheters are inserted into an artery (radial, brachial, femoral, or dorsalis pedis). The arterial catheter is attached to pressure tubing and a transducer. The transducer converts pressure in the artery (mechanical energy) into an electrical signal that is expressed as a visible waveform on an oscilloscope, and a digital numeric value is displayed.

SURGICAL MANAGEMENT. The nurse monitors fluid loss and uses the nonsurgical interventions described on pp. 779-781 to stabilize the client’s hemodynamic status. After a cause has been established, surgical intervention may be necessary to correct the underlying problem. Such interventions include vascular repair or revision, surgical hemostasis of major wounds, closure of bleeding ulcers, and chemical scarring (chemosclerosis) of varicosities.

COLLABORATIVE MANAGEMENT: SEPSIS-INDUCED DISTRIBUTIVE SHOCK (SEPTIC SHOCK)

Assessment Distributive shock caused by sepsis does not resemble other types of shock in that it has two distinctive phases (Figure 37-2).

The first phase is relatively long, often lasting from hours to a day or longer. The clinical manifestations during this phase are subtle. The chance for recovery is good when the client is recognized as being in the first phase of septic shock and the appropriate interventions are made. The second phase of septic shock has a sudden onset and a rapid downhill course. If septic shock progresses without intervention to the second phase, chances for recovery are slim. Identification of the first phase of sepsis-induced distributive shock can make the greatest difference in survival.

HISTORY The nurse collects data about risk factors and causative factors related to septic shock. Age is important because sepsis can develop more easily among older, debilitated people with any degree of immunosuppression. Chart 37-6 lists some of the factors that increase the older adult’s risk for shock.

 Clients are asked specific questions about recent illness, trauma, or procedures or chronic conditions that may lead to sepsis and distributive shock. The use of some medications may directly cause changes leading to shock. A medication regimen may also indicate a disease or problem that can contribute to septic shock. Such medications include aspirin and aspirin-containing drugs, antibiotics, and chemotherapeutic agents.

PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS Many of the clinical manifestations of the first phase are unique to septic shock and are often opposite from those associated with all other types of shock. Chart 37-7 summarizes the clinical manifestations of the first (hyperdynamic) phase of septic shock. These findings result from the body’s reaction to endotoxins and affect the cardiovascular, integumentary, pulmonary, immune, and hematologic systems.

CARDIOVASCULAR MANIFESTATIONS. Endotoxins in the blood interact with white blood cells and blood vessel walls to trigger an inflammatory reaction. Some endotoxins ap- pear to stimulate the heart muscle directly. As a result, cardiac output actually increases during the first phase of septic shock.

This phase is hyperdynamic and also may be called the highoutput or warm-shock phase. Increased cardiac output is reflected by tachycardia, increased stroke volume, a normal-to-elevated systolic blood pressure, and a normal CVP. Increased cardiac output and vasodilation cause good perfusion of the skin so that it appears normal in color with pink mucous membranes and may feel warm to the touch. This situation is temporary, and eventually the cardiac output greatly diminishes in clients in septic shock. As septic shock progresses, disseminated intravascular coagulation (DIC) may occur. The endotoxins and inflammatory reactions stimulate the activation of complement. These actions cause thousands of small clots to form in the tiny capillaries of vascular organs (e.g., liver, kidney, brain, spleen, and heart). These small clots interfere with oxygenation in those organs, causing hypoxia and ischemia and making overall metabolism anaerobic. This enormous number of small clots uses clotting factors and fibrinogen faster than they can be regenerated by the liver, which makes clients much more susceptible to hemorrhage. These occurrences mark the beginning of the second phase of septic shock. Because some of the blood has already clotted, most of the clotting factors are gone, and the blood vessels are dilated. Clients are hypovolemic in this phase of septic shock. Cardiac output, systolic blood pressure, and pulse pressure decrease dramatically.

This phase is called the hypodynamic, lowoutput, or cold-shock phase of septic shock. The clinical manifestations of this phase resemble those of the later stages of all forms of shock.

RESPIRATORY MANIFESTATIONS. In the hyperdynamic phase of septic shock, respiratory rate and depth are increased. Clients often experience a respiratory alkalosis. When septic shock progresses to the hypodynamic phase, the possible life-threatening pulmonary complication of acute respiratory distress syndrome (ARDS) may occur. Although this complication has many causes, ARDS in cases of sepsis is thought to be related to the formation of oxygen free radicals, which damage the pulmonary cells. Oxygen free radicals can form as a result of oxygen therapy and in response to cellular destruction and the subsequent release of oxidizing enzymes. The presence of ARDS in a client with septic shock is an ominous clinical sign and is associated with a high mortality rate.

INTEGUMENTARY MANIFESTATIONS. Clients in the hyperdynamic phase of septic distributive shock often are not recognized as having a problem. The appearance of the skin and mucous membranes leads health care professionals to believe that circulation is unimpaired. Clients feel warm to the touch, and their lips and mucous membranes appear well oxygenated. When septic shock progresses so that circulation is compromised in the hypodynamic phase, the skin is cool and clammy, and pallor or cyanosis is present. In clients with DIC, petechiae and ecchymoses can occur anywhere. Blood may ooze from the gums, other mucous membranes, and venipuncture sites, as well as around IV catheters.

PSYCHOSOCIAL ASSESSMENT The indicator that all is not well with clients at the beginning of septic shock is often a change in affect or behavior. The nurse compares the client’s presenting behavior, verbal responses, and general affect with those assessed earlier in the day or the day before and notes changes. Clients may seem just slightly different in their reactions to greetings, comments, or jokes. They may be less patient than usual or act restless or fidgety. They may verbalize feelings such as, “I feel as if something is wrong, but I don’t know what.If this behavior represents a change from prior assessments, the nurse always considers the possibility of sepsis and shock.

LABORATORY ASSESSMENT The presence of bacteria in the blood and other extracellular fluids supports the diagnosis of sepsis. The nurse obtains specimens of urine, blood, sputum, and any drainage for culture to identify the causative organisms for both diagnostic and therapeutic purposes. Other abnormal laboratory findings associated with septic shock include changes in the white blood cell count; the differential leukocyte count may demonstrate a left shift (see Chapter 20). Changes in hematocrit and hemoglobin levels usually are not evident until late in septic shock, when the client is hemorrhaging. At that point, the hematocrit and hemoglobin levels, fibrinogen levels, and platelet count are low

 Analysis A common collaborative problem for clients with septic shock is Potential for Multiple Organ Dysfunction Syndrome (MODS).

Planning and Implementation

PLANNING: EXPECTED OUTCOMES. The client in septic shock is expected to have normal arterial blood gases, maintain a urine output of at least 20 mL/hr, and have a mean arterial blood pressure within 10 mm Hg of baseline.

INTERVENTIONS. Interventions for the client experiencing septic shock focus on correcting the conditions causing shock and on preventing complications. Chart 37-8 summarizes the best practices for clients experiencing septic shock. Control of fluid volume deficit associated with septic shock is accomplished through supportive and drug therapies. IV therapy is the same as for hypovolemic shock.

OXYGEN THERAPY. Oxygen therapy is useful whenever inadequate tissue perfusion and inadequate oxygenation are present, such as during distributive shock. Oxygen therapy for septic shock is administered in the same ways as for hypovolemic shock.

DRUG THERAPY. The same agents used to enhance cardiac output and restore vascular volume in hypovolemic shock are used for septic shock. A major focus is the administration of antibiotics to combat sepsis. In addition, agents to counteract disseminated intravascular coagulation (DIC) may be required. Septic shock and DIC have two distinctly different phases, and the drug therapies for each phase of septic shock are different. Drug therapy in the first phase is aimed at preventing coagulation and usually consists of heparin administration. Drug therapy in the second, late phase of septic shock is aimed at increasing the blood’s ability to clot and usually consists of the administration of clotting factors, plasma, platelets, or other blood products.

ANTIBIOTICS. Although sepsis and distributive shock can be caused by any microorganism, the most common agents are gram-negative bacteria. When blood cultures have identified specific bacteria, IV antibiotics with known activity against the bacteria are administered. Multiple agents with wide activity are prescribed when the causative agent is not known. A common “triple-antibiotic” regimen includes vancomycin, one of the aminoglycosides (e.g., amikacin, streptomycin, kanamycin, gentamicin), and a systemic penicillin or cephalosporin.

ANTIBODIES. Antibodies against the body’s mediators for inflammation are being tested for their effectiveness in septic shock. Antibodies have been developed against the different substances produced by white blood cells to stimulate the inflammatory response. The mediators thought to start the inflammatory responses in blood vessels and lead to the cascade of septic shock are interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor (TNF). This experimental therapy shows promise in reducing the extensive mortality associated with septic shock (Clochesy, 1996; Workman, 1995).

ANTICOAGULANTS. When clients are identified as being in the early phase of septic shock and are beginning to form numerous small clots, heparin is given to limit unnecessary clotting and to prevent the consumption of clotting factors.

CLOTTING FACTORS AND BLOOD PRODUCTS. When septic shock progresses to the point that small clots have formed to such an extent that the client no longer has sufficient clotting factors to prevent hemorrhage, clotting factors are given intravenously. These factors are obtained from pooled human serum. Infusing fresh frozen plasma also helps to replace clotting factors. In addition, platelets or other blood products may be needed.

PROVIDING A SAFE ENVIRONMENT. Primary prevention is possible for some types of shock by identifying clients at risk for conditions and complications leading to sepsis and preventing those complications. Strict adherence to aseptic technique during invasive procedures and during the manipulation of nonintact skin and mucous membranes in immunocompromised clients can help to prevent or limit sepsis and septic shock. Early detection of the clinical manifestations of shock is a major nursing responsibility. Because shock is a common complication of many conditions found in acute care settings, the nurse always considers the possibility of septic shock. For early detection, the nurse frequently assesses vital signs for specific changes from normal values or from baseline levels. After distributive shock is recognized, health care providers rapidly take action to halt or change the conditions contributing to shock, to support the physiologic compensatory mechanisms, and to prevent life-threatening complications.

Community-Based Care For most clients, shock is a complication of another condition and is resolved before they are discharged from the emergency department or acute care setting. Because more clients are receiving treatment on an outpatient basis and are being discharged earlier from acute care settings, more

HOME CARE MANAGEMENT The nurse or home care aide evaluates the home environment for safety regarding infection hazards. General cleanliness is noted, and particular attention is given to the kitchen and bathrooms. Chart 37-10 lists focused client and environmental assessment data to obtain during a home visit.

 Evaluation: Outcomes  The nurse evaluates the care of the client with sepsis-induced distributive shock. The expected outcomes are that the client:

• Maintains oxygen saturation (as measured by pulse oximetry) of at least 85%

• Maintains a urine output of at least 20 mL/hr Has arterial blood gas values within the normal range

• Has a mean arterial pressure within 10 mm Hg of baseline

• Does not experience multiple organ dysfunction syndrome (MODS)

• Correctly states measures to reduce the risk for sepsis

 

 

Nursing Diagnosis Risk for Shock – NIC NOC

 

Shock is a life-threatening condition that occurs when the body is not getting enough blood flow. This can damage multiple organs. Shock requires immediate medical treatment and can get worse very rapidly.

 

A person in shock has extremely low blood pressure. Depending on the specific cause and type of shock, symptoms will include one or more of the following:

Anxiety or agitation/restlessness

Bluish lips and fingernails

Chest pain

Confusion

Dizziness, lightheadedness, or faintness

Pale, cool, clammy skin

Low or no urine output

Profuse sweating, moist skin

Rapid but weak pulse

Shallow breathing

Unconsciousness

 

NIC: Shock Management

Monitor vital signs, orthostatic blood pressure, mental status, and urine output.

Monitor laboratory values ​​as evidence of tissue perfusion inadekuat (eg increased levels of lactic acid, decreased arterial pH).

Give crystalloid IV fluids as needed (NaCl 0.9%, RL; D5% W)

Give vasoactive medications.

Provide oxygen therapy and mechanical ventilation

Monitor hemodynamic trend.

Monitor fetal heart rate (bradycardia if HR <110 beats / min) or (tachycardia when HR> 160 beats per minute) lasting longer than 10 minutes.

Take blood samples for blood gas analysis and the examination of tissue oxygenation monitor.

Get patency of venous access.

Give fluids to maintain blood pressure or cardiac output.

Monitor critical oxygen delivery to the tissues (SaPO2, hemoglobin level, cardiac output).

Record in the event of bradycardia or decreased blood pressure, or abnormal low systemic arterial pressure as pale, cyanosis or diaphoresis.

Monitor signs and symptoms of respiratory failure (low PaO2, PCO2 increased, paralysis of respiratory muscles)

Monitor blood glucose levels and handle if any abnormality.

Monitor coagulation and complete blood count with WBC differential.

Monitor fluid status include intake and output.

Monitor renal function.

Do a urinary catheter.

Perform installation of NGT and monitor gastric residual.

Position the patient to optimize perfusion.

Provide emotional support to the family.

Provide a realistic hope to the family.

NIC: Shock Management: Cardiac

Auscultation of lung sounds to determine the presence of breath sounds crackles and other extras.

Note the signs and symptoms of decreased cardiac output.

Monitor symptoms of inadequate coronary artery perfusion (eg ST wave changes on EKG or angina).

Monitor the value of coagulation (PT, PTT, fibrinogen, platelets).

Pertahanakan fluid balance by providing fluid and diuretic.

Give positive inotropic drugs or contractility.

Increase preload optimal by improving contractility while minimizing heart failure (giving nitroglycerin).

Increase afterload reduction (giving vasodilators or intraaortic balloon pumping).

Increase coronary artery perfusion (to maintain MAP> 60 mmHg and controls tachycardia).

 

NIC: Shock Management: Vasogenic

Perform wound care to prevent infection and promote healing.

Give antibiotics as scheduled.

Give antihistamines as instructed.

Give epinephrine in an emergency in the event of anaphylaxis.

Provide anti-inflammatory medications as instructed.

Eliminate neurogenic stimulus that causes a reaction.

Treat hyperthermia with antipyretic drugs, air mattress or sponge bath.

Prevent and control shivering with drug delivery and cover extremities.

 

NIC: Shock Management: Volume

Monitor signs and symptoms of persistent bleeding.

Record the value of Hb and HT before and after blood loss.

Give blood products according to instructions (platelets or fresh frozen plasma).

Prevent blood loss by holding the bleeding.

 

NIC: Shock Prevention

Note the bruising, petechiae and conditions of the mucous membrane.

Note color, amount, and frequency of defecation, vomiting and gastric residue.

Urine test to determine the presence of glucose, blood or protein.

Monitor presence of abdominal pain and girth.

Monitor signs and symptoms of ascites.

Monitor initial response to fluid loss: increased HR, decreased blood pressure, orthostatic hypotension, decreased urine output, narrow pulse pressure, decreased capillary refill, skin pale and cold, and diaphoresis.

Monitor early signs of shock cardiogenik: the amount of urine output and cardiac output were decreased, increased SVR and PCWP, pulmonary crackles, S3 and S4 heart sounds, tachycardia.

Monitor early signs of an allergic reaction: wheezing, hoarseness (coarse breath sounds and panting), dyspnea, rash, angioedema, feeling unwell on the gastrointestinal tract, anxiety and restlessness.

Monitor early signs of septic shock: skin warm, dry, shiny, increased cardiac output and temperature.

Maintain airway patency.

Give antiarrhythmic agent.

Give diuretics as instructed.

Give bronchodilator as needed.

 

ACUTE CORONARY SYNDROMES

Unstable angina is chest pain or discomfort that occurs at rest or with minimal exertion and causes marked limitation of activity. An increase in the number of attacks and an increase in the intensity of the pain characterize unstable angina. The pain may last longer than 15 minutes or be poorly relieved by rest or nitroglycerin. Unstable angina describes a broad spectrum of disorders, including new-onset angina, variant (Prinzmetal’s) angina, preinfarction angina, and crescendo angina. A newer way to describe the disorders that make up unstable angina, subendocardial MI, and MI is to call them acute coronary syndromes. In acute coronary syndromes, it is believed that the atherosclerotic plaque in the coronary artery ruptures, resulting in platelet aggregation, thrombus formation, and vasoconstriction. The amount of disruption of the atherosclerotic plaque determines the degree of obstruction of the coronary artery and the specific disease process (unstable angina, subendocardial MI, or MI). Between 10% and 30% of clients with unstable angina progress to having an MI in 1 year, and 29% die from MI in 5 years.

MYOCARDIAL INFARCTION

Myocardial infarction (MI) occurs when myocardial tissue is abruptly and severely deprived of oxygen. When blood flow is acutely reduced by 80% to 90%, ischemia develops. Ischemia can lead to necrosis of myocardial tissue if blood flow is not restored. Most Mis are the result of atherosclerosis of a coronary artery, rupture of the plaque, subsequent thrombosis, and occlusion of blood flow. However, other factors may be implicated, such as coronary artery spasm, platelet aggregation, and emboli from mural thrombi (thrombi lining the walls of the cardiac chambers). Mis often begin with infarction (necrosis) of the subendocardial layer of cardiac muscle. This layer has the longest myofibrils in the heart, the greatest oxygen demand, and the poorest oxygen supply.

Around the initial area of infarction in the subendocardium are two zones: (1) the zone of injury, tissue that is injured but not necrotic, and (2) the zone of ischemia, tissue that is oxygen deprived. This pattern is illustrated in Figure 38-2.

PROCESS OF INFARCTION. Infarction is a dynamic process that does not occur instantly; rather, it evolves over a period of several hours. Hypoxia from ischemia may lead to local vasodilation of blood vessels and acidosis. Imbalances of potassium, calcium, and magnesium, as well as acidosis at the cellular level, may lead to suppression of normal conduction and contractile functions. Automaticity and ectopy are enhanced. Catecholamines released in response to hypoxia and pain may increase the heart’s rate and force of contraction. These factors increase oxygen requirements in tissue that is already oxygen deprived. The area of infarction may extend into the zones of injury and ischemia. The actual extent of the zone of infarction depends on three factors: collateral circulation, anaerobic metabolism, and workload demands on the myocardium. The infarction may involve only the subendocardium (called a subendocardial MI), or it may spread to the epi three layers are involved, the MI is termed transmural. Subendocardial Mis have less effect on wall motion and cardiac output than transmural infarctions do.

PHYSIOLOGIC RESPONSE TO THE INFARCTION. Obvious physical changes do not occur in the heart until 6 hours after the infarction, when the infarcted region appears blue and swollen. After 48 hours, the infarct turns gray with yellow streaks as neutrophils invade the tissue and begin to remove the necrotic cells. By 8 to 10 days after infarction, granulation tissue forms at the edges of the necrotic tissue. Over a 2- to 3-month period, the necrotic area eventually develops into a shrunken, thin, firm scar. Scar tissue permanently changes the size and shape of the entire left ventricle (ventricular remodeling). Remodeling may decrease left ventricular function, cause heart failure, and increase morbidity and mortality.

CLASSIFICATION OF MYOCARDIAL INFARCTION BY LOCATION. The client’s response to an MI also depends on which coronary artery or arteries were obstructed and which part of the left ventricle wall was damaged: anterior, lateral, septal, inferior, or posterior.

Figure 38-3 details the major coronary arteries, and Table 38-1 describes the structures they perfuse. Clients with obstruction of the left anterior descending (LAD) artery usually have anterior or septal Mis because the LAD artery perfuses the anterior wall and most of the septal wall of the left ventricle. Anterior wall Mis account for 25% of all Mis and, at 25%, have the highest mortality rate. Clients with anterior Mis are most likely to experience left ventricular heart failure and ventricular dysrhythmias, because a large segment of the left ventricle wall may have been damaged. The circumflex artery supplies the lateral wall of the left ventricle and possibly portions of the posterior wall or the sinoatrial (SA) and atrioventricular (AV) nodes. Clients with obstruction of the circumflex artery may experience a posterior wall MI (2% of Mis) or a lateral wall MI (3% of Mis) and sinus dysrhythmias. In most people, the right coronary artery perfuses the SA and AV nodes, as well as the inferior or diaphragmatic portion of the left ventricle. Clients with obstruction of the right coronary artery often have inferior Mis. Inferior wall Mis account for approximately 17% of all Mis and have a mortality rate of about 10%. Clients are most likely to experience bradydysrhythmias or AV conduction defects, especially transient second-degree heart blocks. About one third of clients with inferior Mis have a right ventricular MI and right ventricular failure (Braunwald, 1998).

Etiology Atherosclerosis is the primary factor in the development of coronary artery disease (CAD). Numerous risk factors contribute to atherosclerosis (see Chapter 36). Risk factors are classified as nonmodifiable and modifiable.

NONMODIFIABLE RISK FACTORS Nonmodifiable risk factors are personal elements that cannot be altered or controlled. These risk factors, which interact with each other, include age, gender, family history, and ethnic background. The risk of CAD increases with age; 55% of clients who experience a myocardial infarction (MI) are 65 years of age or older. Premenopausal women have a lower incidence of MI than men do. However, for postmenopausal women in their 70s, the incidence of MI equals that of men. Family history is also a risk factor; people whose parents had CAD are more susceptible.

MODIFIABLE RISK FACTORS Modifiable risk factors include elevated serum cholesterol levels, cigarette smoking, hypertension, impaired glucose tolerance, obesity, physical inactivity, and stress.

ELEVATED SERUM CHOLESTEROL LEVELS. The risk of CAD rises as serum cholesterol levels increase. The American Heart Association (AHA) estimates that 52% of Americans have serum cholesterol levels greater than 200 mg/dL and that 20% have levels above 240 mg/dL, putting them at risk for CAD. A 1% reduction in serum cholesterol has been associated with a 2% reduction in CAD. Elevated levels of low-density lipoprotein (LDL) combined with low levels of high-density lipoprotein (HDL) increase the risk further. HDL levels less than 37 mg/dL for men and 47 mg/dL for women are considered to be risk factors for CAD. HDL levels greater than 53 mg/dL for men and 67 mg/dL for women decrease the risk of CAD.

CIGARETTE SMOKING. Cigarette smokers have twice the risk of MI that nonsmokers have and two to four times the risk of sudden cardiac death (Andrews, 1998). An estimated 26.7% of men and 22.8% of women in the United States are smokers (AHA, 1998). Reducing the tar and nicotine content of the cigarettes smoked does not reduce the risk of CAD.

PHYSICAL INACTIVITY. Physical inactivity may be the most important risk factor for the general population because between 40% and 60% of Americans are sedentary. Regular physical activity helps maintain body weight and muscle mass while optimizing blood pressure and lipid values. heart disease. Some evidence indicates that job stress may be associated with left ventricular hypertrophy. Type A behavior, when described as hostility in response to a stressful event, has been associated with a twofold increase in angina.

OTHER FACTORS. Hypertension increases the workload of the heart, which increases the risk of MI. Impaired glucose tolerance (e.g., diabetes) seriously increases the risks, especially in women. Obesity is associated with increased serum cholesterol, elevated blood pressure, and abnormal glucose tolerance. It may also have an independent effect on the risk of CAD. The distribution of adipose tissue seems to be important; women with fat deposited about the waist rather than the hips often have unfavorable lipid profiles and higher rates of CAD. Elevated levels of serum homocysteine are believed by some researchers to be associated with an increased risk of CAD. Clients with multiple risk factors (hypertension, obesity, smoking, high cholesterol levels, and diabetes) have several times the risk of CAD as those without these characteristics. Although many factors place a client at risk for heart disease, there are well-documented, effective ways of promoting cardiovascular health. Some of these interventions are described in Chart 38-1.

 Incidence/Prevalence Approximately 1,100,000 people experience Mis each year in the United States, and about one third of these people die (AHA, 1998). MI is the single largest cause of death for both men and women. Approximately half of the deaths from MI occur in the first hour before reaching the hospital. Approximately 350,000 people experience angina for the first time each year. The AHA estimates that more than 6 million people who have experienced angina or an MI are still living (AHA, 1998). The estimated cost of caring for people with CAD is slightly less than $150 billion yearly.

COLLABORATIVE MANAGEMENT

Assessment

HISTORY If chest discomfort is present at the time of the interview, the nurse delays collection of historical data until interventions for pain, vital sign instability, and dysrhythmias are initiated and the discomfort resolves. The nurse obtains information about how the client has managed the current episode of chest discomfort and which medications he or she is taking. When the client is pain free, information about family history and modifiable risk factors, including eating habits, lifestyle, and physical activity levels, is obtained.

PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS The nurse asks clients to describe the immediate concern. The presence of chest, epigastric, jaw, back, or arm discomfort is noted. The client is asked to rate the discomfort on a scale of 0 to 10, with 10 being the highest level of discomfort. Clients often describe the discomfort as tightness, a burning sensa tion, pressure, or indigestion. The nurse asks them what they have already done to try to relieve the pain. 

PAIN ASSESSMENT. The nurse rapidly yet completely assesses the client with ongoing chest pain. Because chest discomfort may occur from a variety of causes and only 30% of people experiencing chest pain are having a myocardial infarction (MI), it is important to differentiate among the types of chest pain and to identify the source (see Table 33-1).

Both the physician and the nurse may question the client to determine the characteristics of the discomfort. Appropriate questions for the nurse to ask concerning the discomfort include onset, location, radiation, intensity, duration, and precipitating and relieving factors. Chart 38-2 compares and contrasts anginal and infarction pain.

Because anginal pain is ischemic pain, it usually improves when the disparity between oxygen supply and demand is resolved. For example, rest reduces tissue demands, and nitroglycerin improves oxygen supply. Discomfort from an MI does not usually resolve with such simple measures. The nurse also notes the presence of any associated symptoms, including nausea, vomiting, diaphoresis, dizziness, weakness, palpitations, and shortness of breath.

CARDIOVASCULAR ASSESSMENT. The nurse immediately obtains a blood pressure measurement, determines the heart rate, interprets the cardiac rhythm, and assesses for dysrhythmias. Sinus tachycardia with premature ventricular contractions (PVCs) frequently occurs in the first few hours after an MI. If an intravenous (IV) access is available, the nurse ensures that it is patent, because the client will most likely receive IV fluids and medications. If an access is not available, one or preferably two IV accesses are initiated. The nurse may administer oxygen, titrating the fraction of inspired oxygen (Fio2) to the arterial oxygen saturation (Sao2) according to protocols or the physician’s order. Next, the nurse assesses distal peripheral pulses and skin temperature. The skin should be warm, with all pulses palpable. In the client with unstable angina or MI, poor cardiac output may be manifested by cool, diaphoretic skin and diminished or absent pulses. The nurse auscultates for an S3 gallop, which often indicates heart failure, a serious and common complication of MI. The nurse also assesses the respiratory rate and breath sounds for signs of heart failure. An increased respiratory rate is common because of anxiety and pain, but crackles or wheezes may indicate heart failure. Auscultation of an S4 heart sound is a common finding in the client who has had a previous MI or hypertension. The client with MI may experience a temperature elevation for several days after infarction. Temperatures as high as 102°F (38.9° C) may occur in response to myocardial necrosis.

PSYCHOSOCIAL ASSESSMENT Denial is a common early reaction to chest discomfort associated with angina or MI. On average, the client with an acute MI waits more than 2 hours before seeking medical attention. Often the client rationalizes that symptoms are due to indigestion or overexertion. In some situations, denial is a normal part of adapting to a stressful event. However, denial that interferes with identification of a symptom, such as chest discomfort, can be harmful. The nurse explains the significance of reporting any discomfort, emphasizing that health care provisions attempt to relieve the discomfort immediately. Fear, anxiety, and anger are other common reactions of clients and families. Nursing assessment focuses on assisting the client and family members in identifying these feelings. The nurse allows the client and family time to explain their understanding of the event and clarifies any misconceptions.

 LABORATORY ASSESSMENT

SERUM MARKERS OF MYOCARDIAL DAMAGE: CARDIAC ENZYMES. An MI can be confirmed by abnormally high blood levels of cardiac enzymes and isoenzymes. Of all the cardiac enzymes, creatine kinase (CK) is considered the most sensitive and reliable indicator for diagnosis of MI. Total CK levels rise within 3 hours after the onset of chest pain and peak within 24 hours after damage and death of cardiac tissue. Because total CK also rises with brain or muscle injury, an elevation is not specific for myocardial damage. When cardiac muscle tissue dies, the CK specific to myocardial cells (CK-MB isoenzyme) enters the bloodstream (serum does not normally contain CK-MB isoenzyme). Peak elevation of CK-MB isoenzyme levels occurs approximately 12 to 24 hours after the onset of chest pain; levels return to normal 48 to 72 hours later. Confirmation of myocardial damage within 2 hours of emergency department admission is possible with the use of stat determinations of CK and CK subforms. These are gaining popularity as a result of the need to confirm or rule out MI rapidly. The physician may also use serum measurement of lactate dehydrogenase (LDH) to confirm MI. However, identification of LDH is not as reliable as that of CK-MB. LDH levels start to rise within 12 to 24 hours after an MI, peak between 48 and 72 hours, and fall to normal in 7 days. Thus they may be useful in diagnosing an MI in a client who has delayed seeking medical help for several days after the onset of chest discomfort. Serum levels of LDH, isoenzyme rise higher than serum levels of LDH2 in the presence of MI. Newer measurements for detection of cardiac damage, such as troponins T and I, are gaining in popularity for this purpose, since they are more sensitive and specific than LDH.

OTHER SERUM MARKERS OF MYOCARDIAL DAMAGE. Myoglobin is a heme protein found in both skeletal and cardiac muscle. It is released rapidly following myocardial damage and can be detected in the serum in 2 to 3 hours following an MI. Since myoglobin always elevates within 3 to 6 hours following an MI, if it has not increased by 6 hours, it can be determined that an MI has not occurred. Troponins T and I are basic components of the myocardium that are not found in significant levels in the blood of healthy adults. They begin to elevate 3 to 6 hours after an MI and remain elevated for 5 to 7 days. Elevation of troponin T is specific for acute coronary syndromes, identifying the development of unstable angina, subendocardial MI, or MI. Rapid bedside assays are becoming available for the measurement of troponins T and I. No laboratory test can confirm the diagnosis of stable angina. Serum enzyme determinations are not useful in assessing the presence of angina. However, serum markers of myocardial damage remaining withiormal limits are an indication that the client has not had an acute MI. The C-reactive protein (CRP) test is also helpful in determining whether the client has had an acute MI. The level of CRP (normal is 0) correlates with CK-MB levels, but CRP peaks several days later. Levels of CRP are not elevated in clients who have angina.

OTHER LABORATORY TESTS. The finding of an elevated white blood cell count (10,000 to 20,000 cells/mm3) helps in the diagnosis of MI. It typically appears on the second day and lasts up to a week.

 RADIOGRAPHIC ASSESSMENT Unless there is associated cardiac dysfunction (e.g., valvular disease) or heart failure, a chest x-ray film is not diagnostic for angina or MI.

OTHER DIAGNOSTIC ASSESSMENT

ELECTROCARDIOGRAPHY. Twelve-lead electrocardiograms (ECGs) allow the health care provider to examine the heart from varying perspectives and note both the occurrence and the location of ischemia (angina) or necrosis (infarction). Ischemic myocardium does not repolarize normally. Thus 12-lead ECGs obtained during an anginal episode reveal ST depression, T-wave inversion, or both. Variant angina, caused by coronary spasm, usually causes elevation of the ST segment during anginal attacks. These ST- and T-wave changes usually subside when the ischemia is resolved and the pain is relieved. However, the T wave may remain flat or inverted for a period of time. If the client is not experiencing angina at the moment of the test, the ECG for the client with angina is usually normal. When infarction occurs, three ECG changes are usually observed: ST-segment elevation, T-wave inversion, and an abnormal Q wave (wider than 0.04 seconds or more than one third the height of the QRS complex). Figure 38-2 displays the typical ECG changes seen in MI. The Q wave develops because necrotic cells do not conduct electrical stimuli. Hours to days after the MI, the STsegment and T-wave changes will return to normal, but the Q wave usually remains permanently. By identifying the lead in which the ECG changes are occurring, the health care provider can identify the extent and location of the infarction.

STRESS TEST. After the acute stages of an anginal episode or MI, the health care provider often orders an exercise tolerance test (stress test) to assess for ECG changes consistent with ischemia, evaluate medical therapy, and identify clients who might benefit from referral for invasive therapy.

SCANS. Thallium scans use radioisotope imaging to assess for ischemia or necrotic muscle tissue related to angina or MI. Areas of decreased or absent perfusion, referred to as cold spots, identify ischemia or infarction. Multigated acquisition (MUGA) scans may be used to evaluate left ventricular function.

CARDIAC CATHETERIZATION. This procedure may be performed to determine the extent and location of obstructions of the coronary arteries. Cardiac catheterization, the “gatekeeper” to invasive management, allows the cardiologist and cardiac surgeon to identify clients who might benefit from percutaneous transluminal angioplasty (PCTA) or coronary artery bypass grafting (CABG).

 Analysis The client with coronary artery disease (CAD) may have either angina or myocardial infarction (MI). If MI is suspected or cannot be completely ruled out, the client is admitted to a coronary or critical care unit for continuous monitoring.

COMMON NURSING DIAGNOSES AND COLLABORATIVE PROBLEMS

The following are commoursing diagnoses for clients with CAD:

1. Acute Pain related to imbalance between myocardial oxygen supply and demand

2. Ineffective Tissue Perfusion (Cardiopulmonary) related to interruption of blood flow

3. Activity Intolerance related to imbalance between oxygen supply and demand

4. Ineffective Coping related to effects of acute illness, major changes in lifestyle, or loss of control over a body part

For the client experiencing an MI, the following are the most important collaborative problems: 1. Potential for Dysrhythmias 2. Potential for Heart Failure 3. Potential for Recurrent Chest Discomfort and Extension of Injury

ADDITIONAL NURSING DIAGNOSES AND COLLABORATIVE PROBLEMS

In addition to the commoursing diagnoses and collaborative problems, clients with CAD may have one or more of the following: Fear related to threat of death

• Ineffective Sexuality Patterns related to pain and effects of illness

• Impaired Physical Mobility related to pain or fear of movement

Planning and Implementation

ACUTE PAIN

PLANNING: EXPECTED OUTCOMES.

The client with CAD is expected to state that chest discomfort is alleviated.

INTERVENTIONS. The objective of management is to eliminate chest discomfort by providing pain relief, decreasing myocardial oxygen demand, and increasing myocardial oxygen supply.

PAIN MANAGEMENT. The nurse evaluates the chest pain, obtains vital signs, ensures the patency of IV accesses, and notifies the physician of the client’s condition. Chart 38-3 summarizes appropriate interventions for the client with chest discomfort.

DRUG THERAPY. If appropriate, the nurse may administer the prescribed pain medication. One of the initial medications prescribed for chest pain is usually sublingual nitroglycerin (Chart 38-4). Aspirin 325 mg also may be administered orally (chewed) immediately if the client is believed to be experiencing an acute coronary syndrome.

Nitroglycerin. Nitroglycerin, a nitrate often referred to as “nitro,” increases collateral blood flow, redistributes blood flow toward the subendocardium, and causes dilation of the coronary arteries. The nurse instructs the client to hold the tablet under the tongue and provides 5 mL of water, if necessary, to allow the tablet to dissolve. Pain relief should begin within 1 or 2 minutes and be clearly evident in 3 to 5 minutes. After 5 minutes, the nurse rechecks the client’s pain intensity and vital signs. If the blood pressure is less than 100 mm Hg systolic or 25 mm Hg lower than the previous reading, the nurse lowers the head of the bed and notifies the physician. If the client is experiencing some but not complete relief and vital signs remain stable, another nitroglycerin tablet may be used. A total of 3 tablets may be administered in an attempt to relieve anginal pain. Angina usually responds to nitroglycerin. The client typically states that the pain is relieved or markedly diminished. When simple measures, such as taking three sublingual nitroglycerin tablets one after the other, do not relieve chest discomfort, the client may be experiencing an MI. The nurse should inform the physician immediately and prepare the client for transfer to a specialized unit where he or she can be closely monitored and appropriately managed. In a specialized unit the physician may prescribe IV nitroglycerin for management of the chest pain. The nurse begins the nitroglycerin infusion slowly, checking the blood pressure and pain level every 3 to 5 minutes. The nitroglycerin dose is increased until the pain is relieved, the blood pressure falls excessively, or the maximum prescribed dose is reached. The blood pressure is continuously monitored (Chart 38-5).

Morphine Sulfate. The physician may prescribe morphine sulfate (MS) to relieve chest discomfort that is unresponsive to nitroglycerin. Morphine relieves MI pain, decreases myocardial oxygen demand, and reduces circulating catecholamines. It is usually administered in 2- to 5-mg increments intravenously every 5 to 15 minutes until the maximum prescribed dose is reached or until the client experiences relief or signs of toxicity. Signs of morphine toxicity include respiratory depression, hypotension, and severe vomiting. The nurse monitors the client’s vital signs and cardiac rhythm every few minutes. These strategies are often enough to relieve the pain. If these methods are not adequate, additional interventions, identified later under Ineffective Tissue Perfusion (Cardiopulmonary), may be attempted.

OTHER INTERVENTIONS. Several interventions may assist in relieving chest pain. Supplemental oxygen may increase fore oxygen is often prescribed and administered at a flow of 2 to 4 L/min by nasal cannula titrated to maintain an arterial oxygen saturation (Sao2) greater than 92%. If the blood pressure is stable, the nurse may assist the client in assuming any position of comfort. Placing the client in semi-Fowler’s position often enhances comfort and tissue oxygenation. A quiet, calm environment and explanations of interventions often reduce anxiety and assist in relief of chest pain. When the pain has subsided and the client is stabilized, the physician may change the medication to an oral or topical nitrate. During administration of long-term oral and topical nitrates, a 12-hour nitrate-free period should be maintained to prevent tolerance. The client may complain initially of headache. The physician may prescribe acetaminophen (Tylenol, Exdol) to be taken before the nitrate to prevent some of this discomfort.

INEFFECTIVE TISSUE PERFUSION (CARDIOPULMONARY)

NOC PLANNING: EXPECTED OUTCOMES. The client with coronary artery disease (CAD) is expected to exhibit (1) relief of chest discomfort, (2) resolution of ST-segment and Twave changes, (3) sinus rhythm (or normal rhythm for the client) of approximately 60, and (4) blood acceptable range. pressure within

INTERVENTIONS. Because myocardial infarction (MI) is a dynamic process, restoration of perfusion to the injured area often reduces the size of the infarct and improves left ventricular function. Complete, sustained reperfusion of coronary arteries in the first few hours after an MI has decreased mortality in clients with MI.

THROMBOLYTIC THERAPY. Fibrinolytics are used to dissolve thrombi in the coronary arteries and restore myocardial blood flow. Examples of these agents, which target the fibrin component of the coronary thrombosis, include tissue plasminogen activator (t-PA, alteplase [Activase]), anisoylated plasminogen-streptokinase activator complex (APSAC), and reteplase (Retavase). The physician may order the administration of fibrinolytics intravenously or by the intracoronary route during cardiac catheterization. Thrombolytic agents are most effective when administered within the first 6 hours of the coronary event. Thrombolytics are underused nationwide in men and women, young and old. Thrombolytic therapy should be given in a unit where the client can be continuously monitored. It is indicated for clients who have chest pain of greater than 30 minutes’ duration that is unrelieved by nitroglycerin, with indications of transmural ischemia and injury as shown by the ECG. Contraindications include recent abdominal surgery or stroke, because bleeding may occur when fresh clots are lysed (broken down). Table 38-2 lists the current contraindications to thrombolytic therapy.

Before thrombolytic administration, the nurse may need to apply pressure dressings to IV puncture sites or wounds to limit bleeding. Clients who weigh less than 65 kg may need to have their dose of thrombolytic weight adjusted to lessen the likeli immediately reports any indications of bleeding to the physician.

After administration, the nurse observes for signs of bleeding by:

• Documenting the client’s neurologic status

• Observing all IV sites

• Monitoring clotting studies

• Observing for signs of internal bleeding (watching hemoglobin and hematocrit)

• Testing stools, urine, and emesis for occult blood

Some concerns in thrombolytic administration are associated with the specific agent. For example, streptokinase, a firstgeneration thrombolytic agent, is not fibrin specific; thus it may create systemic bleeding problems. Because it is a bacterial protein, streptokinase can cause a hypersensitivity reaction in the client who has had previous exposure. Therefore the nurse questions the client about streptococcal infections or doses of streptokinase within the past year. To prevent an allergic reaction, the physician may prescribe steroids or antihistamines before the administration of streptokinase. During administration, the nurse observes the client closely for hives and shivering, the most common responses. The half-life of the drug is 16 minutes. Second- and third-generation fibrinolytics include tissue plasminogen activator (t-PA, alteplase [Activase]), anisoylated plasminogen-streptokinase activator complex (APSAC; Eminase), reteplase (Retavase), and lanoteplase (n-PA). t-PA is fibrin specific, has a short half-life (3 to 5 minutes), and lacks antigenicity. Because some studies have associated t-PA with a more frequent occurrence of cerebrovascular bleeding, the nurse carefully documents neurologic findings. t-PA is also much more expensive than streptokinase. Reteplase can be given in two boluses V2 hour apart, need not be weight adjusted, and results in greater rates of reperfusion than t-PA. APSAC is a streptokinase derivative; it has a longer half-life (90 to 105 minutes) than streptokinase but has the same antigenic properties. Tenecteplase (TNKase) is the most recent fibrinolytic to be approved for use in clients with Mis. This drug appears to have some advantages over other fibrinolytics. First, it can be easily administered as a single bolus over 5 seconds. Tenecteplase also targets clots more specifically than other fibrinolytics, resulting in slightly less overall bleeding. However, bleeding is still possible, and nursing considerations are similar to the other fibrinolytics. Dosage is based on the client’s weight.

GLYCOPROTEIN IIB/IIIA INHIBITORS. Glycoprotein Ilb/IIIa inhibitors target the platelet component of the thrombus. Abciximab (ReoPro), eptifibatide (Integrilin), and tirofiban (Aggrastat) may be administered intravenously to prevent fibrmogen from attaching to activated platelets at the site of a thrombus. These medications have been used in acute coronary syndromes (especially unstable angina and non-Q-wave MI) during and before percutaneous transluminal coronary angioplasty (PTCA) to ensure patency of the newly opened artery and in conjunction with fibrinolytic agents following MI. If the GP Ilb/IIIa inhibitors are used with a fibrinolytic agent, then the dose of the thrombolytic should be reduced by 25% to 50% to decrease the likelihood of bleeding. Combining a GP Ila/IIIb inhibitor with a fibrinolytic agent following MI appears to improve coronary flow without increasing the risk of hemorrhagic events (Roberts, 1999). During the administration of GP Ila/IIIb inhibitors, the nurse assesses the client closely for indications of bleeding or hypersensitivity reactions. If either occurs, the health care provider is notified immediately regarding administration of the appropriate medications (e.g., antihistamines or corticosteroids) for a hypersensitivity response. For some clients experiencing an MI, primary PTCA may be used to reopen the thrombosed coronary artery. PTCA has been associated with excellent return of blood flow through the coronary artery when it can be performed within 70 minutes of the onset of chest discomfort by a highly experienced practitioner. However, most community hospitals are not capable of performing emergent PTCA. When primary PTCA is not available, the client with MI should receive immediate thrombolytic agents if he or she is an appropriate candidate. PTCA is described in detail later in this chapter.

IDENTIFICATION OF CORONARY ARTERY REPERFUSION. The nurse monitors the client for indications that the clot has been lysed and the artery reperfused. These indications include the following:

·        Abrupt cessation of chest pain

·        Sudden onset of ventricular dysrhythmias

·        Resolution of ST-segment depression

·        A peak at 12 hours of markers of myocardial damage

After clot lysis with thrombolytics, large amounts of thrombin are released into the system, increasing the risk of vessel reocclusion. To maintain the patency of the coronary artery after thrombolytic therapy, the physician usually prescribes aspirin and IV heparin. The nurse monitors the activated partial thromboplastin time (aPTT)—the usual appropriate range is V/2 to 2V2 times the control sample)—and maintains the heparin infusion for 3 to 5 days, as prescribed. Low-molecular weight heparin (enoxaparin) may be substituted for IV heparin.

DRUG THERAPY. Clients who have had an MI, whether receiving thrombolytics or not, should begin aspirin therapy unless contraindicated. They may receive a chewable aspirin immediately and then an enteric-coated aspirin (Ancasal, Ecotrin) 80 to 325 mg daily or every other day to prevent platelet aggregation at the site of the obstruction. Beta-adrenergic blocking agents (e.g., metoprolol [Lopressor, Betaloc]) decrease the size of the infarct, ventricular dysrhythmias, and mortality rates in clients with MI. The physician usually prescribes a cardioselective beta-blocking agent within the first 24 hours after an MI. Beta blockers slow the heart rate and decrease the force of cardiac contraction. Thus these agents prolong the period of diastole and increase myocardial perfusion while reducing the force of myocardial contraction. With beta blockade, the heart is capable of performing 25% to 30% more work without ischemia. During beta-blocking therapy, the nurse: Monitors the heart rate (bradycardia is common) Checks the blood pressure Measures the PR interval Checks the level of consciousness Monitors for any chest discomfort The nurse assesses the lungs for crackles (indicative of heart failure) and wheezes (indicative of bronchospasm). Hypoglycemia, depression, nightmares, and forgetfulness are also problems with beta blockade, especially in older clients (see Chart 38-6).

Physicians frequently prescribe angiotensin-converting enzyme (ACE) inhibitors within 48 hours of an MI to prevent ventricular remodeling and the development of heart failure. ACE inhibitors have been demonstrated to increase survival after an MI. The nurse monitors the client for hypotension, cough, and changes in serum potassium, creatinine, and blood urea nitrogen. For clients with angina, the health care provider may prescribe calcium channel blockers to enhance vasodilation and myocardial perfusion. Calcium channel blockers are indicated for clients with variant angina or for those who are hypertensive and continue to have angina despite therapy with beta blockers. They are not indicated after an MI. The nurse monitors the client receiving calcium channel blockers for hypotension and headaches and reviews the frequency of anginal episodes. The recent Clopidogrel in Unstable Angina to Prevent Recurrent Ischemic Events (CURE) study showed that the combination of clopidogrel (Plavix) and aspirin was more effective in reducing death, MI, and stroke when compared to aspirin alone. The risk of bleeding from using two antiplatelet agents together was not significantly increased (Palatnik, 2001).

ACTIVITY INTOLERANCE

PLANNING: EXPECTED OUTCOMES. The client with coronary artery disease (CAD) is expected to walk at least 200 feet four times a day without chest discomfort or shortness of breath.

INTERVENTIONS. Activity intolerance is reduced by a planned program of cardiac rehabilitation implemented primarily by the nurse and physical therapist.

CARDIAC CARE REHABILITATION. Cardiac rehabilitation is the process of actively assisting the client with cardiac disease in achieving and maintaining a vital and productive life while remaining within the limits of the heart’s ability to respond to increases in activity and stress. It can be divided into three phases.

Phase 1 begins with the acute illness and ends with discharge from the hospital.

Phase 2 begins after discharge and continues through convalescence at home.

Phase 3 refers to long-term conditioning.

In the acute phase (phase 1), the nurse promotes rest and yet ensures some limited mobility. Assistance is provided for some activities of daily living (ADLs), such as bathing and toileting. Clients progress at their own rate to increasing levels of activity, depending on their clinical status, age, and physical capabilities. For example, for the first 24 hours, the client may be restricted to bedrest but allowed to stand to void or to use the bedside commode. The second day, the client may be out of bed sitting in a chair as tolerated, usually for 30 minutes three times a day. The next step in phase 1 is ambulation of the client in the room and to the bathroom. The nurse encourages progressive ambulation in the hallway, usually 50, 100, and then 200 feet three times a day. In addition, the client may begin showering for 5 or 10 minutes with warm water; a stool should be available for him or her to sit on if necessary. The nurse assesses the client’s heart rate, blood pressure, respiratory rate, and level of fatigue with each higher level of activity. Decreases greater than 20 mm Hg in the systolic blood pressure, changes of 20 beats/min in the pulse rate, and complaints of dyspnea or chest pain indicate intolerance of activity. When such signs and symptoms develop, the nurse notifies the physician and does not advance the client to the next level. Older adults with CAD often have needs and concerns different from those of younger adults (Chart 38-6).

INEFFECTIVE COPING

PLANNING: EXPECTED OUTCOMES. The client with CAD is expected to indicate a reduction in anxiety and recognize the beginning of control over life.

INTERVENTIONS. The nurse assesses the client’s level of anxiety while allowing him or her to express any anxiety and attempt to define its origin. Simple, repeated explanations of therapies, expectations, and surroundings may help relieve anxiety.

COPING ENHANCEMENT. During the acute phase of illness, the physician may prescribe anxiolytic (antianxiety) medications, such as alprazolam (Xanax). The nurse identifies the client’s current coping mechanisms; the most common are denial, anger, and depression. Denial allows the client to minimize a threat and use problem- focused coping mechanisms. He or she may avoid discussing what has happened yet comply with treatment regimens. This type of denial decreases anxiety, and the nurse should not discourage it. However, denial that results in a client’s “acting out” and refusing to follow treatment regimens can be harmful. Because this behavior is usually due to extreme anxiety or fear, threats only worsen the behavior. The nurse remains calm and avoids confronting the client but clearly indicates when a behavior is not acceptable and is potentially harmful. Anger may represent an attempt to regain control of life. The nurse encourages the client to verbalize the source of frustration and provides opportunities for decision making and control. Depression may be a client’s response to grief and loss of function. The nurse listens as the client verbalizes feelings of loss, being careful not to offer false or general reassurances. Depression is acknowledged, but the client is expected to perform ADLs and other activities within restrictions. The nurse identifies all improvements in the client’s condition and shares them with him or her. Chart 38-7 summarizes the major NIC intervention activities for clients with CAD.

POTENTIAL FOR DYSRHYTHMIAS

PLANNING: EXPECTED OUTCOMES.

The client with CAD is expected to resume a normal sinus rhythm or normal rhythm for the client and be hemodynamically stable.

INTERVENTIONS. Dysrhythmias are the cause of death in most clients with myocardial infarction (MI) who die before they can be hospitalized. Even in the early period of hospitalization, 70% to 90% of clients with MI experience some abnormality of cardiac rhythm.

Whenever a dysrhythmia develops in a client with CAD, the cardiac nurse:

• Identifies the dysrhythmia

• Assesses the client’s hemodynamic status

• Evaluates the client for chest discomfort

Dysrhythmias are treated when they are causing hemodynamic compromise, are increasing myocardial oxygen requirements, or predispose to lethal ventricular dysrhythmias.

INFERIOR MYOCARDIAL INFARCTION. Typical dysrhythmias for the client with an inferior MI are bradycardias and second-degree AV blocks resulting from ischemia of the AV node. These rhythms tend to be transient. The nurse monitors the cardiac rhythm and rate, and the hemodynamic status. If the client becomes hemodynamically unstable, a temporary pacemaker may be necessary.

ANTERIOR MYOCARDIAL INFARCTION. The client with an anterior MI is likely to exhibit ventricular irritability (premature ventricular contractions [PVCs]). Third-degree or bundle branch block is a serious complication in the client with an anterior MI, because it indicates that a large portion of the left ventricle is involved. The physician may insert a pacemaker. The nurse should observe the client closely to detect the development of heart failure.

POTENTIAL FOR HEART FAILURE

PLANNING: EXPECTED OUTCOMES.

The client with coronary artery disease (CAD) is expected to regain hemodynamic stability as evidenced by the following:

• Blood pressure and pulse rate within the client’s acceptable range

• Adequate urine output

• Mental alertness

• Clear lungs on auscultation

• Palpable peripheral pulses

INTERVENTIONS. Decreased cardiac output related to heart failure is a relatively common complication after an MI. After an MI the client may experience heart failure as a result of left ventricular dysfunction, rupture of the intraventricular septum, papillary muscle rupture with valvular dysfunction, or right ventricular infarction. The most severe form of heart failure, cardiogenic shock, accounts for most in-hospital deaths after an MI. The type of management used to increase cardiac output depends on the location of the MI and the type of heart failure that resulted from the infarction.

MANAGING LEFT VENTRICULAR FAILURE. When a client with MI experiences damage to the left ventricle, rupture of the intraventricular septum, or tear of a papillary mus- cle, a reduction occurs in the amount of blood that the heart can eject. This reduction in ejection fraction results in a decreased cardiac output and greater left ventricular residual volumes. Volume and pressure increase first in the left ventricle and eventually in the pulmonary vasculature. When volume and pressure are markedly increased in the pulmonary vasculature, pulmonary complications develop.

NURSING ASSESSMENT AND MONITORING. The development of left ventricular failure and pulmonary edema is assessed by auscultating for crackles and identifying their location in the lung fields. Wheezing, tachypnea, and frothy sputum may also occur with pulmonary edema. The nurse auscultates the heart, paying particular attention to the presence of an S3 heart sound.

The nurse monitors for the following signs of poor organ perfusion that may result from decreased cardiac output:

• A change in orientation or mental status

• Urine output less than 1 mL/kg/hr or less than 30 mL/hr

• Cool, clammy extremities with decreased or absent pulses

• Unusual fatigue

• Recurrent chest pain

In specialized units, hemodynamic monitoring may be instituted to assess the client’s preload, afterload, and cardiac output. Hemodynamic monitoring in the hospital requires the insertion of a pulmonary artery catheter. The cardiac nurse obtains and records hemodynamic measurements, which include right atrial pressure, pulmonary artery systolic and diastolic pressures, pulmonary artery wedge pressure (PAWP) (a measure of preload), systemic vascular resistance (a measure of afterload), cardiac output, and cardiac index. Single values of these measurements are less significant than the trend of values combined with the client’s clinical manifestations. These measurements help both the nurse and the physician to identify heart failure and guide the administration of fluids and vasoactive drugs.

CLASSIFICATION OF POSTMYOCARDIAL INFARCTION HEART FAILURE.

Killip categorized heart failure after an M I into four classes based on prognosis (Table 38-3).

Class I. Clients with class I heart failure often respond well to reduction in preload with IV diuretics. The nurse monitors the urine output hourly, checks vital signs hourly, continues to assess for signs of heart failure, and reviews the serum potassium level.

Class II and Class III. Clients with class II and class III heart failure may require diuresis and more aggressive medical intervention, such as reduction of afterload or enhancement of contractility. IV nitroprusside or nitroglycerin may be used to decrease both preload and afterload. These drugs are administered as continuous infusions in specialized units where the PAWP and blood pressure can be closely monitored. The blood pressure can drop in response to excessive vasodilation (see Chart 38-5). Positive inotropes, such as dopamine (Intropin), dobutamine (Dobutrex), and amrinone (Inocor), increase the force of cardiac contraction. They are administered by continuous IV infusion. The effects of these drugs on the vasculature and heart rate vary and may be dose dependent. The nurse must understand the anticipated effect of the drug and the desired dosage range. The infusions are titrated to optimize cardiac output. The nurse uses caution when administering these drugs because of the potential risk of increasing myocardial oxygen consumption and further decreasing cardiac output. The client is frequently monitored, paying particular attention to the development of chest pain.

Class IV: Cardiogenic Shock. Class IV heart failure is cardiogenic shock. In cardiogenic shock, necrosis of more than 40% of the left ventricle has occurred. Most clients have a stuttering pattern of chest pain, resulting in piecemeal extension of the MI.

Manifestations of cardiogenic shock include the following:

• Tachycardia

• Hypotension

• Blood pressure less than 90 mm Hg, or 30 mm Hg less than the client’s baseline

• Urine output less than 30 mL/hr

• Cold, clammy skin with poor peripheral pulses

• Agitation, restlessness, or confusion

• Pulmonary congestion

• Tachypnea

• Continuing chest discomfort

Early detection is essential because established cardiogenic shock has a mortality rate of 65% to 100%.

MEDICAL MANAGEMENT. Medical interventions aim to relieve pain and decrease myocardial oxygen requirements through preload and possibly afterload reduction (see Chart 38-5).

The physician orders IV morphine, which is used to decrease pulmonary congestion and relieve pain. Oxygen is administered; intubation and ventilation may be necessary. The nurse uses the information gained from hemodynamic monitoring to titrate drug therapy. Preload reduction may be cautiously attempted with diuretics, nitroglycerin, or nitroprusside, as described for clients with Killip class III heart failure. Because vasodilation may result in a further decline in blood pressure, the nurse monitors systolic pressure constantly. Vasopressors and positive inotropes may be used to maintain organ perfusion, but such drugs increase myocardial oxygen consumption and can worsen ischemia.

Use of an Intra-Aortic Balloon Pump. When clients do not respond to drug therapy with improved tissue perfusion, decreased workload of the heart, and increased cardiac contractility, an intra-aortic balloon pump (IABP) may be inserted. Insertion of an intra-aortic counterpulsation device, such as the IABP, is an invasive intervention that is used to improve myocardial perfusion during an acute MI, reduce afterload, and facilitate left ventricular emptying. The physician can insert an IABP percutaneously or through surgical cutdown. Inflation of the IABP during diastole increases the diastolic pressure and improves coronary perfusion. Deflation of the balloon just before systole reduces afterload at the time of systolic contraction. This facilitates emptying of the left ventricle and improves cardiac output. The balloon catheter is attached to a pump console, which is triggered by an electrocardiogram (ECG) tracing and arterial waveform (Figure 38-4).

Immediate Reperfusion. Immediate reperfusion is an invasive intervention that shows some promise for clients with cardiogenic shock. The client is taken to the cardiac catheterization laboratory, and an emergency left-sided heart catheterization is performed. If the client has a treatable lesion or lesions, the surgeon performs an immediate percutaneous transluminal coronary angioplasty (PTCA) in the catheterization laboratory, or the client is transferred to the operating suite for a coronary artery bypass graft (CABG).

MANAGING RIGHT VENTRICULAR FAILURE. Conditions other than left ventricular failure may result in decreased cardiac output after an MI. In approximately 30% of clients with inferior Mis, right ventricular infarction and failure develop. In this instance, the right ventricle fails independently of the left. Decreased cardiac output with a paradoxical pulse, clear lungs, and jugular venous distention results when the client is in semi-Fowler’s position. A right ventricular MI may be documented by echocardiography and by an ECG using right-sided precordial leads. The goal of medical management is to improve right ventricular stroke volume by increasing right ventricular fiber stretch or preload. To enhance right ventricular preload, the nurse administers sufficient fluids (as much as 200 mL/hr) to increase right atrial pressure to 20 mm Hg, as ordered. The cardiac nurse monitors the pulmonary artery wedge pressure (PAWP) (attempting to maintain it below 15 to 20 mm Hg) and auscultates the lungs to ensure that left-sided failure is not developing. The client’s cardiac output is monitored to ensure that fluid administration is having the desired effect.

POTENTIAL FOR RECURRENT CHEST DISCOMFORT AND EXTENSION OF INJURY

PLANNING: EXPECTED OUTCOMES.

The client with coronary artery disease (CAD) is expected to experience minimal angina while engaging in activities of daily living (ADLs) and an exercise program.

INTERVENTIONS. Recurrent chest discomfort despite medical therapy is one of the major indications for surgical management of CAD. Clients who continue to have chest discomfort despite medical therapy or ischemia during a stress test may require invasive correction by PTCA or CABG to resolve angina or prevent myocardial infarction (MI). Before invasive treatment, a left-sided cardiac catheterization with coronary angiogram is performed to document that the lesions are correctable and that left ventricular pump function is adequate.

PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY. Percutaneous transluminal coronary angioplasty (PTCA) is an invasive but technically nonsurgical technique. It is performed to reduce the frequency and sever

INDICATIONS. Clients who are most likely to benefit from PTCA have single- or double-vessel disease with discrete, proximal, noncalcified lesions. When identifying which lesions are treatable with PTCA, the cardiologist considers the lesion’s complexity and location, as well as the amount of myocardium at risk. PTCA often will not open complex lesions. Treating lesions located in the left main artery would place a large amount of myocardial tissue at risk should the vessel close acutely; therefore these lesions are rarely treated with PTCA. PTCA may also be used for the client with an evolving acute MI, either alone or in conjunction with thrombolytic therapy or GP Ila/IIIb inhibitor, to reperfuse the damaged myocardium. Approximately 50% of clients needing revascularization are initially treated with PTCA.

PROCEDURE. The physician performs PTCA under fluoroscopic guidance in the cardiac catheterization laboratory. A balloon-tipped catheter is introduced through a guidewire to the occlusion in the coronary vessel. The physician activates a compressor that inflates the balloon at 4 to 14 atmospheres of pressure. This process compresses the plaque against the vessel wall and reduces or eliminates the occluding lesion (Figure 38-5).

 Balloon inflation may be repeated until angiography indicates a decrease in the stenosis (narrowing) to less than 50% of the vessel’s diameter. IV heparin is administered in a continuous infusion to prevent thrombus formation; IV or intracoronary nitroglycerin or sublingual nifedipine is given to prevent coronary spasm. PTCA initially reopens the vessel in more than 90% of appropriately selected clients. However, restenosis occurs in a large number of these clients. Glycoprotein (GP) Ila/IIIb inhibitors have demonstrated benefit in preventing restenosis and maintaining the patency of the artery, reducing nonfatal Mis, and preventing deaths following PTCA and are usually administered. Other techniques being used to ensure continued patency of the vessel are laser angioplasty, arthrectomy, and stents. Lasers may be used alone to remove atherosclerotic material from coronary arteries, or they may be used in conjunction with balloon angioplasty to create a smooth lumen about the size of the balloon. Arthrectomy devices can either excise and retrieve plaque or emulsify it. One of the advantages of arthrectomy is that it creates a less bulky vessel with better elastic recoil. Stents are used to maintain the patent lumen obtained by angioplasty or arthrectomy. By providing a supportive scaffold, stents prevent acute closure of the vessel from arterial dissection or vasospasm. Figure 38-6 depicts a stent positioned in a coronary artery.

 POSTPROCEDURE CARE. The nurse monitors for potential problems, which include acute closure of the vessel, bleeding from the insertion site, reaction to the dye used in angiography, hypotension, hypokalemia, and dysrhythmias. The physician usually prescribes a long-term nitrate, calcium channel blocker, and aspirin therapy for clients after PTCA. A beta blocker and an angiotensin-converting enzyme (ACE) inhibitor may be added for clients who have had primary angioplasty following an MI. Many clients continue to have infusions of GP Ila/IIIb inhibitors during the initial hours after PTCA. Clients may experience hypokalemia after the procedure and require careful monitoring and supplementation of potassium. Clients who have intracoronary stents inserted may require anticoagulation with warfarin (Coumadin) for 1 to 3 months until an endothelial covering is laid over the stent. The nursing interventions for clients receiving these medications are described in Chart 38-4. The nurse provides careful explanations of drug therapy and any recommended lifestyle changes.

CORONARY ARTERY BYPASS GRAFT SURGERY. Approximately 598,000 coronary artery bypass graft (CABG) surgeries were performed in the United States in 1996. This represents a 424% increase since 1979. CABG is the most common type of cardiac surgery and the most common procedure for older adults; more than 44% of all CABGs are performed on clients older than 65 years of age. The occluded coronary arteries are bypassed with the client’s own venous or arterial blood vessels or synthetic grafts. The internal mammary artery (IMA) is the current graft of choice because it has a 90% patency rate at 12 years after the procedure. CABG is indicated when clients do not respond to medical management of CAD or when disease progression is evident. The decision for surgery is based on the client’s symptoms and the results of cardiac catheterization.

Candidates for surgery are clients who have the following:

• Angina with greater than 50% occlusion of the left main coronary artery

• Unstable angina with severe two-vessel or moderate threevessel disease

• Ischemia with heart failure

• Acute MI

• Signs of ischemia or impending MI after angiography or PTCA

The vessels to be bypassed should have proximal lesions occluding more than 70% of the vessel’s diameter but good distal runoff. Bypass of less occluded vessels may result in poor perfusion through the graft and early obstruction. CABG is most effective when good ventricular function remains and the ejection fraction is more than 40% to 50%. Clients with lower ejection fractions are poorer risks. For most clients, the risk is low and the benefits of bypass surgery are clear. Surgical treatment of CAD does not appear to affect the life span. Early mortality rates are 1% to 2%. Left ventricular function is the most important long-term indicator of survival. CABG does improve the quality of life for most clients; 80% to 90% of clients are pain free at 1 year after CABG, and 70% remain pain free at 5 years after the proce

PREOPERATIVE CARE. CABG surgery may be planned as an elective procedure or performed on an emergency basis. Clients undergoing elective surgery are often admitted on the morning of the surgery. Preoperative preparations and teaching are completed during prehospitalization interviews. Clients must understand that some medication will need to be adjusted because of the surgery. The nurse ensures that appropriate medications have been discontinued preoperatively and that the necessary ones have been administered (Table 38-4).

Prehospital Preparation. The nurse familiarizes the client and family with the cardiac surgical critical care environment and prepares the client for postoperative care. The nurse demonstrates and has the client return a demonstration of how to splint the chest incision, cough, deep breathe, and perform arm and leg exercises. The nurse stresses the following:

• The client should identify any pain to the nursing staff.

 Most of the pain will be in the sternal incision.

• Pain medication will be available.

The nurse explains that the client should expect to have a sternal incision, possibly a leg incision, one or two chest tubes, a Foley catheter, and several IV fluid catheters postoperatively. An endotracheal tube will be connected to a ventilator for several hours postoperatively. The client and family must understand that the client will not be able to talk while the endotracheal tube is in place. The client should breathe with the ventilator and not fight it. When describing the postoperative course, the nurse emphasizes that close monitoring and the use of sophisticated equipment are standard treatment.

Psychosocial Preparation. Preoperative anxiety is common. Clients often wait 1 to 6 weeks for CABG surgery to be scheduled and performed. As the length of the wait increases, anxiety may increase. An appropriate nursing assessment should identify the level of anxiety and the coping methods clients have used successfully in the past. Some clients may find it helpful to define their fears. Common sources of fear include fear of the unknown, fear of bodily harm, and fear of death. Clients may benefit from detailed information about the surgery, or they may feel overwhelmed by so much material. Some need to discuss their feelings in detail or describe the experiences of people they know who have undergone CABG. The nurse assesses clients’ anxiety level and helps them to cope. Preoperative anxiety has been positively associated with postpericardiotomy delirium.

OPERATIVE PROCEDURE. Coronary artery bypass surgery is performed with the client under general anesthesia and undergoing cardiopulmonary bypass. The anesthesiologist or nurse anesthetist administers anesthesia and intubates the client. Once the client is anesthetized, one surgical team may begin harvesting the saphenous vein if it is to be used for the graft. The cardiac surgical team begins the procedure with a median sternotomy incision and visualization of the heart and great vessels. Cardiopulmonary bypass (CPB) is accomplished by cannulation of the inferior and superior venae cavae. The purpose of CPB is to provide oxygenation, circulation, and hypothermia during induced cardiac arrest. Blood is diverted from the heart to the bypass machine, where it is heparinized, oxygenated, and returned to the circulation through a cannula placed in the ascending aortic arch or femoral artery (Figure 38-7).

 During bypass, the client’s core temperature is cooled to 82.6° to 89.6° F (28° to 32° C). Cooling decreases the rate of metabolism and demand for oxygen. The heart is perfused with a cardioplegic solution containing potassium, which decreases myocardial oxygen consumption and causes the heart to stop during diastole. This process ensures a still operative field and prevents myocardial ischemia. Once the heart is arrested, the grafting procedure can begin. The surgeon uses the internal mammary artery (IMA), a saphenous vein, or both, or a radial artery to bypass lesions in the coronary arteries (Figure 38-8).

The distal end of the IMA is dissected and attached below the lesion on the coronary artery. If the surgeon uses a venous graft or the radial artery, it is anastomosed (sutured) proximally to the aorta and distally to the coronary artery just beyond the occlusion. Thus myocardial perfusion is improved. After flow rates through the grafts are measured, the heart is rewarmed slowly. The cardioplegic solution is flushed from the heart. The heart regains its rate and rhythm, or it may be defibrillated to return it to a normal rhythm. When the procedure is completed, the client is rewarmed by CPB and weaned from the bypass machine while the grafts are observed for patency and leakage. The surgeon then places atrial and ventricular pacemaker wires and mediastinal chest tubes. Finally, the surgeon closes the sternum with wire sutures.

POSTOPERATIVE CARE. After surgery, the client is transported to a post-open heart surgery unit. There the client undergoes mechanical ventilation for 3 to 6 hours. The client requires highly skilled nursing care from a nurse qualified to provide post-cardiac surgery care. The nurse connects mediastinal tubes to water seal drainage systems and grounds the epicardial pacer wires and connects them to the pacemaker box. The nurse monitors pulmonary artery and arterial pressures, as well as the heart rate and rhythm, which are displayed on a monitor. The nurse closely assesses the client for dysrhythmias, such as ventricular ectopic rhythms, bradydysrhythmias, or heart block. The nurse treats symptomatic dysrhythmias according to unit protocol or the physician’s order. If the client has symptomatic bradydysrhythmias or heart block, the nurse turns on the pacemaker and adjusts the pacemaker settings as ordered (see Chapter 34). The nurse also monitors for other complications of CABG, including fluid and electrolyte imbalance, hypotension, hypothermia, hypertension, bleeding, cardiac tamponade, and altered cerebral perfusion. Table 38-5 lists some of the possible postoperative complications of CABG.

Management of Fluid and Electrolyte Imbalance. Assessing fluid and electrolyte balance is a high priority in the early postoperative period. Clients usually have edema, and fluids may be limited to 1500 to 2000 mL. However, decisions concerning fluid administration are made on the basis of the blood pressure, pulmonary artery wedge pressure (PAWP), right atrial pressure, cardiac output, cardiac index, systemic vascular resistance, and urine output. An experienced nurse interprets assessment findings and adjusts fluid administration on the basis of standing unit policies or specific orders from the physician. Serum electrolytes (especially calcium, magnesium, and phosphorus) may be reduced postoperatively and are monitored carefully by both the physician and the nurse. Because the serum potassium level can fluctuate dramatically, electrolyte levels are checked frequently. Potassium depletion is common and may result from hemodilution, diuretic therapy, and nasogastric suction. To prevent dysrhythmias, potassium concentrations are maintained between 4 and 5 mEq/L. If the serum potassium level is depleted, the physician may order IV potassium replacement. The dose of potassium administered exceeds the usual recommended level of no more than 20 mEq of potassium per hour. For a potassium bolus, as much as 40 to 80 mEq may be mixed in 100 mL of IV solution and given at a rate as high as 40 mEq/hr. The drug must be given through a central catheter, and the rate of administration controlled by an infusion pump. The client must be on a cardiac monitor for extremely careful observation.

Management of Hypotension. Hypotension (systolic blood pressure less than 90 mm Hg) is a significant problem because it may result in the collapse of a vein graft. The nurse reviews the assessment parameters to identify what might be causing the hypotension. Decreased preload (decreased PAWP) can result from hypovolemia or vasodilation. If the client is hypovolemic, it might be appropriate to increase fluid administration or administer blood. The physician may treat the client with a low PAWP, decreased systemic vascular resistance, and vasodilation with vasopressor therapy to increase the blood pressure. However, if hypotension is the result of left ventricular failure (increased PAWP), IV inotropes might be necessary.

Management of Hypothermia. Although the client is rewarmed to 98.6° F (37° C) before being removed from bypass, it is not uncommon for the body temperature to drift downward after the client leaves the surgical suite. The nurse monitors the body temperature and institutes rewarming procedures should the temperature drop below 96.8° F (36° C). Rewarming may be accomplished with warm blankets, rewarming lights, or thermal blankets. The danger of rewarming a client too quickly is that he or she may begin shivering, resulting in metabolic acidosis and hypoxia. To prevent shivering, rewarming should proceed at a rate no faster than 1.8° F (1° C)/hr. The nurse discontinues rewarming when the body temperature approaches 98.6° F (37° C) and the client’s extremities feel warm.

Management of Hypertension. Hypothermia is a significant risk for the client following CABG surgery because it promotes vasoconstriction and hypertension. Other factors contributing to hypertension in the CABG client include CPB, medications, and the client’s own sympathetic activity. Most CABG clients experience hypertension (if hypertension is defined as a systolic blood pressure greater than 140 to 150 mm Hg). Hypertension is dangerous because increased pressure promotes leakage from suture lines and may cause bleeding. To return the blood pressure to acceptable limits, the nurse titrates IV nitroprusside or nitroglycerin (see Chart 38-4).

Management of Bleeding. Bleeding occurs to a limited extent postoperatively in all clients. Mediastinal and chest tube drainage is measured at least hourly, and drainage exceeding 150 mL/hr is reported to the surgeon. Clients with IMA grafts may have more chest drainage. The nurse may autotransfuse the chest drainage to assist with volume management when 500 mL has accumulated or 4 hours has elapsed, depending on the clinical pathway or the physician’s order. The nurse must maintain the patency of the mediastinal and chest tubes. One effective way of promoting chest tube drainage is to prevent a dependent loop from forming in the tubing.

Management of Cardiac Tamponade. If the client is bleeding and the mediastinal tubes are not kept patent, blood may accumulate around the heart. The myo-cardium is compressed, and cardiac tamponade results. The fluid accumulating around the heart compresses the atria and ventricles, prevents them from filling adequately, and reduces cardiac output. The following are hallmarks of cardiac tamponade: • Sudden cessation of previously heavy mediastinal drainage • Jugular venous distention but clear lung sounds • Pulsus paradoxus (blood pressure greater than 10 mm Hg higher on expiration than on inspiration) • An equalizing of PAWP and right atrial pressure Tamponade can be confirmed by echocardiogram or chest x-ray study. Pericardiocentesis (see Chapter 35) may not be appropriate for tamponade after CABG, because the blood in the pericardium may have clotted. Volume expansion and emergency sternotomy with drainage are then the treatments of choice.

Management of Altered Levels of Consciousness. The client may demonstrate changes in the level of consciousness, which may be permanent or transient. Transient changes related to anesthesia, CPB, air emboli, or hypothermia occur in as many as 75% of clients. Transient neurologic deficits may include slowness to arouse, memory loss, and confusion. Clients with transient neurologic deficits usually return to baseline neurologic status within 4 to 8 hours.

Permanent client may demonstrate the following:

• Abnormal pupillary response

• Failure to awaken from anesthesia

• Seizures

• Absence of sensory or motor function

The nurse checks the client’s neurologic status every 30 to 60 minutes until the client has awakened from anesthesia; the nurse then checks every 2 to 4 hours.

Pain Management. The nurse must differentiate between sternotomy pain, which is expected after CABG, and anginal pain, which might indicate graft failure. Typical sternotomy pain is localized, does not radiate, and often becomes worse when the client coughs or breathes deeply. The client may describe the pain as sharp, aching, or burning. Pain may stimulate the sympathetic nervous system, which increases the heart rate and vascular resistance while decreasing cardiac output. The nurse administers the prescribed medication, in adequate doses, frequently enough to limit pain. However, during the process of weaning the client from mechanical ventilation, it may be necessary to use short-acting analgesics and to limit pain medication because of the respiratory depressant effects of analgesia.

Transfer from the Special Care Unit. Ventilation is usually provided for 3 to 6 hours postoperatively, until the client is breathing adequately and is hemodynamically stable. During the first day, the client usually has pacer wires, hemodynamic monitoring lines, and mediastinal tubes removed and is transferred to an intermediate care unit. All CABG clients, but especially those with IMA grafts, are at high risk for atelectasis, so the nurse encourages the client to splint, cough, turn, and deep breathe to raise secretions. The nurse guides him or her in a gradual resumption of activity. Two hours after extubation, the client should be dangled as tolerated and turned side to side. Within 4 to 8 hours after extubation, the client should be out of bed in a chair. By the first day after surgery, the client should be out of bed in a chair and ambulating 25 to 100 feet three times a day as tolerated.

The nurse continues to monitor for decreased cardiac output, pain, dysrhythmias, and infection. The nurse assesses the neurovascular status of the donor arm of clients who have had the radial artery used as a conduit in CABG. Every hour initially, and eventually every 4 hours, the nurse assesses the hand color, temperature (pulse both ulnar and radial stump), and capillary refill. In addition, the fingertips, hand, and arm are assessed for sensation and mobility at least every 4 hours. Approximately one third of clients with CABG and two thirds of those with valve replacements experience supraventricular dysrhythmias (especially atrial fibrillation) during the postoperative period, most commonly on the second or third postoperative day. The nurse examines the monitor pattern for atrial fibrillation. When auscultating the heart, the nurse listens for an irregular rhythm. (See Chapter 34 for interventions for atrial fibrillation.) Sternal wound infections develop between 5 days and several weeks postoperatively in about 2% of clients and represent a significant complication (Hussey & Leeper, 1998).

The nurse is alerted to the presence of mediastinitis by the following:

• Fever continuing beyond the first 4 days after CABG

• Instability (bogginess or stepping) of the sternum

• Redness or purulent drainage from suture sites

• An increased white blood cell coun

The physician may perform a needle biopsy to confirm a sternal infection. Surgical debridement, antibiotic wound irrigation, and IV antibiotics are usually indicated. Four to 6 weeks of IV antibiotics are required if sternal osteomyelitis has developed.

Postpericardiotomy syndrome is a source of chest discomfort in 10% to 40% of post-cardiac surgery clients. The syndrome is characterized by pericardial and pleural pain, pericarditis, a friction rub, an elevated temperature and white blood cell count, and dysrhythmias. Postpericardiotomy syndrome may occur days to weeks after surgery and seems to be associated with blood remaining in the pericardial sac. The nurse observes for the development of pericardial or pleural pain. For most clients, the syndrome is mild and self-limiting. However, the client may require treatment similar to that for pericarditis. The nurse should be prepared to detect pericardial tamponade. Older adults may have different needs and experience slightly different problems after CABG. Nursing concerns related to the older CABG client are detailed in Chart 38-8.

MINIMALLY INVASIVE DIRECT CORONARY ARTERY BYPASS.

The minimally invasive direct coronary artery bypass (MIDCAB) may be indicated for clients with a lesion of the left anterior descending (LAD) artery. In one of the most common MIDCAB procedures, after a 2-inch left thoracotomy incision is made and the fourth rib removed, the left internal mammary artery (IMA) is dissected and attached to the still-beating heart below the level of the lesion in the LAD. Cardiopulmonary bypass (CPB) is not required. Nurses must assess postoperatively for chest pain and electrocardiogram (ECG) changes (Q waves and ST-segment and T-wave changes in leads V2 to V6) because occlusion of the IMA graft occurs acutely in 10% of clients. If there is any question of acute graph closure, the nurse notifies the surgeon immediately. Clients tend to have more incisional pain after MIDCAB than after traditional CABG surgery, but the pain can usually be managed with oxycodone or codeine. Because they have a thoracotomy incision and a chest tube or smaller lumen vacuum chest device, clients are encouraged to cough, deep breathe, and use an incentive spirometer for a week postoperatively. Most clients spend less than 6 hours in a critical care unit and are discharged in 2 or 3 days.

TRANSMYOCARDIAL LASER REVASCULARIZATION. Transmyocardial laser revascularization is a new procedure for clients with unstable angina and inoperable CAD with areas of reversible myocardial ischemia. After a single-lung intubation, a left anterior thoracotomy is performed and the heart is visualized. A laser is used to create 20 to 24 long, narrow channels through the left ventricular muscle to the left ventricle. These channels will eventually allow oxygenated blood to flow during diastole from the left ventricle to nourish the muscle. After the surgery, the client is transported to a critical care unit, where the nurse institutes hemodynamic monitoring and monitors for anginal episodes and bleeding disturbances. Although many clients report decreases in anginal episodes following the procedure, researchers have been unable to document why clients experience such an improvement.

Community-Based Care

CASE MANAGEMENT

Case management is most appropriate for clients who meet high-cost, high-volume, and high-risk criteria. Clients with coronary artery disease (CAD) clearly meet all of these criteria. Clinical pathways and case management programs for clients who have CAD are in effect in most U.S. hospitals. By focusing on cardiovascular risk reduction and improving the continuity of care, health care professionals have reduced the length and cost of hospital stays. Posthospital case management should reduce hospital readmission rates and improve client health.

 HOME CARE MANAGEMENT Clients who have experienced a myocardial infarction (MI), angina, or coronary artery bypass graft (CABG) surgery are usually discharged to home or to a subacute care setting with pharmacologic therapy and specific activity prescriptions. Hospital stays are approximately 5 to 7 days for clients with MI or those undergoing CABG, and only 2 days for those undergoing percutaneous transluminal coronary angioplasty (PTCA); therefore clients are still recovering when they are discharged. They may require a home care nurse for assessment and teaching following discharge and an aide for assistance with activities of daily living (ADLs) if they are older or weaker (Chart 38-9).

In addition, women, who tend to be older and living alone when coronary events occur, may have a greater need for home assistance after CABG surgery (see the Evidence-Based Practice for Nursing box above). Clients who were residents in long-term care may be returned there after hospitalization for unstable angina, MI, or CABG surgery. Cardiac rehabilitation is available in many communities for clients after an MI or CABG surgery, but only 10% to 30% of clients participate in structured rehabilitation programs. The most frequently cited reasons for nonparticipation are lack of insurance coverage, a physician’s directive that it is unnecessary, and the client’s decision that it is not necessary. Clients who participate in structured rehabilitation programs report greater improvement in exercise tolerance and improved ability to control stress. However, there is no difference in their return to work.

HEALTH TEACHING Because hospital stays are short and clients are quite ill during hospitalization, most in-hospital education programs concentrate on the skills essential to self-care after discharge. As part of home visits or a cardiac rehabilitation program, the nurse identifies the additional educational needs of the client and family, as well as their readiness to learn. The nurse then develops a teaching plan, which usually includes education about the normal anatomy and physiology of the heart, the pathophysiology of angina and MI, risk factor modification, activity and exercise protocols, cardiac medications, and when to seek medical assistance. The nurse informs the client about the normal function of the heart and coronary arteries and explains angina and MI. Clients are taught that myocardial healing after an MI begins early and is usually complete in 6 to 8 weeks. Clients who have undergone CABG are told that the sternotomy heals in about 6 to 8 weeks. Clients who have undergone CABG require instruction on incisional care for the sternum and the graft site. They should inspect the incisions daily for any redness, swelling, or drainage. The leg of a saphenous vein donor site is often edematous. The nurse instructs clients to avoid crossing legs, to wear elastic stockings until the edema subsides, and to elevate the surgical limb when sitting in a chair. Clients who have had a radial artery graft are instructed to open and close the hand vigorously 10 times every 2 hours.

 RISK FACTOR MODIFICATION. Modification of risk factors is a necessary part of a client’s management and involves changing his or her health maintenance patterns. Such modifications may include smoking cessation, altered dietary habits, regular exercise, blood pressure control, and blood glucose control.

SMOKING CESSATION. For clients who smoke, the nurse explains the detrimental effects on the cardiovascular system of smoking tobacco, especially cigarettes. Many clients spontaneously quit smoking soon after an MI. Nurse counseling has been demonstrated to be a cost-effective way to assist clients in stopping smoking. Clients who use nicotine replacement are two to three times more likely to be successful in abstaining from cigarettes permanently. However, the nurse advises the client that nicotine replacement is not recommended for those who have acute coronary syndromes or recently experienced an MI. If the client relapses and begins smoking again, the nurse reassures him or her that most former smokers relapsed several times before quitting permanently. Other methods of smoking cessation include acupuncture, acupressure, and hypnosis (see Chapter 4).

CHOLESTEROL CONTROL. The mainstays of cholesterol control are diet therapy and administration of antihyperlipidemic agents.

DIET THERAPY. The nurse collaborates with the dietitian to encourage the client to follow a prudent diet. Less than 30% of the calories in the diet should be from fat, and the fat consumed should be primarily monounsaturated or polyunsaturated. Clients should avoid saturated fats and foods rich in cholesterol. The nurse or dietitian also instructs the client not to add salt at the table. Booklets and cookbooks that can assist the client in learning to cook with reduction of fats, oils, and salt are available from the American Heart Association (AHA). Merely making such printed information available for clients to peruse has been demonstrated to result in decreased consumption of fat and increased fiber intake (Bereford et al, 1997). Weight reduction caormalize plasma lipid and lipoprotein levels in overweight clients. The cardiac rehabilitatiourse collaborates with the dietitian and physical therapist to provide multifactorial rehabilitation, including nutrition education, counseling, behavior modification, and exercise training, to help the overweight client lose weight permanently.

ANTIHYPERUPIDEMIC AGENTS. Reduction of cholesterol levels with antihyperlipidemic agents, such as pravastatin (Pravachol), has been demonstrated to reduce significantly the risk of further CAD (including recurrent MI), death from CAD, and the need for revascularization procedures. Thus many clients with both normal and high cholesterol levels are encouraged to take these agents after CAD develops. An area of controversy is the use of antioxidants (such as vitamin E). Some researchers report that the use of such agents counteracts the adverse effects of oxygen free radicals (derived from high cholesterol levels) on blood vessels and protects arteries. Other reports point out that excessive vitamin E increases the risk for liver damage and that the longterm effects of antioxidants are not known.

PHYSICAL ACTIVITY. The nurse collaborates with the physical therapist to establish an activity and exercise schedule as part of client rehabilitation. The nurse instructs the client to remaiear home during the first week after discharge and to continue a walking program. The client may engage in light housework or any activity done while sitting and that does not precipitate angina. During the second week, he or she is encouraged to increase social activities and possibly to return to work part time. By the third week, he or she may begin to lift objects as heavy as 15 pounds (such as 2 gallons of milk) but should avoid lifting or pulling heavier objects for the first 6 to 8 weeks. Chart 38-10 lists suggested instructions for exercise. The client may begin a simple walking program by walking 400 feet twice a day at the rate of 1 mile/hr the first week after discharge and increasing the distance and rate as tolerated, usually weekly, until he or she can walk 2 miles at 3 to 4 miles/hr. The nurse instructs the client to take a pulse reading before, halfway through, and after exercise. The client should stop exercising if the target pulse rate is exceeded or if dyspnea or angina develops. After a limited exercise tolerance test, the physical therapist or nurse encourages the client to join a formal exercise program, ideally one that assists the client in monitoring cardiovascular progress. The program should include 5- to 7-minute warm-up and cool-down periods, as well as 30 minutes of aerobic exercise. The client should engage in aerobic exercise a minimum of three (and preferably five) times a week.

COMPLEMENTARY AND ALTERNATIVE THERAPIES. Additional therapies can aid in reducing the client’s anxiety about progressive activity both in the immediate postoperative period and during the rehabilitation phase. Such techniques as progressive muscle relaxation, guided imagery, and music therapy have been shown to decrease anxiety, reduce depression, and increase compliance with activity/exercise regimens after CABG.

SEXUAL ACTIVITY. Sexual activity is often a subject of great concern to clients and their partners. The nurse informs the client and partner that engaging in their usual sexual activity is unlikely to cause any damage to the heart. Clients can resume sexual intercourse on the advice of the physician, usually after exercise tolerance is assessed. The client who can walk one block or climb two flights of stairs without symptoms can usually safely resume sexual activity. The nurse suggests that initially clients schedule intercourse after a period of rest. They might try having intercourse in the morning when they are well rested or wait I 1/2 hours after exercise or a heavy meal. The position selected should be comfortable for both the client and his or her partner (e.g., side-lying position) so that no undue stress is placed on the heart or suture line.

BLOOD PRESSURE CONTROL. The nurse may make arrangements for the client to have blood pressure measurements taken at regular intervals and collaborates with the primary care provider to establish parameters for reporting the blood pressure to the provider. Lifestyle modifications such as weight reduction, physical activity, and reducedsodium diets may assist in the management of hypertension. If the client is taking medication, the nurse assesses his or her compliance with the medication regimen.

BLOOD GLUCOSE CONTROL. Clients with diabetes mellitus are assessed for their participation in efforts to control hyperglycemia. The nurse reviews the prescribed dosage of insulin or oral hypoglycemic agents with the client and family. The client should demonstrate accurate testing of blood for glucose levels.

CARDIAC MEDICATIONS. The nurse assists the client in understanding the type of cardiac medications prescribed, the benefit of each drug, potential side effects to watch for, and the correct dosage and time of day to take each drug. Medication regimens vary considerably among clients. However, many clients with angina are discharged while taking aspirin, a beta blocker, a calcium channel blocker, an antihyperlipidemic agent, and a nitrate. Clients who have experienced an MI may require aspirin, a beta blocker, an antihyperlipidemic agent, and an angiotensin-converting enzyme (ACE) inhibitor. The regimen can be complex. The nurse must determine that the client can comply with the instructions. Use of sublingual nitroglycerin deserves special attention. The nurse instructs the client to carry nitroglycerin tablets at all times and to keep the tablets in a light-resistant container. Nitroglycerin tablets should be replaced every 3 to 5 months, before they lose their potency and stop producing a tingling sensation when placed under the tongue. Chart 38-11 gives instructions for clients concerning management of chest discomfort at home.

SEEKING MEDICAL ASSISTANCE.

Clients are encouraged to notify their health care provider if they experience the following:

·        Heart rate remaining less than 50 after arising

·        Wheezing or difficulty breathing

·        Weight gain of 3 pounds in 1 week

·        Slow persistent increase iitroglycerin use

·        Dizziness, faintness, or shortness of breath with activity

Clients are encouraged to call for transportation to the hospital if they experience the following:

·        Chest discomfort that does not improve after 20 minutes or 3 nitroglycerin tablets

·        Extremely severe chest discomfort with weakness, nausea, or fainting.

HEALTH CARE RESOURCES

The AHA is an excellent source for booklets, films, video cassettes, cookbooks, and professional service referrals for the client with CAD. Many local affiliates have their own cardiac rehabilitation programs. Within the community, cardiac rehabilitation programs may be affiliated with local hospitals, community centers, or other facilities, such as clinics. Many shopping malls open before shopping hours to allow a measured walking program indoors; this is particularly popular with older clients and also provides a good support group. Mended Hearts is a nationwide program with local chapters that provides education and support to CABG clients and their families. Smoking cessation programs and clinics, as well as weight reduction programs, are found within the community. Many hospitals sponsor health fairs, blood pressure screening, and risk factor modification programs as well.

 Evaluation: Outcomes

The nurse evaluates the client with CAD on the basis of the identified nursing diagnoses and collaborative problems. The expected outcomes are that the client will:

• State that the chest discomfort is alleviated, appear comfortable, and have resolution of ST-segment and T-wave changes

• Remain hemodynamically stable: maintain a normal sinus rhythm or normal rhythm for the client at a rate of approximately 60, as well as maintain blood pressure within an acceptable range, adequate urine output, mental alertness, palpable pedal pulses, and clear lungs on auscultation

• Walk 200 feet four times a day without chest discomfort or shortness of breath

• Indicate decreased anxiety

• Indicate a sense of having some control over life

• Experience minimal angina while engaging in activities of daily living (ADLs) or an exercise program  

 

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