MS CH 26 Nursing Care of Patients With Heart Failure PDF

4068_Ch26_521-546 15/11/14 1:44 PM Page 521 Nursing Care of Patients With Heart Failure KATHY BERCHEM LEARNING OUTCOMES 1. Describe the pathophysiology of left- and right-sided heart failure. 2. Define acute heart failure. 3. List causes of acute and chronic heart failure. 4. Identify signs and sym...

4068_Ch26_521-546 15/11/14 1:44 PM Page 521 Nursing Care of Patients With Heart Failure KATHY BERCHEM LEARNING OUTCOMES 1. Describe the pathophysiology of left- and right-sided heart failure. 2. Define acute heart failure. 3. List causes of acute and chronic heart failure. 4. Identify signs and symptoms of acute and chronic heart failure. 5. Plan nursing care for patients undergoing diagnostic tests for heart failure. 6. Explain medical treatments used for acute and chronic heart failure. 7. Plan nursing care for acute and chronic heart failure. 8. Plan teaching for patients with heart failure and their families. 26 KEY TERMS afterload (AFF-ter-lohd) cor pulmonale (KOR PUL-mah-NAH-lee) cyanosis (SYE-an-NOH-siss) hepatomegaly (HEP-aa-toh-MEH-gah-lee) orthopnea (or-THOP-knee-ah) paroxysmal nocturnal dyspnea (PEAR-ox-IS-mul knock-TURN-al DISP-knee-ah) peripheral vascular resistance (puh-RIFF-uh-ruhl VASkyoo-lar ree-ZIS-tense) preload (PREE-lohd) pulmonary edema (PULL-muh-NARE-ee eh-DEE-muh) splenomegaly (SPLEE-noh-MEG-ah-lee) 521 4068_Ch26_521-546 15/11/14 1:44 PM Page 522 522 UNIT FIVE Understanding the Cardiovascular System OVERVIEW OF HEART FAILURE Heart failure (HF) is a clinical syndrome that occurs as a result of the inability of the ventricle(s) to fill or pump enough blood to meet the body’s oxygen and nutrient needs. It may cause dyspnea, fatigue, and fluid v olume overload in the intra vascular and interstitial spaces, resulting in reduced quality and length of life. Causes of HF are varied and may include coronary artery disease (most often), myocardial infarction (MI), cardiomyopathy, heart valve problems, and hypertension. Any heart problem can potentially lead to HF . In the older adult, the most common cause of HF is cardiac ischemia. It may develop rapidly (acute), as with cardiogenic shock and pulmonary edema, or over time (chronic) as a result of another disorder, such as hypertension or pulmonary disease. The incidence of HF is growing as the older adult population and patient survi val rates increase. According to the American Heart Association (AHA; Go et al, 2014), 5.1 million people ha ve HF with more than 670,000 ne w cases each year. HF is the most common reason for hospital admission in the older adult. The patient may e xperience many functional limitations and symptoms, and according to the Centers for Disease Control and Pre vention (2013), the mortality rate is as high as 597,000 deaths per year . Quality of life is often impaired. Readmission rates to hospitals soon after dischar ge for HF treatment are high and pose a challenge for health care providers (HCPs). For more information, visit www.americanheart.org. • When too much water builds up behind the dam, the riverbanks are flooded; in HF, if too much blood builds up behind the failing ventricle, the lungs (pulmonary edema) or peripheral tissues are flooded (peripheral edema). • HF can be the result of systolic (contractile) dysfunction, diastolic (relaxation) dysfunction, or a mixed systolic and diastolic dysfunction. Systolic dysfunction is a contractile problem in which the ventricle is unable to generate enough force to pump blood from the ventricle. Diastolic dysfunction is a problem with the ventricle’s ability to relax and fill. Mixed systolic and diastolic dysfunction is a combination of the two defects. Conditions that cause HF can af fect one or both of the heart’s pumping systems. Therefore, HF can be classified as right-sided HF, left-sided HF, or biventricular HF. The left ventricle typically weakens first because it has the greatest workload to eject blood against the resistance in the aorta. Because the right and left sides of the heart’s pumping system work together in a closed system, failure of one side eventually leads to failure of the other side. Congestive Heart Failure Congestive HF is an older term for HF. It is still used inter changeably by some to indicate HF, the preferred term. This is because volume overload or “congestion” either in the lungs or periphery is not present in e veryone with HF or at all times. Pathophysiology The heart is divided into two separate pumping systems, the right side of the heart and the left side of the heart. Proper cardiac functioning requires each ventricle to pump out equal amounts of blood over time. If the amount of blood returned to the heart becomes more than either v entricle can handle, the heart can no longer function effectively as a pump. LEARNING TIP To understand HF, compare it to a dam in a river: • In a river without a dam, the water flows freely; in the normal circulatory system, blood flows freely. • In a river with a dam, the water is blocked by the dam and builds up behind it; in HF, the failing ventricle acts like a dam in the river, causing blood to back up behind it. LEARNING TIP To visualize and understand the effects of HF, trace the flow of blood backward from each ventricle. Along the backward path from the failing ventricle, congestion develops and produces the signs and symptoms seen in HF. If you understand the backward path of congestion, you can identify the signs and symptoms specifically associated with right- or left-sided HF. Left-Sided Heart Failure The left ventricle must generate a certain amount of force during a contraction to eject blood into the aorta through the aortic valve. This force is referred to as afterload. The pressure within the aorta and arteries acts as resistance and influences the force required to open the aortic valve to pump blood into the aorta. This pressure is called peripheral vascular resistance (PVR). Hypertension is one of the major causes of left-sided HF because it increases the pressure within arteries. Increased pressure in the aorta makes the left ventricle work harder to pump blood into the aorta. Over time the strain caused by the increased workload causes the left v entricle to weaken and fail. Other conditions that can lead to left-sided HF are described in Table 26.1. 4068_Ch26_521-546 15/11/14 1:44 PM Page 523 Chapter 26 TABLE 26.1 CAUSES OF LEFT-SIDED HEART FAILURE Cause Aortic stenosis Primary Effect on Left Ventricular Workload Increased volume to pump from restricted blood outflow Cardiomyopathy Increased workload from impaired contractility Coarctation of the aorta Restricted outflow and increased resistance from narrowing of aorta Hypertension Resistance increased from elevated pressure Heart muscle infection Increased workload from damaged myocardium Myocardial infarction Increased workload from impaired contractility Mitral regurgitation Increased volume to pump from backward blood flow With left-sided HF, blood backs up from the left ventricle into the left atrium and then into the four pulmonary veins and lungs (Fig. 26.1). This increases pulmonary pressure, causing movement of fluid f irst into the interstitium and then into the alveoli. Alveolar edema is more serious because it reduces gas exchange across the alveolar capillary membrane. Shortness of breath and c yanosis may result from the decreased Nursing Care of Patients With Heart Failure 523 oxygenation of the blood leaving the lungs. If the fluid buildup is severe, acute pulmonary edema occurs, which requires immediate medical treatment. Right-Sided Heart Failure Conditions causing right-sided HF increase the w ork of the right ventricle. They increase the amount of contractile force needed or require pumping of e xcess blood volume (preload). Causes of right-sided HF are described in Table 26.2. The major cause of right-sided HF is left-sided HF. When the left side fails, fluid backs up into the lungs and pulmonary pressure is increased. The right ventricle must continually pump blood against this increased fluid and pressure in the pulmonary artery and lungs. Over time this additional strain eventually causes it to f ail. When the right v entricle hypertrophies or fails because of increased pulmonary pressures, it is referred to as cor pulmonale. When the right ventricle fails, it does not empty normally, and there is a backw ard buildup of blood in the systemic blood vessels. As the blood backs up from the right ventricle, right atrial and systemic venous blood volume increases. The jugular neck veins, which are not normally visible, become distended and can be seen when the person is in a 45-degree upright position. Edema may occur in the peripheral tissues, and the abdominal organs can become engorged (Fig. 26.2). Fluid congestion in the gastrointestinal (GI) tract causes anorexia, nausea, and abdominal pain. As the failure progresses, blood pools in the hepatic v eins, and the liver becomes congested (hepatomegaly). This liver congestion also • WORD • BUILDING • cor pulmonale: cor—heart + pulm—lung hepatomegaly: hep—liver + mega—large TABLE 26.2 CAUSES OF RIGHT-SIDED HEART FAILURE Cause Atrial septal defect FIGURE 26.1 Left-sided HF. Shaded areas indicate areas of congestion from blood backup caused by the failing left side of the heart. Primary Effect on Right Ventricular Workload Left atrial blood flow into right atrium increases right ventricular volume to pump Cor pulmonale Resistance increased from elevated pressure Left-sided HF Resistance increased from backup of fluid and elevated pressures Pulmonary hypertension Resistance increased from elevated pressure Increased volume to pump from Pulmonary restricted right ventricular blood valve stenosis outflow 4068_Ch26_521-546 15/11/14 1:44 PM Page 524 524 UNIT FIVE Understanding the Cardiovascular System released from the pituitary gland to conserv e water, causing decreased urine output. This adds to the fluid retention problem already found in HF. Over time the heart responds to the increased workload by enlarging its chambers (dilation) and increasing its muscle mass (hypertrophy), referred to as remodeling. In dilation, the heart muscle fibers stretch to increase the force of myocardial contractions, which is kno wn as the FrankStarling phenomenon. In hypertrophy, the muscle mass of the heart increases, creating more contractile force. Both of these compensatory mechanisms temporarily impro ve patient symptoms b ut also increase the heart’ s oxygen needs, which further contrib utes to HF. Additionally, the heart walls stiffen, which further reduces pumping ability. PULMONARY EDEMA (ACUTE HEART FAILURE) FIGURE 26.2 Right-sided HF. Shaded areas indicate areas of congestion from blood backup due to the failing right side of the heart. causes pain in the right upper quadrant of the abdomen and impairs liver function. Systemic venous congestion also leads to engorgement of the spleen (splenomegaly). LEARNING TIP To understand the signs and symptoms of leftsided versus right-sided HF, remember that left-sided signs and symptoms are found in the lungs. Left begins with L, as does Lung: Left = Lungs = L. Any signs and symptoms not related to the lungs (L) are caused by right-sided failure. COMPENSATORY MECHANISMS TO MAINTAIN CARDIAC OUTPUT Compensatory mechanisms help ensure that an adequate amount of blood is being pumped out of the heart. Although these mechanisms are designed to maintain cardiac output, they contribute to a cycle that, instead of being helpful, leads to further HF. When the sympathetic nervous system detects low cardiac output, it speeds up the heart rate by releasing epinephrine and norepinephrine. Although this raises cardiac output (cardiac output = heart rate × stroke volume), the increased heart rate also increases the oxygen needs of the heart. In response to the resulting low renal blood flow, the kidneys activate the reninangiotensin-aldosterone system, and antidiuretic hormone is Pulmonary edema, also known as acute HF, is sudden severe fluid congestion in the alveoli of the lungs and is life threatening. Pulmonary edema occurs with an acute event such as a MI or when the heart is se verely stressed, causing the left ventricle to fail. Complications of pulmonary edema include dysrhythmias and cardiac arrest. Pathophysiology First, pressure rises in the lung’ s venous blood vessels as blood builds up. As pressures continue to rise, fluid moves into the interstitial spaces. Then, with continued pressure increases, fluid containing red blood cells (RBCs) leaks into the alveoli. Finally, the alveoli and airways become filled with fluid, reducing gas exchange and oxygen levels. Signs and Symptoms Signs and symptoms of pulmonary edema are listed in Table 26.3. Pink, frothy sputum is a classic symptom of pulmonary edema caused by the increased lung congestion and pressures that allow leaking of fluid and RBCs into the alv eoli. Compensatory mechanisms increase the heart rate and blood pressure; however, as pulmonary edema w orsens, the blood pressure may fall. Diagnostic Tests Diagnostic studies are listed in Table 26.3. The congestion in the pulmonary system can be seen on x-ray e xamination. Arterial blood gases (ABGs) show a decrease in PaO2 that continues as the edema worsens and an increase in PaCO2, causing respiratory acidosis. The pulmonary artery catheter sho ws elevated pulmonary pressures and a decreased cardiac output. Therapeutic Measures Immediate treatment is needed to pre vent patients from drowning in their own secretions (see Table 26.3). The goal • WORD • BUILDING • splenomegaly: splen—spleen + mega—large 4068_Ch26_521-546 15/11/14 1:44 PM Page 525 Chapter 26 TABLE 26.3 ACUTE HEART FAILURE SUMMARY Signs and Symptoms Rapid respirations with accessory muscle use Severe dyspnea, orthopnea Crackles and wheezes Coughing Pink, frothy sputum Anxiety, restlessness Pale skin and mucous membranes Clammy, cold skin Diagnostic Tests Chest x-ray examination Arterial blood gases Electrocardiogram Hemodynamic monitoring Therapeutic Measures Oxygen via cannula, mask, or mechanical ventilation Positioning in high or semi-Fowler’s position Bedrest Intravenous (IV) drugs: morphine, diuretics, inotropic agents, vasodilators Frequent vital signs, urinary output Pulmonary pressures Daily weights Treatment of underlying cause Priority Nursing Diagnoses Impaired Gas Exchange Decreased Cardiac Output Excess Fluid Volume Nursing Care of Patients With Heart Failure 525 of therapy is to reduce the w orkload of the left v entricle in order to impro ve cardiac output and reduce the patient’ s anxiety. Placing the patient in F owler’s position allows the lungs to expand more easily. Ask the patient what position provides him or her the most comfort in breathing. Oxygen is given, usually by mask to pro vide higher amounts. In severe cases of pulmonary edema, endotracheal intubation and mechanical ventilation may be necessary. Medications are given intravenously to reduce anxiety, relax airways, increase peripheral blood pooling to decrease preload, reduce fluid congestion, strengthen heart contractions, reduce arterial pressure (afterload) and sodium and water retention to relieve dyspnea. Nursing Care The patient is typically critically ill and in an intensi ve care unit (ICU). Psychosocial supportive care is important because the patient will be anxious if alert. CHRONIC HEART FAILURE Signs and Symptoms Chronic HF is a progressi ve disorder. Signs and symptoms worsen over time (Table 26.4). Fatigue and Weakness Fatigue and weakness are the earliest symptoms of HF . They occur from the decreased amount of oxygen reaching the tissues. During the day, the fatigue worsens, especially with activity. Dyspnea Dyspnea is a common symptom of left-sided HF. It is a result of the pulmonary congestion that impairs gas exchange TABLE 26.4 CHRONIC HEART FAILURE SUMMARY Right-Sided Heart Failure Left-Sided Heart Failure Signs and Symptoms Jugular venous distention Dependent peripheral edema Ascites Weight gain Splenomegaly Hepatomegaly Gastrointestinal pain, anorexia, nausea Fatigue, weakness Tachycardia Nocturia Dyspnea on exertion Dry hacking cough, especially when supine Crackles, wheezing Orthopnea Paroxysmal nocturnal dyspnea Cheyne-Stokes respirations Cyanosis Tachypnea, tachycardia Nocturia Diagnostic Tests History and physical examination Electrocardiogram Chest x-ray Two-dimensional echocardiography with Doppler Exercise stress test Coronary angiography Continued 4068_Ch26_521-546 15/11/14 1:44 PM Page 526 526 UNIT FIVE Understanding the Cardiovascular System TABLE 26.4 CHRONIC HEART FAILURE SUMMARY—cont’d Cardiac magnetic resonance imaging Nuclear imaging studies Cardiac catheterization Serum laboratory tests: CBC, BNP, electrolytes, BUN, creatinine, liver function tests, thyroidstimulating hormone, fasting blood glucose, lipid profile, ferritin Arterial blood gases Urinalysis Sleep studies Hemodynamic monitoring Complications Hepatomegaly Splenomegaly Pleural effusion Left ventricular thrombus and emboli Cardiogenic shock Therapeutic Measures Noninvasive Treat underlying cause Oxygen by cannula or mask Drug therapy (see Table 26.5) Individualized activity plan Dietary sodium restriction Fluid restriction Daily weights Invasive Pacemaker ICD Resynchronization therapy Mechanical assistive devices Intra-aortic balloon pump Left ventricular assist device Total artificial heart Surgery: CABG, valvuloplasty, heart valve replacement, cardiac transplant Priority Nursing Diagnoses Impaired Gas Exchange Decreased Cardiac Output Excess Fluid Volume Note. BNP = brain natriuretic peptide; BUN = blood urea nitrogen; CABG = coronary artery bypass graft; CBC = complete blood count; ICD = implantable cardioverter defibrillator. between the alv eoli and capillaries. Dyspnea stimulates compensatory mechanisms that produce short, rapid respirations. Dyspnea is classified in several ways: • Exertional dyspnea is shortness of breath that increases with activity. • Orthopnea is dyspnea that increases when lying flat. In an upright position, gravity holds fluid in the lower extremities. In a supine position, gravitational forces are removed, allowing fluid to move from the legs to the heart, which overwhelms the already congested pulmonary system. When orthopnea is present, two or more pillows are often used for sleeping. Documentation should state the number of pillows used. For example, use of three pillows would be “three-pillow orthopnea.” • Paroxysmal nocturnal dyspnea (PND) is sudden shortness of breath that occurs after lying flat for a time. PND results from excess fluid accumulation in the lungs. The sleeping person awakens with feelings of • WORD • BUILDING • orthopnea: orth—straight + pnea—to breathe 4068_Ch26_521-546 15/11/14 1:44 PM Page 527 Chapter 26 suffocation and anxiety. Relief is obtained by sitting upright for a short time, which reduces the amount of fluid returning to the heart. Nursing Care of Patients With Heart Failure 527 up to 30 seconds and is then follo wed by the shallo w to deeper respiratory pattern of Cheyne-Stokes as carbon dioxide levels rise again. Cough Edema A chronic, dry cough is common in HF . The coughing increases when lying down from increased irritation of the lung mucosa. This irritation is due to the increase in pulmonary congestion that occurs when gravity no longer keeps fluid in the legs and more fluid returns to the heart and lungs. Pulmonary congestion causes abnormal breath sounds such as crackles and wheezes. Crackles are produced from fluid buildup in the alveoli resulting from increased pressure in the pulmonary capillaries. Wheezes occur from bronchiolar constriction caused by the increased fluid. Edema occurs in HF as a result of (1) systemic blood v essel congestion and (2) sympathetic compensatory mechanisms that cause the kidneys to activate the renin-angiotensin-aldosterone system, in which antidiuretic hormone is released from the pituitary gland, causing sodium and water to be retained. Systemic edema or pulmonary edema can occur in HF . The effect of backward buildup of pressure in the systemic blood vessels is seen with distention of the jugular v eins, swelling of the legs and feet, sacral edema in the indi vidual on bed rest, and increased fluid within the abdominal cavity and organs (ascites). An acute buildup of fluid in the lungs produces pulmonary edema. Tachycardia Anemia The sympathetic nervous system compensates for the decreased cardiac output in HF by releasing epinephrine and norepinephrine to increase the heart rate. Normally , this is helpful because the increased heart rate increases the amount of blood ejected by the heart to maintain an adequate cardiac output. However, whenever the heart works faster, the heart itself also requires more oxygen, which the failing heart finds difficult to supply. Many patients with HF are anemic due to hemodilution from fluid overload, and decreased angiotensin-converting enzyme (ACE) action. The reduced ACE action decreases erythropoietin release, resulting in decreased production of RBCs. Crackles and Wheezes LEARNING TIP To simulate the sound of crackles, open a piece of Velcro or rub hair together next to your ear. These sounds are similar to the sound of crackles heard with a stethoscope. Chest Pain Chest pain may occur from ischemia in the patient with HF. Decreased cardiac output results in decreased oxygen delivery to the heart itself via the coronary arteries. Compensatory mechanisms designed to maintain cardiac output increase the workload and oxygen needs of the heart and are counterproductive in HF. Tachycardia increases the oxygen needs of the heart. The kidneys compensate by retaining sodium and fluid, which increases the fluid volume returning to the heart (preload) and therefore the heart’s workload and oxygen needs. Pain also increases oxygen requirements, adding further to the cycle of HF. Cheyne-Stokes Respiration A breathing pattern of shallow respirations building to deep breaths followed by a period of apnea characterizes CheyneStokes breathing. The apneic period occurs because the deep breathing causes carbon dioxide levels to drop to a level that does not stimulate the respiratory center. This apnea may last Nocturia Nocturia is an increase in urine output at night during sleep. After lying down, fluid in the lower legs returns to the circulatory system. Renal blood flo w and filtration are increased, resulting in greater urine production and the need to urinate frequently during the night. Nocturia may occur up to six times per night, contributing to the patient’s fatigue from lack of sleep. NURSING CARE TIP Patients will often void shortly after going to bed due to fluid in the legs returning to the heart and then the kidneys for filtering after they lie down. To help patients get as much undisturbed rest as possible, teach them to recline with their legs at or above heart level for at least 30 minutes before going to bed. Then they can void before going to bed, instead of soon after. Cyanosis The skin, nail beds, or mucous membranes may appear blue, or cyanotic, from decreased oxygenation of the blood. Cyanosis is a late sign of HF. It is associated primarily with left-sided HF. Altered Mental Status Reduced cardiac output decreases the amount of oxygen delivered to the brain. As a result, restlessness, insomnia, confusion, decreased le vel of consciousness, and impaired memory may occur. 4068_Ch26_521-546 15/11/14 1:44 PM Page 528 528 UNIT FIVE Understanding the Cardiovascular System Malnutrition Several factors contribute to malnutrition in the person with chronic HF. Altered mental status, dyspnea, and fatigue interfere with the ability to eat. Anorexia and GI upset occur from pressure exerted by excess fluid surrounding the GI structures (ascites). This pressure may also impair absorption of food. CRITICAL THINKING Mr. Shepard—Part 1 ■ Mr. Shepard, age 66, has a f amily history of cardiac disease. He has been hypertensive for 10 years and takes captopril (Capoten) daily. His baseline vital signs are BP 122/78 mm Hg, pulse 80 beats per minute (beats/min), respirations 18 per minute, height 66 inches, and weight 170 lb. During a visit to his HCP , he states that he has been short of breath during his daily 2-mile walk and has been using two pillows at night for sleep. As he talks, the HCP notes that he has an intermittent dry cough. His physical examination shows BP 140/86 mm Hg, pulse 106 beats/min, respiration 24 per minute, weight 178 lb, and bilateral crackles in the lung bases. 1. What signs and symptoms of HF does Mr. Shepard have? 2. Do the signs and symptoms reflect right- or leftsided HF? 3. Why are each of the signs and symptoms occurring? 4. Why is Mr. Shepard using two pillows for sleeping? 5. What health care team members might collaborate on Mr. Shepard’s care during the course of his HF? Suggested answers are at the end of the chapter. Complications of Heart Failure Complications of HF are listed in Table 26.4. The liver and spleen enlarge from the fluid congestion, which causes impaired function, cellular death, and scarring. The elevated pressures in the capillaries of the lung can cause a pleural effusion, which is a leakage of fluid from the capillaries of the lung into the pleural space. Thrombosis and emboli can occur as a result of poor emptying of the ventricles, which leads to stasis of blood. Aspirin or anticoagulants are often prescribed to prevent thrombus formation in patients with HF . Cardiogenic shock, often caused by an MI that damages the left ventricle, occurs when the left v entricle is unable to supply the tissues with enough oxygen and nutrients to meet their needs. Cardiogenic shock is a life-threatening condition that requires immediate treatment (see Chapter 9). Diagnostic Tests Diagnostic tests are done to identify the cause of HF and determine the degree of failure present (see Table 26.4): • Serum laboratory tests can evaluate contributing factors for HF, such as elevated serum blood urea nitrogen (BUN) and serum creatinine from renal failure, elevated liver enzymes from liver damage, elevated ferritin with hemochromatosis (iron overload), and thyroid function tests. • A serum B-type natriuretic peptide (BNP) or N-terminal proBNP (NT-proBNP) level may be obtained. Elevated levels indicate HF and severity; higher levels of this cardiac biomarker correlate with a worse prognosis. BNP is made by the heart to regulate blood volume to reduce cardiac workload. When the heart has to work harder over time, it releases more BNP. • Elevated serum cystatin C (a protein produced by all nucleated cells) is a risk factor for HF. • A chest x-ray examination shows the size, shape, and any enlargement of the heart as well as congestion in the pulmonary vessels. • Cardiac dysrhythmias that precipitate and contribute to HF are diagnosed with an electrocardiogram (ECG; see Chapters 21 and 25). • Echocardiography may measure ventricular size, wall thickness, motion, and ejection fraction and assess valvular function. • Exercise stress testing and nuclear imaging studies show activity tolerance, which is usually limited in HF. • Cardiac magnetic resonance imaging (MRI) shows both moving and still pictures of the heart and major blood vessels. Cardiac structure and function are analyzed to determine treatment for cardiac disease. • Cardiac catheterization and angiography are used to detect underlying heart disease that may be the cause of HF. • Sleep studies may be done because sleep apnea or breathing disorders can contribute to HF. • Measurement of the pressure in the heart and lungs is done with hemodynamic monitoring to guide medical therapy. CRITICAL THINKING Mr. Shepard—Part 2 ■ Mr. Shepard’s chest x-ray e xamination shows an enlarged heart (cardiomegaly). 1. Why is Mr. Shepard’s heart enlarged? 2. What is the significance of an enlarged heart? Suggested answers are at the end of the chapter. Therapeutic Measures The overall goal of medical treatment for chronic HF is to improve the heart’s pumping ability and decrease the heart’s oxygen demands. Treatment of HF focuses on (1) identifying and correcting the underlying cause, (2) increasing the strength of the heart’s contraction, (3) maintaining optimum water and sodium balance, and (4) decreasing the heart’ s workload. HF management requires a team approach that may involve physicians, nurse practitioners, case managers, 4068_Ch26_521-546 15/11/14 1:44 PM Page 529 Chapter 26 nurses, dietitians, physical therapists, occupational therapists, pharmacists, social w orkers, and clergy. HF critical pathways (treatment guidelines) as well as HF clinics are used to ensure quality-based outcomes while reducing treatment costs. The severity of HF determines the individualized therapy selected. Noninvasive approaches are usually tried f irst. If noninvasive treatment is not ef fective, invasive approaches may be used. Often, multiple therapies are used in combination for optimum patient outcomes. Oxygen Therapy One of the major problems caused by HF is a reduction in oxygen delivered to the tissues. The signs and symptoms of this are fatigue, dyspnea, altered mental status, and cyanosis. Oxygen therapy may assist in supplying the oxygen needs of the tissues. In mild HF , oxygen may be deli vered via nasal cannula. For more severe cases, ABG values guide oxygen delivery, either via masks that provide high concentrations of oxygen or with mechanical ventilation. Nursing Care of Patients With Heart Failure 529 in survival along with a reduction in need for emergency treatment. Implications for Nursing Practice Cardiac rehabilitation programs for chronic HF patients have been shown to improve quality of life. Nurses should initiate referrals to cardiac rehabilitation programs and educate patients on their value toward overall cardiac health. REFERENCES Belardinelli, R., Georgiou, D., Cianci, G., & Purcaro, A. (2012). 10-year exercise training in chronic heart failure: A randomized controlled trial. Journal of the American College of Cardiology, 60, 1521–1528. Porto, E. F., Kumpel, C., Leite, J. R., Andrade, A. A., Oliveira, N. C., & Portes, L. A. (2012). Quality of Life after Cardiac Rehabilitation for Patients with Heart Failure: 18 months followup. American Journal of Medicine and Medical Sciences, 2(5): 89–95. Activity Activity tolerance depends on the se verity of HF signs and symptoms. Severe symptoms may require bed rest with restricted activity until treatment reduces the symptoms. For stable HF, a regular exercise program, such as one set up with referral to a cardiac rehabilitation program, has shown to improve cardiac function and reduce HF effects (see “EvidenceBased Practice”). Patients should be encouraged to stay as active as possible within the parameters of the collaborati ve plan set up with the health care team.An individualized walking program that increases acti vity over time is often prescribed. Patients are educated on how to exercise safely and how to identify symptoms they may have to prevent overexertion and worsening of symptoms. EVIDENCE-BASED PRACTICE Clinical Question Do cardiovascular rehabilitation programs improve quality of life for HF patients? Evidence In a randomized controlled study of 123 medically stable HF patients over 10 years, exercise training demonstrated improved functional capacity and quality of life over patients who did not exercise regularly (Belardinelli, Georgiou, Cianci, & Purcaro, 2012). Cardiac rehabilitation has shown long-term benefits also in a randomized controlled trial (Porto et al, 2012). In the study, patients with chronic HF who participated in a supervised cardiac rehabilitation program, compared with nonparticipants, demonstrated improved cardiovascular fitness, functional capacity, quality of life, and an increase Sodium Restriction and Weight Control Dietary sodium is restricted to decrease fluid retention. Salt substitutes often use potassium in place of sodium, so the patient and HCP should discuss their use.A healthy weight range should be maintained, and a dietitian consult can include a plan for a low-sodium diet and weight reduction if needed. BE SAFE! In severe HF with abdominal discomfort present, malnutrition is a concern. The patient can be anorexic, but the weight gain that occurs with fluid retention can mask the weight loss occurring from the anorexia. Monitor food intake to ensure that weight gain from fluid retention does not allow malnutrition to go undetected. Drug Therapy There is no cure for HF . Medications, however, can improve symptoms and quality of life. The American College of Cardiology Foundation/American Heart Association (ACC/AHA) 2013 guidelines recommend medication classes with qualifiers for the following stages of HF development (Yancy et al, 2013): • Stage A refers to people at high risk of HF. • Stage B is those who have no HF symptoms but do have structural heart disease. • Stage C applies to people with current or past symptoms of HF with structural heart disease. This includes most patients with HF. • Stage D includes those with refractory HF, which requires extraordinary support or hospice care. 4068_Ch26_521-546 15/11/14 1:44 PM Page 530 530 UNIT FIVE Understanding the Cardiovascular System In general, drug cate gories begin with angiotensinconverting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) to control hypertension if present in Stage A, then add beta blockers (bisoprolol, carvedilol, metoprolol succinate SR) along with the ACE inhibitors or ARBs for Stage B, then diuretics for fluid retention, and consideration of aldosterone antagonists, nitrates, digitalis, and hydralazine (Apresoline) for Stage C (Table 26.5). Anticoagulants are also used on an individual risk basis. LEARNING TIP To help you identify ACE inhibitors, remember that their generic names end with -pril. ANGIOTENSIN-CONVERTING ENZYME INHIBITORS. ACE inhibitors are considered the first-choice drug over angiotensin receptor blockers (ARBs). They are used for their vasodilation effect, which lowers blood pressure and reduces workload on the heart. They also offer additional benefit by preventing remodeling, which is an effect that leads to progressive cardiac deterioration. ANGIOTENSIN RECEPTOR BLOCKERS. ARBs are an alternative to ACE inhibitors for inhibiting the renin-angiotensinaldosterone system, thereby lo wering blood pressure and workload on the heart. They should be used carefully if ACE inhibitors are also used because hypotension, hyperkalemia, and renal dysfunction risks increase. BETA-ADRENERGIC BLOCKERS. Initially the sympathetic nerv- ous system (SNS) acts to compensate for HF . Long-term TABLE 26.5 MEDICATIONS USED FOR HEART FAILURE Medication Class/Action ACE Inhibitors First-line therapy to decrease afterload. Decrease cardiac hypertrophy. Examples Nursing Implications captopril (Capoten) benazepril (Lotensin) enalapril (Vasotec) fosinopril (Monopril) lisinopril (Prinivil, Zestril) moexipril (Univasc) quinapril (Accupril) perindopril (Aceon) ramipril (Altace) trandolapril (Mavik) Check apical pulse and blood pressure (BP). If pulse less than 60 beats/min or systolic BP less than 90 mm Hg, notify HCP. Give 1 hour before meals. Give captopril and moexipril on empty stomach. Teaching: Take first doses at night to adjust to lower BP. Rise slowly. Check BP weekly. Report if persistent cough or other side effects develop. Angiotensin II Receptor Inhibitors (ARBs) candesartan (Atacand) Block angiotensin II receptor irbesartan (Avapro) blockers to prevent losartan (Cozaar) hypertension. May be used valsartan (Diovan) if ACE inhibitor not tolerated. Beta-Adrenergic Blockers Reduce sympathetic nervous system input, cardiac remodeling; improve cardiac output to reduce symptoms, reduce disease progression and sudden death. Loop Diuretics Decrease fluid overload. • Potassium wasting • Potassium sparing Check apical pulse and BP. If pulse below 60 beats/min or systolic BP below 100 mm Hg, notify HCP. Teaching: Rise slowly. Report rash, sore throat/mouth, fever, swelling, difficulty breathing, chest pain, or irregular heartbeat. bisoprolol (Zebeta) carvedilol (Coreg) metoprolol succinate (Toprol XL) Check apical pulse and BP. If pulse below 60 beats/min or systolic or BP below 100 mm Hg, notify HCP. Teaching: Take pulse daily and notify HCP if below 60. Take BP biweekly. Rise slowly. bumetanide (Bumex) furosemide (Lasix) torsemide (Demadex) Check BP and pulse before giving. Monitor electrolyte levels (especially potassium and in those on digitalis) and fluid status (daily weight, intake, output, thirst, dry mouth, weakness, oliguria) throughout therapy. Administer per patient lifestyle (usually in the morning) to avoid nocturia. spironolactone (Aldactone) Do not give potassium-sparing diuretic if hyperkalemic. Teaching: Report signs of hyperkalemia: weakness, fatigue, confusion, dyspnea, arrhythmias, confusion. 4068_Ch26_521-546 15/11/14 1:44 PM Page 531 Chapter 26 Nursing Care of Patients With Heart Failure 531 TABLE 26.5 MEDICATIONS USED FOR HEART FAILURE—cont’d Medication Class/Action Thiazide Diuretics Decrease fluid overload. Potassium wasting Examples Nursing Implications chlorothiazide (Diuril) hydrochlorothiazide (Hydro DIURIL, HCTZ, Microzide) metolazone (Zaroxolyn) Monitor potassium. Teaching: Use of potassium supplements and, if on digitalis, increased risk of toxicity with hypokalemia. Monitor weight daily, and report 2- to 3-lb change over 1–2 days. Use sunscreen. Inotropes—Cardiac Glycoside (Positive Inotrope and Negative Chronotrope) digoxin (Lanoxin) Take apical pulse for 1 minute; if below 60 beats/min, Increase force and contraction notify HCP. of myocardium, which Older patients are more susceptible to toxicity. increases cardiac output. Periodically monitor drug level and electrolytes Slow heart rate to reduce (hypokalemia, hypomagnesemia, and hypercalcemia workload of heart and make more susceptible to toxicity). control atrial fibrillation, Teaching: Take medication exactly as directed, at the if present. same time each day. Take pulse before taking medication; if below 60 beats/min hold and contact HCP. Signs of digitalis toxicity: abdominal pain, anorexia, nausea, vomiting, visual changes (blurred, yellowgreen halos, photophobia, diplopia), bradycardia, dysrhythmias Vasodilators Decrease afterload, which increases cardiac output and reduces cardiac workload. Used for patients who cannot take ACE inhibitors. isosorbide dinitrate (Isorbid, Isordil) hydralazine (Apresoline) nitroglycerin Take blood pressure and pulse before giving. Notify HCP if not within normal limits. Teaching: Rise slowly. Headache common initially, treated with aspirin. ACE = angiotensin-converting enzyme. sympathetic effects, however, are not helpful in HF . Betablockers block the adverse effects of the SNS. Improved cardiac output, reduced symptoms, reduced disease progression, and reduced sudden death are benefits of this therapy. DIURETICS. Diuretics reduce fluid v olume and decrease pulmonary venous pressure, which in turn decreases cardiac workload. Because they are given to help prevent edema, edema does not need to be present for their use. Diuretics act on various areas of the kidneys to promote the excretion of edema fluid. A combination of diuretics may be used to achieve the desired effect. Electrolytes (especially potassium levels to prevent hypokalemia) and fluid balance (to prevent dehydration) should be carefully monitored during therapy. Potassium supplements are often gi ven with potassiumwasting diuretics. ALDOSTERONE ANTAGONISTS. Spironolactone (Aldactone) blocks the effects of aldosterone, which causes the retention of sodium and fluid. Potassium must be monitored carefully, because spironolactone is a potassium-sparing agent and the risk of hyperkalemia increases if ACE inhibitors or ARBs are also used. BE SAFE! Always check potassium levels before giving a potassium-wasting diuretic such as the loop diuretics furosemide (Lasix), bumetanide (Bumex), or torsemide (Demadex) or before giving a potassium supplement, which the patient may be taking due to diuretic therapy. Do not give a diuretic if the potassium level is low or a potassium supplement if the potassium level is high. INOTROPIC AGENTS. Inotropic drugs strengthen ventricular contraction to increase cardiac output. Inotropic agents include digitalis (digoxin), sympathomimetics (dobutamine), and phosphodiesterase inhibitors (milrinone). The sympathomimetics and phosphodiesterase inhibitors are usually used short term. Digitalis. In addition to improving contraction strength, digitalis preparations decrease conduction time within the heart, 4068_Ch26_521-546 15/11/14 1:44 PM Page 532 532 UNIT FIVE Understanding the Cardiovascular System which slows the heart rate to allow more complete emptying of the ventricles. Obtaining an apical pulse rate before administration of digitalis is required. Digitalis may increase myocardial oxygen needs, so it is used cautiously. Monitoring of serum drug levels is necessary to detect toxic levels of the drug. If toxic levels are present, the drug is stopped to allow digitalis levels to decrease over time. CRITICAL THINKING Mr. Shepard—Part 3 ■ During Mr. Shepard’s visit, the HCP tells him to continue the ACE inhibitor, the diuretic, and a 2-g sodium diet. 1. 2. 3. 4. Why is the ACE inhibitor continued? Will the ACE inhibitor affect preload or afterload? Why is the diuretic ordered? What lab test result is checked before administering diuretics? 5. Why is a 2-g sodium diet ordered? 6. What is the overall goal of the ordered treatment? Suggested answers are at the end of the chapter. Pacemakers and Implantable Cardioverter Defibrillator For patients at risk of sudden death, pacemak ers and implantable cardioverter defibrillators (ICDs) are used along with medication therapy. They can pace the heart rate and rhythm or deliver an electric countershock if a life-threatening rhythm occurs. replacement heart. Technology in this area is continually changing. For current information and to see pictures of these devices, see DavisPlus. INTRA-AORTIC BALLOON PUMP. For acute care, an intra- aortic balloon pump (IABP) increases circulation to the coronary arteries and reduces the w ork of the heart. The IABP catheter is inserted into the femoral artery and positioned in the descending aortic arch (Fig. 26.3). It is attached to a computer that senses ventricular contraction and controls the balloon. While the heart is relax ed (diastole), the balloon is inflated, sending more blood into the coronary arteries. Just before the heart contracts (systole), the balloon deflates to allow blood to flow past it. The deflation of the balloon creates a suction effect, which allows the blood to flo w past it with less resistance (decreased afterload) into the aorta. The IABP is inserted in a cardiac catheterization laboratory, critical care unit, or surgical suite and is used short term for several days. VENTRICULAR ASSIST DEVICES. Ventricular assist de vices (VADs) are implanted mechanical devices that assist cardiac pumping (Fig. 26.4). These devices maintain cardiac output and allow the failing ventricle to rest. VADs are used temporarily as a bridge to transplantation (while awaiting a donor heart), bridge to recovery (for hearts that potentially can recover), or as destination therapy (long-term therapy) for those who are not candidates for heart transplant. They may also be referred to as left v entricular assist devices (LVADs) if used in the left ventricle only, right ventricular assist devices (RVADs) if used in the right v entricle only, or bi-VADs Cardiac Resynchronization Therapy With HF, the ventricles do not al ways beat in normal synchrony with each other. This dyssynchrony results in less effective pumping by the ventricles and reduced stroke volume. Cardiac resynchronization therapy (CRT) restores normal contraction timing of the ventricles. It reduces symptoms and improves quality of life. A biventricular cardiac pacing system is used. An atrial lead senses or paces the atria as needed. A right and left v entricular lead stimulates the v entricles to synchronize their contractions in response to the atrial event. Left ventricular filling and thus contraction is then improved. CRT therapy is also a vailable with an implantable car dioverter defibrillator (CRT-D). For more information and pictures of CRT devices, visit www.medtronic.com. Mechanical Assistive Devices Mechanical assistive devices can provide temporary support to patients in cardiogenic shock and act as a bridge to transplantation, destination therap y (long-term solution when other options are not available for the failing heart), or heart replacement. These devices increase the cardiac output of the patient. They include the intra-aortic balloon pump, ventricular assist devices, total artificial heart, and implantable Diastole Systole FIGURE 26.3 Intra-aortic balloon pump. 4068_Ch26_521-546 15/11/14 1:44 PM Page 533 Chapter 26 Nursing Care of Patients With Heart Failure 533 Surgical Management Aorta Inflow valve Outflow valve Battery pack System controller HF causes may be treated surgically with coronary artery bypass for coronary artery disease or v alve replacement for valvular disease (see Chapters 23 and 24). Once these conditions are treated, HF symptoms should resolve. Surgical ventricular reconstruction (SVR) reduces left ventricular volume in HF patients. It is often done along with coronary artery bypass surgery. The STICH trial data on further analysis sho wed that coronary artery bypass graft (CABG) with SVR increased survival when certain parameters occurred (end systolic v olume index 70 mL/m 2 or less; Michler et al, 2013). Nursing Process for the Patient With Chronic Heart Failure Data Collection Prosthetic left ventricle While obtaining data for the patient with HF, focus on areas that might indicate the presence of HF (Table 26.6). FIGURE 26.4 Schematic of a left ventricular assist device. Nursing Diagnoses, Planning, Interventions, and Evaluation (biventricular assist devices) if used in both ventricles. VADs can pump blood directly from either the right atrium to the pulmonary artery (right ventricular failure) or the left atrium to the aorta (left ventricular failure). Two devices are used for biventricular failure. See the “Nursing Care Plan for the Patient With Chronic HF” for common nursing diagnoses. The major focus of nursing care for chronic HF patients is to impro ve oxygenation and decrease the body’s need for oxygen with rest, positioning, medications, fluid balance, and oxygen consumption control. TABLE 26.6 NURSING DATA COLLECTION FOR THE PATIENT WITH CHRONIC HEART FAILURE Subjective Data History Respiratory Lung disease? How many flights of stairs can be climbed without dyspnea? How many pillows used for sleeping? Dyspnea at rest or that awakens from sleeping? Cardiovascular Any cardiac disease history: hypertension, myocardial infarction, valvular problem, anemia, dysrhythmias, palpitations? Chest pain: precipitating factors, severity, relieving factors? Can activities of daily living be performed? Can activities performed 6 months, 4 months, 2 months, 2 weeks ago still be done? Any dizziness (vertigo) or fainting (syncope)? Fluid retention Daily sodium intake? Weight gain? Are shoes tight? Do ankles swell? Gastrointestinal Is appetite good? Any nausea, vomiting, or abdominal pain? Urinary Decrease in daytime urine output? How often does patient go to the bathroom at night (nocturia)? Neurologic Any change in behavior? Continued 4068_Ch26_521-546 15/11/14 1:44 PM Page 534 UNIT FIVE 534 Understanding the Cardiovascular System TABLE 26.6 NURSING DATA COLLECTION FOR THE PATIENT WITH CHRONIC HEART FAILURE—cont’d Medications Knowledge of Condition Coping Skills Respiratory Objective Data Tachypnea, crackles, wheezing, respiratory effort, dyspnea with exertion Cardiovascular Tachycardia, dysrhythmias, jugular venous distention, peripheral edema (degree of pitting) Gastrointestinal Abdominal distention, ascites, hepatomegaly, splenomegaly Neurologic Confusion, decreased level of consciousness, restlessness, impaired memory Integumentary Cold, clammy skin; pallor; cyanosis General Weight Diagnostic Test Findings OXYGEN. Oxygen therapy is ordered by the HCP and guided by blood gas analysis and patient symptoms. Before starting oxygen therapy, explain the therapy to the patient. For chronic HF, oxygen is administered at 2 to 6 L/min via nasal cannula. The effects of the oxygen should be monitored carefully. REST AND ACTIVITY. Reduction of the body’s oxygen demands decreases the workload of the heart. A balance of rest and activity that does not produce signs or symptoms of oxygen deprivation is essential. The activity level of the patient is determined by the severity of the HF. During times of exertion, monitor the patient’s vital signs and respiratory ef fort for oxygen deprivation. If activity intolerance develops, the activity should be stopped. Semi-Fowler’s or high-F owler’s position makes breathing easier. In upright positions, the lungs are able POSITIONING. to expand more fully and gravity decreases the amount of fluid returned to the heart, thereby reducing the heart’s workload. FLUID RETENTION. Monitoring daily weights for weight gain is important in detecting fluid retention. Edema is usually not observed until 5 to 10 pounds of e xtra fluid are present. A baseline weight should be obtained when HF is diagnosed. Daily weights should be measured on the same scale, at the same time of day, and with the same type of clothing worn to ensure accuracy. A good time to obtain a daily weight is in the morning after the bladder is emptied. Documentation of daily weights should include the date and time of the weight, the scale used, the clothing w orn, and the weight measurement. The patient can keep a weight journal. Tell patients to report weight gains of 2 to 3 pounds over 1 to 2 days. NURSING CARE PLAN for the Patient With Chronic Heart Failure Nursing Diagnosis: Activity Intolerance related to fatigue caused by oxygen imbalance Expected Outcome: The patient will show increased activity tolerance with vital signs within normal limits (WNL) in response to activity. Evaluation of Outcome: Does the patient participate in activities and maintain vital signs WNL? Intervention Provide rest, space activities, and conserve energy. Rationale Myocardial oxygen need is decreased with rest and energy conservation. Evaluation Does patient participate in activity with minimal pulse rate or ECG changes? Intervention Assist as needed with activities of daily living (ADLs). Rationale Conserve energy by assisting with ADLs. Evaluation Are patient’s ADLs met? 4068_Ch26_521-546 15/11/14 1:44 PM Page 535 Chapter 26 Nursing Care of Patients With Heart Failure 535 NURSING CARE PLAN for the Patient With Chronic Heart Failure—cont’d Intervention Teach use of assistive devices and lifestyle changes. Rationale Assistive devices can overcome limitations to increase activity. Evaluation Does patient incorporate assistive devices into lifestyle changes? GERIATRIC Intervention Increase time allowed to complete activities. Rationale Independence and participation are increased if extra time is allowed for tasks. Evaluation Does patient report greater ability to complete activities with fewer symptoms? Nursing Diagnosis: Excess Fluid Volume related to HF and the secondary reduction in renal blood flow for filtration Expected Outcomes: The patient will remain free from edema and dyspnea, have clear lung sounds, and maintain baseline weight at all times. Evaluation of Outcomes: Does patient have clear lung sounds with baseline weight maintained? Intervention Monitor for edema, weight gain, jugular venous distention (JVD), lung crackles. Rationale Excess fluid is indicated by edema, sudden weight gain, JVD, and crackles in the lungs. Evaluation Are edema, weight gain, JVD, or crackles present? Are they worsening or improving? Intervention Monitor intake and output (I&O). Rationale I&O will show imbalances. Evaluation Are I&O balanced for 24 hours? Intervention Administer diuretics. Rationale Diuretics promote fluid excretion. Evaluation Is output increased and edema or dyspnea reduced? Intervention Decrease sodium intake as ordered. Rationale Sodium retains fluid. Evaluation Does patient restrict sodium intake? Intervention Maintain fluid restriction as ordered. Rationale Excess fluid intake contributes to edema. Evaluation Does patient restrict fluid intake? Nursing Diagnosis: Disturbed Sleep Pattern related to nocturia and inability to lie down and sleep comfortably Expected Outcome: The patient will awaken refreshed and be less fatigued during the day at all times. Evaluation of Outcome: Does patient wake up less frequently during the night and feel more refreshed with less fatigue during the day? Intervention Identify barriers to sleep. Rationale Anxiety, nocturia, diuretics, orthopnea, or paroxysmal nocturnal dyspnea can make sleep difficult. Evaluation Does patient identify sleep barriers? Intervention Assist patient in identifying positions of comfort for sleeping. Rationale Use of pillows or a recliner can decrease orthopnea. Evaluation Can patient identify a position of comfort? Intervention Teach patient cause of dyspnea at night. Rationale Anxiety about falling asleep and waking up short of breath is reduced. Evaluation Can patient explain cause of dyspnea? Intervention Encourage patient to recline for 30 to 60 minutes before bedtime. Rationale Reclining before bedtime redistributes fluid to the kidneys so that the patient can void before going to sleep instead of soon afterward. Evaluation Is patient awakened to void after going to bed less often? GERIATRIC Intervention Encourage patient to take diuretics according to sleep patterns. If sleeps during nighttime hours, then take diuretic early in the day. If sleeps during daytime hours, then take medications after rising. Rationale Nocturia is reduced if diuretics are taken earlier in the day. Evaluation Does patient take diuretics early and report less nocturia? 4068_Ch26_521-546 15/11/14 1:44 PM Page 536 536 UNIT FIVE Understanding the Cardiovascular System OXYGEN CONSUMPTION. Increased oxygen consumption by the heart should be avoided. Sustained tachycardia increases the oxygen needs of the heart and should be reported promptly to the HCP for treatment. Older patients are especially vul nerable to the effects of tachycardia because of their decreased reserves. Constipation should be prevented because straining during defecation, known as the Valsalva maneuver, increases the heart’s workload by increasing venous return to the heart. Stool softeners should be administered, as ordered, to prevent straining. Patients should be taught methods of saving energy while performing ADLs. Fatigue should be avoided by alternating activity with periods of rest. A referral to occupational therapy and physical therapy can be helpful for developing techniques that allo w the patient to conserv e energy during self-care. Some suggestions for conserving ener gy include placing frequently used objects at waist level to avoid reaching overhead, planning bathing activities to include rest periods, and using Velcro fasteners to make dressing easier. MEDICATIONS. HF is a progressive, chronic condition, and patients may require lifetime medication. Combination drug therapy is often needed, and taking multiple pills daily can be challenging. Financial resources, adherence to therap y regimen, and ongoing monitoring are issues that must be considered. Diuretics. Diuretics require monitoring of the patient’s potas- sium levels and blood pressure. To prevent hypokalemia, potassium supplements may be prescribed during diuretic therapy, and a diet with high-potassium foods is encouraged. If too much fluid is remo ved, the patient may become hypotensive, and orthostatic hypotension can de velop. The patient may then be dizzy and at risk of f alling. Caution the patient to change positions and rise slo wly to prevent falls during diuretic therapy. Digitalis. Before administration of a digitalis drug, which slows the heart rate, the patient’ s apical pulse should be counted for 1 minute. If the pulse is below 60 beats/min, notify the HCP to determine if the drug should be given. Some patients are given digitalis even if their heart rates are between 50 and 60 beats/min, as long as their heart’s conduction system is normal or if the rate is due to other medications such as a beta block er. When giving digitalis, be aware that hypokalemia increases the heart’ s sensitivity to digitalis. A patient can become toxic on a normal dose of digitalis when hypokalemia is present. This is important to note because many people on digitalis also take diuretics, which may lower potassium levels. Monitoring for signs and symptoms of digitalis toxicity should be done routinely during patient assessment. Early signs and symptoms of digitalis toxicity are anorexia, nausea, and vomiting; bradycardia or other dysrhythmias; visual problems; and mental changes. Older adults are especially prone to the toxic effects of this drug and may exhibit confusion when levels are toxic. Vasodilators. Medications with vasodilating effects reduce the heart’s workload by decreasing vascular pressure. Blood pressure is monitored when administering vasodilators. Medication Teaching. Patients and their f amilies are taught the purpose, side effects, and precautions for prescribed medications. Patients should understand the importance of taking their medication as prescribed, even if they do not have symptoms. A schedule should be developed so patients remember to take their medications. Teach them to report side effects to the HCP. If dizziness occurs from drugs that reduce blood pressure, the drugs can be staggered so that the y are not all taken at the same time. P atients taking digitalis or a beta blocker should be taught to take their pulse and to notify their HCP if it is below 60 beats/min or below the lower limit heart rate set by their HCP. Patients on diuretics should be taught the following: • Take drug during the day before 1600 to decrease being awakened at night to void (if desired). • Have a readily available and obstacle-free bathroom or commode to prevent incontinence and falls. • Eat high-potassium foods if taking a potassium-wasting diuretic. • Weigh oneself daily, and report weight gains of 2 to 3 pounds over 1 to 2 days. LOW-SODIUM DIET AND WEIGHT CONTROL. A dietitian consult helps the patient and f amily understand the need for adherence to a special diet and ways to provide menus that are appealing and easy to use. Eating should remain pleasurable for the patient to a void malnutrition. Discuss foods the patient likes and can still have rather than talking about only foods the y cannot have. Patients are taught to read food labels to determine which foods are high and low in sodium content. They are also taught that salt substitutes may contain potassium. With this knowledge, patients can help design a daily meal plan using low-sodium foods that are appealing to them. Food preparers are taught not to salt food during cooking, and table salt should be eliminated. Spices, herbs, and lemon juice may be suggested to flavor unsalted foods. For overweight patients, weight reduction may help eliminate the underlying cause of HF. Diet counseling and support should be given to the obese patient to encourage weight loss. The body mass inde x (BMI) and w aist-to-hip rat