Heart Failure

Compensatory Mechanisms

Renin-Angiotensin-Aldosterone-System (RAAS) 1. Homeostatic regulatory system - BP control and fluid and electrolyte balance 2. Fluid and sodium retained in response to stress - Causes vasoconstriction to ↑ BP The RAAS is a regulatory system that works to maintain normal homeostasis. The activation of the RAAS results in BP control and fluid and electrolyte balance. In response to stress, the role of the RAAS is to promote retention of fluid and sodium, and cause vasoconstriction to raise BP. However, recurrent activation of the RAAS in HF is what is responsible for the signs and symptoms that develop. Neurohormonal response - RAAS - As CO falls, blood flow to kidneys ↓ and is sensed as ↓ volume 1. SNS is activated to ↑ BP and HR 2. Release of aldosterone from adrenal cortex results in sodium and water retention 3. Peripheral vasoconstriction and ↑ BP 4. Pituitary gland releases ADH which results in water reabsorption The outcome of the cascade results in further water and sodium retention in an already overloaded state, and increased workload of the failing heart. Other factors contributing to development of HF 1. Endothelin is produced - Causes further arterial vasoconstriction and ↑ cardiac contractility and hypertrophy 2. Cytokines are released - Further depress heart function by causing hypertrophy, contractile dysfunction, and cell death Other factors also contribute to the development of HF. The production of endothelin, a potent vasoconstrictor produced by the vascular endothelial cells, is stimulated by ADH, angiotensin II, and catecholamines. This results in further arterial vasoconstriction and an increase in cardiac contractility and hypertrophy. Locally, proinflammatory cytokines are released by heart cells in response to various forms of cardiac injury (e.g., MI). Two cytokines, tumor necrosis factor (TNF) and interleukin-1 (IL-1), further depress heart function by causing hypertrophy, contractile dysfunction, and cell death. Over time, a systemic inflammatory response also occurs. Neurohormonal response - SNS - Inadequate stroke volume and CO 1. Release of catecholamines (epinephrine and norepinephrine) - ↑ HR - ↑ Myocardial contractility - Peripheral vasoconstriction 2. Initially helpful but then harmful In response to an inadequate stroke volume and CO, the SNS is activated, resulting in the release of catecholamines (epinephrine and norepinephrine). The circulating catecholamines enhance peripheral vasoconstriction and cause an increase in the HR (chronotropy) and myocardial contractility (inotropy). Initially, the compensatory mechanisms are beneficial with a result of increased CO. However, over time these factors become harmful and counterproductive, as they increase the workload, preload (volume), and oxygen requirement in an already failing heart. Ventricular remodeling - Continuous activation of neuro-hormonal responses (RAAS and SNS) - Hypertrophy of ventricular myocytes - Ventricles larger but less effective in pumping - Can cause life-threatening dysrhythmias and sudden cardiac death In HF, continuous activation of the neurohormonal responses (RAAS and SNS) lead to elevated levels of norepinephrine, angiotensin II, aldosterone, ADH, endothelin, and proinflammatory cytokines. Together, these factors result in an increase in the heart's workload, ventricular dysfunction, and ventricular remodeling. Remodeling involves hypertrophy of the ventricular myocytes. This results in large, abnormally shaped contractile cells. This altered shape of the ventricles eventually leads to increased ventricular mass, increased wall tension, increased oxygen consumption, and impaired contractility. Although the ventricles become larger, they become less effective pumps. Ventricular remodeling is a risk factor for life-threatening dysrhythmias and sudden cardiac death (SCD). Drug therapies to prevent or reverse remodeling and decrease mortality are recommended. These include ACE-inhibitors, β-adrenergic blockers (β-blockers), and aldosterone antagonists. Dilation - Enlargement of chambers of heart that occurs when pressure in left ventricle is elevated - Initially effective - Eventually this mechanism becomes inadequate and CO decreases Dilation is an enlargement of the chambers of the heart. It occurs when pressure in the heart chambers (usually the LV) is elevated over time. The muscle fibers of the heart stretch in response to the volume of blood in the heart at the end of diastole. The degree of stretch is directly related to the force of the contraction (systole) (this is the Frank-Starling law). This increased contraction initially leads to increased CO and maintenance of BP and perfusion. Dilation starts as an adaptive mechanism to cope with increasing blood volume. Eventually this mechanism becomes inadequate because the elastic elements of the muscle fibers are overstretched and can no longer contract effectively, thereby decreasing the CO. Hypertrophy - Increase in muscle mass and cardiac wall thickness - Initially effective - Over time leads to poor contractility, increased O2 needs, poor coronary artery circulation, and risk for ventricular dysrhythmias Hypertrophy is an increase in the muscle mass and cardiac wall thickness in response to overwork and strain. It occurs slowly because it takes time for this increased muscle tissue to develop. Initially, the increased contractile power of the muscle fibers leads to an increase in CO and maintenance of tissue perfusion. Over time, hypertrophic heart muscle has poor contractility, requires more oxygen to perform work, has poor coronary artery circulation (tissue becomes more easily ischemic), and is prone to dysrhythmias.

Chronic HF Patient Teaching

Signs and symptoms of HF exacerbations - what to do/report Importance of early detection Can have positive outlook with chronic health problem if treatment plan is followed Review the signs and symptoms of HF exacerbations with the patient and caregiver. Give them a clear action plan to follow should symptoms occur. Early detection of worsening HF may help to prevent an acute episode requiring hospitalization. Patients with HF are at risk for anxiety and depression. Emphasize to the patient that it is possible to live productively with this chronic illness. Patients with HF usually need to take drugs for the rest of their lives. This often becomes difficult because a patient may be asymptomatic when HF is under control. You must stress that the disease is chronic, and that drugs must be continued to keep the HF under control. Drug therapy - Expected actions - Signs of drug toxicity - How to take HR and what to report - Signs and symptoms of hypokalemia and hyperkalemia - BP monitoring as needed Teach the patient the expected actions of the ordered drugs and the signs of drug toxicity. Also teach the patient and caregiver how to take a HR. The HR should always be taken for 1 full minute. A HR less than 50 beats/minute may be a contraindication to taking a digitalis preparation or β-blocker unless specified otherwise by the HCP. However, in the absence of symptoms (e.g., heart block, ventricular ectopy, syncope), a HR less than 50 beats/minute may be acceptable. Include clear information about when a drug, especially digitalis and beta blockers, should be held and a HCP called. Teach the patient the symptoms of hypokalemia and hyperkalemia if diuretics that deplete or spare potassium are ordered. Weakness, fatigue, constipation, and muscle cramping may occur but often there are no physical signs of hypo- or hyperkalemia. Frequently the patient who takes thiazide or loop diuretics is given supplemental potassium. It may also be appropriate to teach patients home BP monitoring, especially those with hypertension. Dietary therapy - Written plan - Reading labels for sodium - No added salt - Daily weights - Smaller, more frequent meals Dietary Therapy 1. Consult the written diet plan and list of permitted and restricted foods. 2. Examine labels to determine sodium content. Also examine the labels of over-the-counter drugs, such as laxatives, cough medicines, and antacids for sodium content. 3. Avoid using salt when preparing foods or adding salt to foods. 4. Weigh yourself at the same time each day, preferably in the morning, using the same scale and wearing the same or similar clothes. 5. Eat smaller, more frequent meals. Activity/rest - Energy-conserving and energy-efficient behaviors - Exercise training (cardiac rehab) - Increase gradually - Avoid heat and cold extremes - Rest after exertion - Avoid emotional upsets Activity Program 1. Increase walking and other activities gradually, provided they do not cause fatigue or dyspnea. Consider a cardiac rehabilitation program. 2. Avoid extremes of heat and cold. Rest The physical therapist, occupational therapist, or you can instruct the patient in energy-conserving and energy-efficient behaviors after an evaluation of daily activities has been done. For example, once you understand the patient's daily routine, suggestions can be made to simplify work or modify an activity. Exercise training (e.g., cardiac rehabilitation) improves symptoms of chronic HF but is often underprescribed. Exercise for patients with HF has been found to be safe and to improve the overall sense of well-being. It has also been correlated with mortality reduction. Increase walking and other activities gradually, provided they do not cause fatigue or dyspnea. Avoid extremes of heat and cold. Frequently the patient needs a prescription for rest after an activity. Many hard-driving persons need the "permission" to not feel "lazy." Avoid emotional upsets. Verbalize any concerns, fears, feelings of depression, etc., to HCP. Ongoing monitoring - Know FACES - Reappearance of symptoms - What to report - Regular follow-up - Support group Health promotion - Vaccinations - Reduce risk factors Ongoing Monitoring 1. Know the signs and symptoms of worsening heart failure. FACES: fatigue, limitation of activities, chest congestion/cough, edema, shortness of breath. 2. Recall the symptoms experienced when illness began. Reappearance of previous symptoms may indicate a recurrence. 3. Report immediately to health care provider any of the following: Weight gain of 3 lb (1.4 kg) in 2 days, or 3 to 5 lb (1.4 to 2.3 kg) in a week Difficulty breathing, especially with exertion or when lying flat Waking up breathless at night Frequent dry, hacking cough, especially when lying down Fatigue, weakness Swelling of ankles, feet, or abdomen; swelling of face or difficulty breathing (if taking ACE inhibitors) Nausea with abdominal swelling, pain, and tenderness Dizziness or fainting 4. Follow up with HCP on regular basis. 5. Consider joining a local support group with your family members and/or caregiver(s). Health Promotion 1. Obtain annual flu vaccination. 2. Obtain pneumococcal vaccine (e.g., Pneumovax) and revaccination after 5 years (for people at high risk of infection or serious disease). 3. Develop plan to reduce risk factors (e.g., BP control, smoking cessation, weight reduction).

Heart Failure Complications

Pleural effusion - Pleural effusion is a common complication in HF. There are two pleural layers or membranes: the visceral pleura lines the lungs, whereas the parietal pleura lines the chest cavity. Normally a small amount of fluid is between the two layers for lubrication and to aid breathing. A pleural effusion occurs when excess fluid builds up in the pleural cavity of the lungs secondary to increasing pressure in the pleural capillaries. Fluid then moves from these capillaries into the pleural space. Pleural effusions may result in symptoms of dyspnea, cough, and chest pain. (Pleural effusion is discussed in Chapter 27.) Dysrhythmias - atrial and ventricular - Chronic HF causes enlargement of the chambers of the heart. This enlargement can cause changes in the normal electrical pathways. When numerous sites in the atria fire spontaneously and rapidly (atrial fibrillation), the organized atrial depolarization (contraction) no longer occurs. Atrial fibrillation also promotes thrombus formation within the atria. Thrombi may break loose and form emboli. This places patients with atrial fibrillation at risk for stroke. They require treatment with anticoagulants, cardioversion, ablation and antidysrhythmic drugs. - Patients with HF are also at risk for ventricular dysrhythmias (e.g., ventricular tachycardia [VT], ventricular fibrillation [VF]). Patients with decreased LV function are at the greatest risk for SCD. Guidelines recommend implantation of a prophylactic implantable cardioverter-defibrillator (ICD). Left ventricular thrombus - With ADHF or chronic HF, the enlarged LV and decreased CO combine to increase the risk of thrombus formation in the LV. Once a thrombus has formed, it may also decrease left ventricular contractility, decrease CO, and worsen the patient's perfusion. The development of emboli from the thrombus also places the patient at risk for stroke. Hepatomegaly - HF can lead to severe hepatomegaly, especially with RV failure. The liver becomes congested with venous blood. The hepatic congestion leads to impaired liver function. Eventually liver cells die, fibrosis occurs, and cirrhosis can develop (see Chapter 43). Renal failure - The decreased CO that accompanies chronic HF results in decreased perfusion to the kidneys and can lead to renal insufficiency or failure (see Chapter 46). Diagnostic Studies - Determine and treat underlying cause 1. Echocardiogram - Provides information on EF, heart valves and heart chambers 2. ECG, chest x-ray, 6-minute walk test, MUGA scan, cardiopulmonary exercise stress test, heart catheterization, EMB 3. BNP levels Diagnosing HF is often difficult. Patient signs and symptoms are not highly specific and may mimic those associated with many other medical conditions (e.g., anemia, lung disease). A primary goal in diagnosis is to find the underlying cause of HF. An echocardiogram is a common diagnostic tool used in patients with HF. It provides information on the EF. This helps to differentiate between HFpEF and HFrEF. An echocardiogram also provides information on the structure and function of the heart valves. Heart chamber enlargement or stiffness can also be assessed. Other useful tests include electrocardiogram (ECG), chest x-ray, 6-minute walk test, multi-gated acquisition (MUGA) scan, cardiopulmonary exercise stress test, and heart catheterization. Studies for obstructive sleep apnea may be done in select patients. An endomyocardial biopsy (EMB) may be done as part of a heart catheterization in select acutely ill patients who develop unexplained, new onset HF that is unresponsive to usual care. Laboratory studies also aid in the diagnosis of HF. In general, BNP levels correlate positively with the degree of LV failure. Many agencies routinely measure the N-terminal prohormone of BNP (NT-proBNP). This is a more precise test to aid in the diagnosis of HF. Levels are temporarily higher in patients receiving nesiritide (Natrecor) and may be high in patients with chronic, stable HF. Increases in BNP or NT-proBNP levels can be caused by conditions other than HF. These include pulmonary embolism, renal failure, and acute coronary syndrome.

Heart Transplantation

Treatment of choice for patients with refractory end-stage HF, inoperable CAD, and cardiomyopathy - 3,000 on list; average 2,000 available - Survival rate of 85%-90% at 1year; 75% at 3 Selection process identifies patients who would most benefit from a new heart Candidates must undergo physical, diagnostic, and psychologic evaluation Heart transplantation is the transfer of a healthy donor heart to a patient with a diseased heart. This surgery is used to treat a variety of terminal or end-stage heart conditions. Retransplantation (i.e., a second or third heart transplant) is also done. In the United States, approximately 3000 patients are listed for heart transplants. However, on average only 2000 hearts become available. The 1-year transplant survival rate is 85% to 90%, whereas the 3-year survival rate is approximately 75%. A careful selection process ensures that hearts are distributed fairly and to those who will benefit most from the donor heart. The United Network for Organ Sharing (UNOS) is in charge of a system that gives organs fairly to people. Once a person meets the criteria for heart transplantation, a complete physical examination and diagnostic workup are done. In addition, the patient and caregiver undergo a comprehensive psychologic evaluation. This includes assessing coping skills, support systems, and commitment to follow the rigorous regimen that is essential to a successful transplantation. The complexity of the transplant process may be overwhelming to a patient with inadequate support systems and a poor understanding of the lifestyle changes needed after transplant Transplant candidates are placed on a list - Stable patients wait at home and receive ongoing medical care - Unstable patients may require hospitalization for more intensive therapy - Overall waiting period for a heart is long; many patients die during this time Donor and recipient matching is based on body and heart size, and an immunologic evaluation. The immunologic assessment includes ABO blood type, antibody screen, panel-reactive antibody (PRA) level, and human leukocyte antigen typing (explained in Chapter 13). Once a person is accepted as a transplant candidate (this may happen quickly during an acute illness or after a longer period), he or she is placed on a transplant list. Patients may wait at home and receive ongoing medical care if their condition is stable. If their condition is not stable, they may require hospitalization for more intensive therapy. Therapy may include implantation of bridge devices (VADs) to assist the heart while awaiting transplant. Unfortunately, the overall waiting period for a new heart is long. Many patients die while waiting for a transplant. Several devices are available as a bridge to transplantation (BTT), but only two have received FDA approval for heart recovery after a life-threatening cardiac event. 1. Heart retrieval first step 2. Second step is removal of recipient's heart except for portions of atria (2 different approaches) and venous connections 3. Final step is implantation of donor heart The surgical procedure actually involves multiple surgeries. First, the donor heart is retrieved. The donor is usually someone who has suffered irreversible brain injury (brain death). Most donor hearts are obtained at sites distant from the institution performing the transplant. A team of physicians, nurses, and technicians goes to the hospital of the donor to remove donated organs once brain death of the donor has been determined. The retrieved organs are transported on ice until they can be implanted. For the heart, this is optimally less than 4 hours. Often the donor heart is flown to the recipient's hospital. Second, the donated heart is implanted into the recipient. Two different approaches are used in this surgery. In the biatrial approach, the recipient's damaged heart is removed at the midatrial level and the donor heart connected at the left atrium, pulmonary artery, aorta, and right atrium. In the bicaval approach, the right atrium of the recipient's heart (with the SA node and maintenance of atrial conduction) is preserved and then the donor heart is connected. Cardiopulmonary bypass is needed during the surgical procedure to maintain oxygenation and perfusion to vital organs. Posttransplantation monitoring - Acute rejection - Infection - Malignancy - Cardiac vasculopathy Immunosuppressive therapy Endomyocardial biopsy (EMB) A variety of complications can occur after the transplant, including a risk for SCD. Acute rejection is an immediate posttransplant complication, and immunosuppressive therapy is the key in posttransplant management. In the first year after transplantation, the major causes of death are acute rejection and infection. Later on, malignancy (especially lymphoma) and cardiac vasculopathy (accelerated CAD) are major causes of death. Most immunosuppressive regimens include corticosteroids, calcineurin inhibitors (cyclosporine [Sandimmune, Neoral], tacrolimus [Prograf]), and antiproliferative drugs (mycophenolate mofetil [CellCept]). Because of the use of immunosuppression therapy, infection is a primary complication after transplant surgery. On a long-term basis, immunosuppressive therapy increases the risk for cancer. To detect rejection, an EMB is obtained on a weekly basis for the first month, monthly for the following 6 months, and yearly thereafter. In this procedure, a catheter is inserted into the jugular vein and moved into the right ventricle. The catheter uses a bioptome, a device with two small cups that can be closed, to remove small samples of heart muscle. Endomyocardial biopsies are obtained from right ventricle weekly for the first month, monthly for following 6 months, and yearly thereafter to detect rejection In an EMB, a catheter is put into the jugular vein and is advanced into the right ventricle. The catheter has a bioptome at its end—a set of two small cups that can be closed to pinch off and remove small samples of heart muscle. Nursing care focuses on - Promoting patient adaptation to the transplant process - Monitoring cardiac function - Managing lifestyle changes - Providing ongoing teaching Nursing management throughout the posttransplant period focuses on promoting patient adaptation to the transplant process, monitoring cardiac function, managing lifestyle changes, and providing ongoing teaching to the patient and caregiver.

Chronic HF Nursing Assessment

Subjective Data 1. Past health history - Any cardiac history or diseases that increase risk for cardiac dysfunction 2. Drugs - Any cardiac drugs, estrogens, corticosteroids, NSAIDs, OTC drugs, herbs Obtain the following important health information from the patient: Past health history: CAD (including recent MI), hypertension, cardiomyopathy, valvular or congenital heart disease, diabetes mellitus, hyperlipidemia, renal disease, thyroid or lung disease, rapid or irregular heart rate. Drugs: Use of and compliance with any cardiac drugs; use of diuretics, estrogens, corticosteroids, nonsteroidal antiinflammatory drugs (NSAIDs), over-the-counter drugs, herbal supplements. Carefully review the patient's current prescription and over-the-counter drugs. Assess for use of any NSAIDs as they can contribute to sodium retention. Subjective Data - Fatigue, depression, anxiety - Usual sodium intake - Nausea/vomiting/anorexia - Stomach bloating - Weight gain - Ankle swelling - Nocturia - Decreased daytime urine output - Constipation - Dyspnea, orthopnea, cough - Palpitations - Dizziness, fainting - Number of pillows used for sleeping - Paroxysmal nocturnal dyspnea - Insomnia - Chest pain or heaviness - RUQ pain, abdominal discomfort - Behavioral changes - Visual changes Obtain the following important health information related to pertinent functional health patterns: Health perception-health management: Fatigue, depression, anxiety Nutritional-metabolic: Usual sodium intake; nausea, vomiting, anorexia, stomach bloating; weight gain, ankle swelling Obtain the following important health information related to pertinent functional health patterns: Elimination: Nocturia, decreased daytime urinary output, constipation Activity-exercise: Dyspnea, orthopnea, cough (e.g., dry, productive); palpitations; dizziness, fainting Obtain the following important health information related to pertinent functional health patterns: Sleep-rest: Number of pillows used for sleeping; paroxysmal nocturnal dyspnea, insomnia Cognitive-perceptual: Chest pain or heaviness; RUQ pain, abdominal discomfort; behavioral changes; visual changes Objective Data - Skin color and temperature - Edema - Respiratory rate and sounds - Frothy, blood-tinged sputum - Heart rate and sounds - Abdominal distention - Changes in LOC - Serum electrolytes - BUN, creatinine - Liver function tests - NT-proBNP or BNP - Chest x-ray - Echocardiogram - ECG - O2 saturation Additional focused assessment findings include: Integumentary Cool, diaphoretic skin; cyanosis or pallor, peripheral edema (right-sided heart failure) Respiratory Tachypnea, crackles, rhonchi, wheezes; frothy, blood-tinged sputum Cardiovascular Tachycardia, S3, S4, murmurs; pulsus alternans, PMI displaced inferiorly and posteriorly, lifts/heaves, jugular vein distention Gastrointestinal Abdominal distention, hepatosplenomegaly, ascites Neurologic Restlessness, confusion, decreased attention or memory Possible Diagnostic findings Altered serum electrolytes (especially Na+ and K+) ↑ BUN, creatinine, or liver function tests ↑ NT-proBNP or BNP Chest x-ray demonstrating cardiomegaly, pulmonary congestion, and interstitial pulmonary edema Echocardiogram showing increased chamber size, decreased wall motion, decreased EF or normal EF with evidence of diastolic failure Atrial and ventricular enlargement on ECG ↓ O2 saturation

Left-Sided Heart Failure

Blood backs up into left atrium and pulmonary veins Increased pulmonary pressure causes fluid leakage →→ pulmonary congestion and edema Left-sided HF results from left ventricular dysfunction. This prevents normal, forward blood flow and causes blood to back up into the left atrium and pulmonary veins. The increased pulmonary pressure causes fluid leakage from the pulmonary capillary bed into the interstitium and then the alveoli. This manifests as pulmonary congestion and edema.

Chronic HF Nursing Intervention

Basic principles of care - HF is a progressive disease: establish treatment plans and quality-of-life goals - Use of self-management tools for symptom management - Restrict salt (and water at times) - Conserve energy - Maintain support systems - Monitor respiratory status - Administer oxygen therapy - Semi-Fowler's position - Monitor hemodynamic status - Daily weights - I and O - Administer prescribed drugs - Monitor edema - Alternate rest with activity - Provide diversionary activities - Monitor response to activity - Collaborate with OT/PT - Reduce anxiety - Evaluate support system - Patient teaching Many persons with HF will experience one or more episodes of ADHF. When they do, they are usually admitted through the ED, first stabilized, and then cared for in an ICU, an intermediate care unit, or a specialized HF unit with continuous ECG monitoring capability. Successful HF care depends on several important principles: (1) HF is a progressive disease, and treatment plans are established along with quality of life goals; (2) symptom management is controlled by the patient with self-management tools (e.g., daily weights, drug regimens, diet, and exercise plans); (3) salt and, at times, water must be restricted; (4) energy must be conserved; and (5) support systems are essential to the success of the entire treatment plan. Reduction of anxiety is an important nursing function, since anxiety may increase the SNS response and further increase myocardial workload. Reducing anxiety may be facilitated by a variety of nursing interventions and the use of sedatives (e.g., benzodiazepines, morphine sulfate). The Joint Commission has selected three core measures in the management of patients with HF to reflect standards of evidence-based care. The AHA has developed a program, Get With The Guidelines-Heart Failure, to improve adherence to standards of evidence-based care of patients hospitalized with HF. Together, these approaches work to ensure high-quality care for patients with HF. Respiratory Monitoring Monitor pulse oxymetry, respiratory rate, rhythm, depth, and effort of respirations to evaluate changes in respiratory status. Auscultate breath sounds, noting areas of decreased/absent ventilation and presence of adventitious sounds to detect presence of pulmonary edema. Monitor for increased restlessness, anxiety, and work of breathing to detect increasing hypoxemia. Oxygen Therapy Administer supplemental O2 or other noninvasive ventilator support (e.g., bilevel positive airway pressure [BiPAP]) as needed to maintain adequate O2 levels. Monitor the O2 liter flow rate and position of O2 delivery device to ensure O2 is adequately delivered. Change O2 delivery device from mask to nasal prongs during meals as tolerated to sustain O2 levels while eating. Monitor the effectiveness of O2 therapy to identify hypoxemia and establish range of O2 saturation. Positioning Position to alleviate dyspnea (e.g., semi-Fowler's position), as appropriate, to improve ventilation by decreasing venous return to the heart and increasing thoracic capacity. Hemodynamic Monitoring Perform a comprehensive assessment of peripheral circulation (e.g., check peripheral pulses, edema, capillary refill, color, and temperature of extremity) to determine circulatory status. Note signs and symptoms of decreased cardiac output (e.g., chest pain, S3, S4, jugular vein distention) to detect changes in status. Monitor fluid balance (e.g., I/O and daily weight) to evaluate renal perfusion. Continuously monitor cardiac rhythm to detect dysrhythmias. Administer prescribed diuretics, as appropriate, to treat hypervolemia. Monitor for therapeutic effect of diuretic (e.g., increased urine output, decreased CVP/PCWP, and decreased adventitious breath sounds) to assess response to treatment. Monitor potassium levels after diuresis to detect excessive electrolyte loss. Monitor changes in peripheral edema to assess response to treatment. Encourage alternate rest and activity periods to reduce cardiac workload and conserve energy. Provide calming diversionary activities to promote relaxation to reduce O2 consumption and to relieve dyspnea and fatigue. Monitor patient's O2 response (e.g., pulse rate, cardiac rhythm, and respiratory rate) to self-care or nursing activities to determine the level of activity that can be performed. Collaborate with occupational and/or physical therapists to plan and monitor activity/exercise program. Instruct patient and caregivers on activity restriction and progression to allay fears and anxiety. Establish a supportive relationship with the patient and caregiver(s) to promote adherence with the treatment plan. Evaluate and encourage use of support systems. Teach patient and caregiver techniques of self-care that will minimize O2 consumption (e.g., self-monitoring and pacing techniques for performance of ADLs). Inform the patient of the purpose for and benefits of the prescribed activity/exercise.

Chronic Heart Failure Clinical Manifestations

Dependent on age, underlying type and extent of heart disease, and which ventricle is affected FACES Fatigue Limitation of Activities Chest congestion/cough Edema Shortness of breath Chronic HF is characterized as progressive worsening of ventricular function and chronic neurohormonal activation that result in ventricular remodeling. This process involves changes in the size, shape, and mechanical performance of the ventricle. The clinical manifestations of chronic HF depend on the patient's age, underlying type and extent of heart disease, and which ventricle is failing to pump effectively. The Heart Failure Society of America (HFSA) developed the acronym, FACES (fatigue, limitation of activities, chest congestion/cough, edema, and shortness of breath) to help educate patients on identifying HF symptoms Fatigue Dyspnea Orthopnea Paroxysmal nocturnal dyspnea Tachycardia Fatigue Fatigue is one of the earliest symptoms of chronic HF. The patient notes fatigue after usual activities and eventually limits these activities. The fatigue is caused by decreased CO, impaired perfusion to vital organs, decreased oxygenation of the tissues, and anemia. Anemia can result from poor nutrition, renal disease, or drug therapy (e.g., angiotensin-converting enzyme [ACE] inhibitors). Dyspnea Dyspnea is a common manifestation of chronic HF. It is caused by increased pulmonary pressures secondary to interstitial and alveolar edema. Dyspnea can occur with mild exertion or at rest. Orthopnea often accompanies dyspnea. Careful questioning of patients often reveals adaptive behaviors, such as sleeping with two or more pillows or in a chair to aid breathing. Paroxysmal nocturnal dyspnea (PND) occurs when the patient is asleep. The patient awakes in a panic, has feelings of suffocation, and a strong desire to sit or stand up. PND is caused by the reabsorption of fluid from dependent body areas when the patient is flat. A cough is often associated with HF and may be the first clinical symptom. It begins as a dry, nonproductive cough and may be misdiagnosed as asthma or other lung disease. The cough is not relieved by position change or over-the-counter cough medicine. Tachycardia Tachycardia is an early clinical sign of HF. One of the body's first responses to compensate for a failing heart is to increase the HR via activation of the SNS. This works to increase CO. Initially this response is favorable, but over time, persistent tachycardia is harmful and may exacerbate HF. Adequate HR control in patients with chronic HF has been associated with better clinical outcomes, including decreased hospitalizations and mortality. Edema - Dependent, liver, abdominal cavity, lungs - Edema may be pitting in nature - Sudden weight gain of >3 lb (1.4 kg) in 2 days may indicate ADHF, an exacerbation of chronic HF - Edema is a common sign of HF. It may occur in dependent body areas (peripheral edema), liver (hepatomegaly), abdominal cavity (ascites), and lungs (pulmonary edema and pleural effusion). If the patient is in bed, sacral and scrotal edema may develop. Pressing the edematous skin with the finger may leave a transient depression (pitting edema). The development of dependent edema or a sudden weight gain of more than 3 lb (1.4 kg) in 2 days is often a sign of ADHF. It is important to note that not all lower extremity edema is a result of HF. Hypoproteinemia, immobility, venous insufficiency, and certain drugs can cause peripheral edema. Nocturia - Nocturia is the tendency to urinate excessively during the night. Chronic HF is frequently associated with poor renal perfusion and function. Patients develop increased peripheral and systemic edema. At night when lying flat, extravascular fluid is reabsorbed from the interstitial spaces back into the circulatory system. This results in increased perfusion to the kidneys. The increased renal blood flow results in diuresis. The patient may complain of having to urinate frequently throughout the night. Skin changes - Because tissue capillary oxygen extraction is increased in a person with chronic HF, the skin may appear dusky. Often the lower extremities are shiny and swollen, with diminished or absent hair growth. Chronic swelling may result in pigment changes. This causes the skin to appear brown or brawny in areas covering the ankles and lower legs. Behavioral changes - Cerebral circulation may be reduced with chronic HF secondary to decreased CO. The patient or caregiver may report unusual behavior, including restlessness, confusion, and decreased attention span or memory. This may also be secondary to poor gas exchange and worsening HF. It is often seen in the late stages of HF. Co-existing psychologic disorders, especially depression and anxiety, contribute a two-fold risk of mortality and higher readmission rates and health care costs in patients with HF. Approximately 1 in 5 patients with HF have clinical depression. In addition, patients with psychologic disorders have poorer adherence to treatment plans. Assess patients with HF for depression and anxiety and, if needed, initiate appropriate consults. Chest pain - HF can precipitate chest pain (angina) due to decreased coronary artery perfusion from decreased CO and increased myocardial work. Chest pain may accompany either ADHF or chronic HF. Weight changes - Many factors contribute to weight changes. First there may be a progressive weight gain from fluid retention. Renal failure may also contribute to fluid retention. Abdominal fullness from ascites and hepatomegaly frequently causes anorexia and nausea. As HF advances, the patient may have cardiac cachexia with muscle wasting and fat loss. This can be masked by the patient's edematous condition and may not be seen until after the edema subsides.

ADHF Drug Therapy

Diuretics - Decrease volume overload (preload) - Loop diuretics - Furosemide (Lasix) - Diuretics are the mainstay of treatment in patients with volume overload. They act to decrease sodium reabsorption at various sites within the nephrons, thereby enhancing sodium and water loss. Decreasing intravascular volume with the use of diuretics reduces venous return (preload) and subsequently the volume returning to the LV. This allows the LV to pump more efficiently. CO is increased, pulmonary vascular pressures are decreased, and gas exchange is improved. Loop diuretics (e.g., furosemide [Lasix]) can be given by IV push and act rapidly in the kidneys. Vasodilators - Reduce circulating blood volume and improve coronary artery circulation - IV nitroglycerin - Sodium nitroprusside - Nesiritide (Natrecor) - IV nitroglycerin is a vasodilator that reduces circulating blood volume. It also improves coronary artery blood flow by dilating the coronary arteries. Therefore nitroglycerin reduces preload, slightly reduces afterload (in high doses), and increases myocardial oxygen supply. When titrating IV nitroglycerin, monitor BP frequently (every 5 to 10 minutes) to avoid hypotension. Sodium nitroprusside (Nipride) is a potent IV vasodilator that reduces both preload and afterload, thus improving myocardial contraction, increasing CO, and reducing pulmonary congestion. Complications of IV sodium nitroprusside include hypotension and thiocyanate toxicity, which can develop after 48 hours of use. Sodium nitroprusside is given in an ICU, since symptomatic hypotension is the main adverse effect. Nesiritide, given IV, is a recombinant form of BNP. It causes both arterial and venous dilation. The main hemodynamic effects of nesiritide include (1) a reduction in PAWP and (2) a decrease in systemic BP. Although classified as a vasodilator, nesiritide is also a neurohormonal blocking agent. It can be used for short-term treatment of ADHF. Nesiritide does not require titration after the initial IV bolus. It can be given in the emergency department (ED) and non-ICU setting. Because the main adverse effect of nesiritide is symptomatic hypotension, monitor BP closely. Morphine - Reduces preload and after load - Relieves dyspnea and anxiety - Morphine sulfate reduces preload and afterload. It is frequently used in the treatment of HF and acute coronary syndrome (see Chapter 33). It dilates both pulmonary and systemic blood vessels. When morphine is used, the patient often experiences relief from dyspnea and, consequently, the anxiety often associated with dyspnea. Use morphine cautiously in patients with ADHF. Morphine is related to more adverse events, including a greater need for mechanical ventilation, more ICU admissions, prolonged hospitalization, and higher mortality rates in these patients. Positive inotropes - β-agonists (dopamine, dobutamine, norepinephrine [Levophed]) - Phosphodiesterase inhibitor (milrinone) - Digitalis - Inotropic therapy increases myocardial contractility. Drugs include β-agonists (e.g., dopamine [Intropin], dobutamine [Dobutrex], norepinephrine [Levophed]), the phosphodiesterase inhibitor milrinone (Primacor), and digitalis. The β-agonists are only used as a short-term treatment of ADHF. Milrinone is a phosphodiesterase inhibitor that has been called an inodilator. It increases myocardial contractility (inotropic effect) and promotes peripheral vasodilation. Inhibition of phosphodiesterase increases cyclic adenosine monophosphate (cAMP). This enhances calcium entry into the cell and improves myocardial contractility. Milrinone increases CO and reduces BP (decrease afterload). Like dopamine and dobutamine, this drug is available only for IV use. Adverse effects include dysrhythmias, thrombocytopenia, and hepatotoxicity. Digitalis is a positive inotrope that improves LV function. Digitalis increases contractility but also increases myocardial oxygen consumption. Because digitalis requires a loading dose and time to work, it is not recommended for the initial treatment of ADHF. Currently, inotropic therapy is only recommended for use in the short-term management of patients with ADHF who have not responded to conventional drug therapy (e.g., diuretics, vasodilators, morphine).

Chronic HF Drug Therapy

Diuretics - Reduce edema, pulmonary venous pressure, and preload - Promote sodium and water excretion - Loop diuretics - Thiazide diuretics - Monitor potassium levels (hypokalemia) - Diuretics are used to reduce edema, pulmonary venous pressure, and preload. If excess extracellular fluid is removed, blood volume returning to the heart can be reduced and cardiac function improved. Diuretics act on the kidney by promoting excretion of sodium and water. Many varieties of diuretics are available. Loop diuretics (e.g., bumetanide [Bumex]) are potent diuretics. These drugs act on the ascending loop of Henle to promote sodium, chloride, and water excretion. Problems in using loop diuretics include reduction in serum potassium levels, ototoxicity, and possible allergic reaction in patients sensitive to sulfa-type drugs. Thiazide diuretics inhibit sodium reabsorption in the distal tubule, thus promoting excretion of sodium and water. They can be added to loop diuretics to obtain results if patients become resistant to loop diuretics. Thiazide diuretics also can cause severe reductions in potassium levels. Diuretics are effective in relieving the congestive symptoms of HF. However, their use does activate the SNS and RAAS, which can exacerbate the HF syndrome. In chronic HF, the lowest effective dose of diuretic should be used. RAAS inhibitors - ACE inhibitors - Angiotensin II receptor blockers - Aldosterone antagonists - Monitor potassium levels (hyperkalemia) Angiotensin-Converting Enzyme Inhibitors ACE inhibitors are the primary drug of choice for blocking the RAAS system in HF patients with systolic failure. The conversion of angiotensin I to the potent vasoconstrictor angiotensin II needs ACE. ACE inhibitors block this enzyme, resulting in reduced levels of angiotensin II. The end result of the neurohormonal blockade is decreased plasma aldosterone levels, decreased SNS activity, vasodilation, and sodium and water excretion. ACE inhibitors also decrease the development of ventricular remodeling by inhibiting ventricular hypertrophy. These drugs can cause symptomatic hypotension, intractable cough, hyperkalemia, angioedema (allergic reaction involving edema of the face and airways), and renal insufficiency (high doses of ACE inhibitors). Angiotensin II Receptor Blockers For patients who are unable to tolerate ACE inhibitors, angiotensin II receptor blockers (ARBs) are recommended. These agents prevent the vasoconstrictor and aldosterone-secreting effects of angiotensin II by binding to the angiotensin II receptor sites. Aldosterone Antagonists Spironolactone (Aldactone) and eplerenone (Inspra) are aldosterone antagonists. They block the harmful neurohormonal effects of aldosterone on the heart blood vessels. Aldosterone antagonists may prolong survival in patients with HFrEF. They are also potassium-sparing diuretics that promote sodium and water excretion while retaining potassium. These effects occur because these agents bind to receptors at the aldosterone-dependent sodium-potassium exchange site in the distal renal tubule. β-Blockers - Β-Blockers directly block the negative effects of the SNS (e.g., increased heart rate) on the failing heart. Vasodilators - Nitrates - Nitrates cause vasodilation by acting directly on the smooth muscle of the vessel wall. Nitrates are of particular benefit in the management of myocardial ischemia related to HF because they promote vasodilation of the coronary arteries. Combination therapy - BiDil - Combination therapy with hydralazine and isosorbide dinitrate (Bidil) may be helpful in African American patients with HF who are getting optimal therapy with ACE inhibitors and β-blockers. The same benefit is not found in white patients. The combination of the two drugs is also associated with a significant improvement in LV EF and exercise tolerance. Although the evidence of benefit is stronger in African American patients, the combination therapy may be used in patients of other races who are already on optimal therapy. Positive inotropic agents - Digitalis - Digitalis preparations (e.g., digoxin [Lanoxin]) increase the force of cardiac contraction (inotropic action). Inhibitor of cardiac sinus node 1. Ivabradine (Corlanor) 2. Must be in sinus rhythm with resting HR of > 70 bpm and taking highest dose β-blockers - Inhibits sinus node - Reduces HR - Decreases risk of hospitalization for worsening HF Ivabradine (Corlanor) is new category of oral drug that inhibits the sinus node and reduces HR. It is used for patients who have symptoms of chronic HF. They must be in sinus rhythm with a resting HR of at least 70 beats per minute and taking β-blockers at the highest dose tolerated. Ivabradine also reduces the risk of hospitalization for worsening HF. The most common side effects of ivabradine include symptomatic bradycardia, high BP, atrial fibrillation, and vision disturbance (i.e., flashes of light). Tell patients to call their HCP if they experience symptoms of an irregular HR, feel that the heart is pounding or racing, have chest pressure, or worsened dyspnea. Low HR is a common side effect of ivabradine and can be serious. Patients should tell their HCP if they have experience dizziness, weakness, or fatigue.

Classification of Heart Failure

Left-sided HF 1. Most common form of HF 2. Results from inability of LV to - Empty adequately during systole - Fill adequately during diastole 3. Further classified as - Systolic - Diastolic - Mixed systolic and diastolic The most common form of HF is left-sided HF. Left-sided HF results either from (1) the inability of the left ventricle (LV) to empty adequately during systole or (2) fill adequately during diastole. Left-sided HF can be further classified as systolic, diastolic, or mixed systolic and diastolic failure. Involves diastolic or systolic dysfunction A defect in either ventricular filling (diastolic dysfunction) or ventricular ejection (systolic dysfunction) are the key manifestations of HF.

Chronic HF Nutritional Therapy

Low sodium diet - Individualize recommendations and consider cultural background (www.nhlbi.nih.gov/health/index.htm#recipes) - Recommend Dietary Approaches to Stop Hypertension (DASH) diet - Sodium is usually restricted to 2 g/day Poor adherence to a low-sodium diet and failure to take prescribed drugs as directed are the two most common reasons for readmissions of HF patients to the hospital. Therefore, it is critical that you accurately assess a patient's diet and teach both the patient and caregiver about the importance of diet. Obtain a detailed diet history. Determine not only what foods the patient eats but also when, where, and how often the patient dines out. In addition, assess the cultural value of food. Use this information to assist the patient in making appropriate dietary choices when developing a diet plan. The National Heart, Lung, Blood Institute (NHLBI) provides helpful dietary guidelines for heart-healthy food preparation for people of various cultures (e.g., Hispanics, Asian Americans). These are available online at www.nhlbi.nih.gov/health/educational/lose_wt/menuplanner.html The edema associated with chronic HF is often treated by dietary restriction of sodium. The Dietary Approaches to Stop Hypertension (DASH) diet is effective as a first-line therapy for many individuals with hypertension (discussed in Chapter 32). This diet is now also widely used for the patient with HF, with or without hypertension. The average American adult's daily intake of sodium ranges from 7 to 15 g. A commonly prescribed diet for a patient with HF is a 2-g sodium diet. All foods high in sodium (over 400 mg per serving) should be avoided. Fluid restriction not generally required If required, < 2L/day - Ice chips, gum, hard candy, ice pops to help thirst Daily weights important - Same time, same clothing each day Weight gain of 3 lb (1.4 kg) over 2 days or a 3- to 5-lb (2.3 kg) gain over a week should be reported to HCP Fluid restrictions are not commonly ordered for the patient with mild to moderate HF. However, in moderate to severe HF and renal insufficiency, fluids are limited to less than 2 L/day. Helping patients deal with thirst as a side effect of the drugs is important. To deal with the thirst, suggest ice chips, gum, hard candy, or ice pops. Tell patients to weigh themselves daily as this is important for monitoring fluid status. Tell patients to weigh themselves at the same time each day. Ideally this should be before breakfast, using the same scale, wearing the same type of clothing. This helps ensure valid comparisons from day to day and helps identify early signs of fluid retention. For patients with visual limitations, suggest scales with larger numbers and/or an audible response. Tell patients to call the HCP if they see a weight gain of 3 lb (1.4 kg) over 2 days or a 3- to 5-lb (2.3-kg) gain over a week.

Chronic HF Interprofessional Care

Main treatment goals - Treat the underlying cause and contributing factors - Maximize CO - Reduce symptoms - Improve ventricular function - Improve quality of life - Preserve target organ function - Improve mortality and morbidity With the addition of new drugs and devices, the management of HF has dramatically changed in the past few years. Because of the large number of patients and the high cost of care related to hospital readmissions, strategies to improve outcomes have been developed. One example is the use of guideline-directed medical therapy as defined by the AACF/AHA. Another example is specialized HF inpatient units with transitional programs to the outpatient setting to help manage these patients. These units are staffed with multidisciplinary HF teams, including nurses who are educated in the care of these patients. The main goals in the treatment of chronic HF are to treat the underlying cause and contributing factors, maximize CO, reduce symptoms, improve ventricular function, improve quality of life, preserve target organ function, and improve mortality and morbidity risks. Oxygen therapy - Relieves dyspnea and fatigue Physical and emotional rest - Conserve energy and decrease oxygen needs - Dependent on severity of HF Structured exercise program - CR associated with better outcomes In a person with HF, oxygen saturation of the blood can be reduced because the blood is not adequately oxygenated in the lungs. The use of supplemental oxygen improves saturation and assists in meeting tissue oxygen needs. This helps to relieve dyspnea and fatigue. Optimally, either pulse oximetry or arterial blood gases (ABGs) are used to monitor the need for and effectiveness of oxygen therapy. Physical and emotional rest allows the patient to conserve energy and decreases the need for additional oxygen. The degree of rest recommended depends on the severity of HF. A patient with severe HF may be on bed rest with limited activity. A patient with mild to moderate HF can be ambulatory with restriction of strenuous activity. The patient should be told to participate in prescribed activities with adequate recovery periods. A structured exercise program, such as cardiac rehabilitation (CR), should be considered for all patients with chronic HF. CR has been associated with decreased hospitalizations and reduced mortality. Patients enrolled in CR programs have also reported improved quality of life and less depression. CardioMems system - The CardioMems system is a new device to help monitor patient's pulmonary pressures. It is implanted in a patient's distal pulmonary artery during a right heart catheterization. The permanent device is approved for patients with NYHA Class III HF symptoms. It allows for close monitoring of changes in pulmonary pressures. Implantable cardioverter-defibrillator (ICD) Biventricular pacing/cardiac resynchronization therapy (CRT) IABP and VADs as bridge to transplant (BTT) or as destination therapy (DT) Patients with an EF less than 35% are at an increased risk of SCD from ventricular tachycardia or fibrillation. An ICD is recommended for SCD prophylaxis. In HF, neurohormonal effects and cardiac remodeling can result in dyssynchrony of the LV and RV. This contributes to poor CO. In these patients, biventricular pacing, known as cardiac resynchronization therapy (CRT), is recommended. In CRT an extra pacing lead is placed through the coronary sinus to a coronary vein of the LV. This lead coordinates right and left ventricular contractions. The ability to have normal electrical conduction (synchrony) between the RV and the LV increases left ventricular function and CO. At times, patients may need both CRT and an ICD Several mechanical options are available to sustain HF patients with deteriorating conditions, especially those awaiting heart transplantation. These include the IABP and VADs. However, the limitations of bed rest and the risk of infection and vascular complications preclude long-term use of the IABP. VADs provide highly effective long-term support and have become standard care in many heart transplant centers. The heart pump is operated via a driveline that exits the abdominal wall and is attached to a system controller with patient specific settings. VADs operate on AC current or batteries.

Pathophysiology Mixed Heart Failure

Mixed systolic and diastolic failure 1. Seen in disease states such as dilated cardiomyopathy (DCM) 2. Poor EFs (<35%) 3. High pulmonary pressures 4. Biventricular failure - Both ventricles may be dilated and have poor filling and emptying capacity Mixed systolic and diastolic failure is seen in disease states such as dilated cardiomyopathy (DCM). DCM is a condition in which poor systolic function is further compromised by a dilated LV wall that is unable to relax. These patients often have extremely low EFs (less than 35%), high pulmonary pressures, and biventricular failure (both ventricles are dilated and have poor filling and emptying capacity).

Pathophysiology Right-Sided Heart Failure

RV fails to pump effectively Fluid backs up in venous system Fluid moves into tissues and organs Left-sided HF is most common cause - Other causes include RV infarction, PE, and cor pulmonale (RV dilation and hypertrophy) Right-sided HF occurs when the right ventricle (RV) fails to pump effectively. When the RV fails, fluid backs up into the venous system. This causes movement of fluid into the tissues and organs (e.g., peripheral edema, abdominal ascites, hepatomegaly, jugular venous distention). The most common cause of right-sided HF is left-sided HF. As the LV fails, fluid backs up into the pulmonary system, causing increased pressures in the lungs. The RV has to work harder to push blood to the pulmonary system. Over time, this increased workload weakens the RV and gradually it fails. Other causes of right-sided HF (independent of the function of the LV) include RV infarction, pulmonary embolism, and cor pulmonale (RV dilation and hypertrophy caused by pulmonary disease).

Pulmonary Edema

As pulmonary edema progresses, it inhibits oxygen and carbon dioxide exchange at the alveolar-capillary interface. A. Normal relationship. B. Increased pulmonary capillary hydrostatic pressure causes fluid to move from the vascular space into the pulmonary interstitial space. C. Lymphatic flow increases in an attempt to pull fluid back into the vascular or lymphatic space. D. Failure of lymphatic flow and worsening of left heart failure result in further movement of fluid into the interstitial space and into the alveoli.

The home care nurse visits a patient with chronic heart failure who is taking digoxin (Lanoxin) and furosemide (Lasix). The patient complains of nausea and vomiting. Which action is most appropriate for the nurse to take? A. Perform a dipstick urine test for protein. B. Notify the health care provider immediately. C. Have the patient eat foods high in potassium. D. Ask the patient to record a weight every morning.

Answer: B Rationale: Administration of furosemide increases excretion of potassium and may cause hypokalemia. The risk for digitalis toxicity increases if potassium levels are below normal and digoxin is administered. Signs and symptoms of digitalis toxicity include anorexia, nausea and vomiting, visual disturbances (such as "yellow" vision), and dysrhythmias.

A patient with left-sided heart failure is prescribed oxygen at 4 L/min per nasal cannula, furosemide (Lasix), spironolactone (Aldactone), and enalapril (Vasotec). Which assessment should the nurse complete to best evaluate the patient's response to these drugs? A. Observe skin turgor B. Auscultate lung sounds C. Measure blood pressure D. Review intake and output

Answer: B Rationale: Left-sided heart failure will prevent normal blood flow and will cause blood to back up into the left atrium and into the pulmonary veins. The increased pulmonary pressure causes fluid extravasation from the pulmonary capillary bed into the interstitium and then the alveoli, which manifests as pulmonary congestion and edema. The most important assessment to determine if the drugs are improving the patient's condition is to auscultate lung sounds. The other assessments are important, but the best indicator of improvement of left ventricular function is a reduction in adventitious lung sounds (crackles).

A patient with a history of chronic heart failure is hospitalized with severe dyspnea and a dry, hacking cough. Assessment findings include pitting edema in both ankles, BP 170/100 mm Hg, pulse 92 beats/minute, and respirations 28 breaths/minute. Which explanation, if made by the nurse, is most accurate? A. "The assessment indicates that venous return to the heart is impaired, causing a decrease in cardiac output." B. "The manifestations indicate impaired emptying of both the right and left ventricles, with decreased forward blood flow." C. "The myocardium is not receiving enough blood supply through the coronary arteries to meet its oxygen demand." D. "The patient's right side of the heart is failing to pump enough blood to the lungs to provide systemic oxygenation."

Answer: B Rationale: The patient is experiencing acute decompensated heart failure with symptoms of both right- and left-sided heart failure. Left-sided heart failure prevents normal, forward blood flow and causes pulmonary congestion. Right-sided heart failure causes a backup of blood and results in venous congestion.

Pulmonary Edema Clinical Manifestations

Anxious, pale, cyanotic Cool and clammy skin Dyspnea Orthopnea Tachypnea Use of accessory muscles Cough with frothy, blood-tinged sputum Crackles and wheezes Tachycardia Hypotension or hypertension Abnormal S3 or S4 Clinical manifestations of pulmonary edema are distinct. The patient has dyspnea and orthopnea (unable to lie flat due to shortness of breath). Jugular venous distention is often present and is the most sensitive and specific sign for elevated LV filling pressures. The patient is usually anxious, pale, and possibly cyanotic. The skin is clammy and cold from vasoconstriction caused by stimulation of the SNS. Respiratory rate is often greater than 30 breaths/minute, and use of accessory muscles to breathe may be seen. There may be wheezing and coughing with the production of frothy, blood-tinged sputum. Breath sounds may reveal crackles and wheezes throughout the lungs. The absence of crackles does not rule out ADHF as many patients with a history of chronic HF develop increased lymphatic drainage of the alveolar edema. The patient's HR is rapid, and an abnormal S3 or S4 heart sound may be auscultated. BP may be elevated or decreased depending on the severity of the HF.

Pathophysiology Diastolic HF

HFpEF - HF with preserved EF Impaired ability of the ventricles to relax and fill during diastole, resulting in decreased stroke volume and CO Diastolic failure, or HFpEF, is the inability of the ventricles to relax and fill during diastole. Approximately 50% of patients with HF have HFpEF. Hypertension is the most important cause of diastolic failure. Other risk factors include older age, female gender, diabetes, and obesity. In diastolic failure, the LV is generally stiff and noncompliant. Diastolic failure is characterized by high filling pressures because of stiff ventricles. Decreased filling of the ventricles results in decreased stroke volume and CO. The end result of diastolic failure is the same as systolic failure (e.g., pulmonary congestion). HFpEF is diagnosed by the following criteria: (1) signs and symptoms of HF, (2) normal EF, and (3) evidence of LV diastolic dysfunction by echocardiography or cardiac catheterization. Therapies for HFpEF are targeted at reducing underlying risk factors and treating comorbidities. Result of left ventricular hypertrophy from hypertension, older age, female, diabetes, obesity Same end result as systolic failure Diastolic failure, or HFpEF, is the inability of the ventricles to relax and fill during diastole. Approximately 50% of patients with HF have HFpEF. Hypertension is the most important cause of diastolic failure. Other risk factors include older age, female gender, diabetes, and obesity. In diastolic failure, the LV is generally stiff and noncompliant. Diastolic failure is characterized by high filling pressures because of stiff ventricles. Decreased filling of the ventricles results in decreased stroke volume and CO. The end result of diastolic failure is the same as systolic failure (e.g., pulmonary congestion). HFpEF is diagnosed by the following criteria: (1) signs and symptoms of HF, (2) normal EF, and (3) evidence of LV diastolic dysfunction by echocardiography or cardiac catheterization. Therapies for HFpEF are targeted at reducing underlying risk factors and treating co-morbidities.

Pathophysiology Systolic HF

HFrEF - HF with reduced EF Inability to pump blood forward Caused by - Impaired contractile function - Increased afterload - Cardiomyopathy - Mechanical abnormalities Decreased LV ejection fraction (EF) Systolic failure, also known as HFrEF, results from an inability of the heart to pump blood effectively. The hallmark of systolic failure is a decrease in the EF. The amount of blood pumped by the left ventricle with each heart beat is called the ejection fraction (EF). The American Academy of Cardiology Foundation (ACCF) has adopted the terms heart failure with reduced EF (HFrEF) and heart failure with preserved EF (HFpEF) to describe systolic and diastolic HF. Normal EF is 55% to 60%. Patients with HFrEF generally have an EF less than 45%. It can be as low as 5% to 10%. HFrEF is caused by impaired contractile function (e.g., MI), increased afterload (e.g., hypertension), cardiomyopathy, and mechanical abnormalities (e.g., valvular heart disease). The LV in systolic failure loses its ability to generate enough pressure to eject blood forward through the aorta. Over time, the LV becomes dilated and hypertrophied. The weakened heart muscle cannot generate adequate stroke volume, which affects CO. Because the LV cannot effectively push blood forward, end diastolic volumes and pressures in the LV increase. When the LV fails, blood backs up into the left atrium. This causes fluid accumulation in the lungs. The increased pulmonary hydrostatic pressure causes fluid leakage from the pulmonary capillary bed into the interstitium and then the alveoli. This results in pulmonary congestion and edema.

Chronic HF Nursing Implementation

Health Promotion - Interprofessional communication and decision-making with patient and caregiver - Identify and treat risk factors for HF to prevent or slow progression Communication and joint decision making among the patient, caregiver, and interprofessional team are integral to selection and delivery of high-quality, patient-centered care. Currently, the emphasis is on aggressively identifying and treating risk factors for HF to prevent or slow the progression of the disease. For example, teach a patient with hypertension or hyperlipidemia ways to manage BP or cholesterol with drugs, diet, and exercise. Encourage patients to obtain vaccinations against the flu and pneumonia. Patients with valvular disease should be evaluated for valve replacement procedures if they are contributing to HF and symptoms. Coronary revascularization procedures should be considered in patients with CAD. The use of antidysrhythmic drugs or pacing therapy is indicated for patients with serious dysrhythmias or conduction disturbances.

Placement of Pacing Leads in Cardiac Resynchronization Therapy

1. Right atrial lead 2. right ventricular lead 3. coronary sinus 4. left ventricular lead

Acute Decompensated Heart Failure (ADHF) Clinical Manifestations

ADHF - Sudden onset of signs and symptoms of HF - Requires urgent medical care - Pulmonary and systemic congestion due to ↑ left-sided and right-sided filling pressures Acute decompensated HF (ADHF) is defined as the sudden onset of signs and symptoms of HF, requiring urgent medical care. The universal finding in ADHF is pulmonary and systemic congestion due to elevated left-sided and right-sided filling pressures. Early → increased pulmonary venous pressure - Increase in the respiratory rate - Decrease in Pao2 Later → interstitial edema - Tachypnea Further progression → alveolar edema - Respiratory acidemia In acute decompensated HF (ADHF), the pulmonary venous pressure increases caused by failure of the LV. This results in engorgement of the pulmonary vascular system. As a result, the lungs become less compliant, and there is increased resistance in the small airways. To help compensate, the lymphatic system increases its flow to help maintain a constant volume of the pulmonary extravascular fluid. This early stage is clinically associated with a mild increase in the respiratory rate and a decrease in partial pressure of oxygen in arterial blood (Pao2). If pulmonary venous pressure continues to increase, the increase in intravascular pressure causes more fluid to move into the interstitial space than the lymphatics can remove. Interstitial edema occurs at this point. Tachypnea develops and the patient becomes symptomatic (e.g., short of breath). If the pulmonary venous pressure increases further, the alveoli lining cells are disrupted and a fluid containing red blood cells (RBCs) moves into the alveoli (alveolar edema). As the disruption becomes worse from further increases in the pulmonary venous pressure, the alveoli and airways are flooded with fluid. This is accompanied by a worsening of the arterial blood gas values (i.e., lower Pao2 and possible increased partial pressure of carbon dioxide in arterial blood [Paco2] and progressive respiratory academia). Can manifest as pulmonary edema Life-threatening situation - alveoli fill with fluid Most commonly associated with left-sided HF ADHF can manifest as pulmonary edema. This is an acute, life-threatening situation in which the lung alveoli become filled with serosanguineous fluid. The most common cause of pulmonary edema is left-sided HF secondary to CAD. Based on hemodynamic and clinical status, patients can be categorized into one of four groups 1. Dry-warm 2. Dry-cold 3. Wet-warm (most common) 4. Wet-cold Patients with ADHF can be categorized into one of four groups based on hemodynamic and clinical status: dry-warm, dry-cold, wet-warm, and wet-cold. The most common presentation in patients with ADHF is the wet and warm patient. A patient is "wet" due to volume overload (e.g., congestion, dyspnea), but "warm" due to adequate perfusion (warm skin, positive pulses).

Dilated and Hypertrophied Heart Chambers

Compare and contrast dilation and hypertrophy; dilation refers to size of filling space; hypertrophy refers to thickness of muscle.

ADHF Interprofessional Care

Continuous monitoring and assessment - VS, O2 saturation, urinary output Hemodynamic monitoring if unstable Supplemental oxygen Mechanical ventilation if unstable High Fowler's position Patients with ADHF need continuous monitoring and assessment. This is done in an intensive care unit (ICU) if the patient is unstable. In the ICU, monitor heart rhythm and oxygen saturation continuously. Assess vital signs and urine output at least every hour. The patient may have hemodynamic monitoring, including arterial BP and pulmonary artery pressures. If a pulmonary artery catheter is placed, evaluate CO and pulmonary artery wedge pressure (PAWP). Therapy is titrated to maximize CO and reduce PAWP. A normal PAWP is generally between 8 and 12 mm Hg. Patients with ADHF may have a PAWP as high as 30 mm Hg. (Hemodynamic monitoring is discussed in Chapter 65.) Provide supplemental oxygen to help increase the percentage of oxygen in inspired air. (Oxygen therapy is discussed in Chapter 28.) In severe pulmonary edema, the patient may need noninvasive positive pressure ventilation (e.g., bilevel positive airway pressure [BiPAP]) or intubation and mechanical ventilation. BiPAP is also effective in decreasing preload. (Ventilatory support is discussed in Chapter 65.) Some patients with ADHF require hospitalization but are more stable. They are often admitted to a telemetry or stepdown unit for treatment. Assess these patients every 4 hours (e.g., vital signs, pulse oximetry) for adequate oxygenation. Record intake and output and daily weights to evaluate fluid status. If the patient has dyspnea, place in a high Fowler's position with the feet horizontal in the bed or dangling at the bedside. This position helps decrease venous return because of the pooling of blood in the extremities. This position also increases the thoracic capacity, allowing for improved breathing. Ultrafiltration (aquapheresis) for patients with volume overload and resistance to diuretics Circulatory assist devices for patients with deteriorating HF - Intraaortic balloon pump (IABP) - Ventricular assist devices (VADs) Ultrafiltration (UF), or aquapheresis, is an option for the patient with volume overload. It is a process to remove excess salt and water from the patient's blood. UF can rapidly remove intravascular fluid volume while maintaining hemodynamic stability. The ideal patients for UF are those with major pulmonary or systemic volume overload who have shown resistance to diuretics and are hemodynamically stable. UF also may be an appropriate adjunctive therapy for patients with HF and coexisting renal failure. (UF is discussed in Chapter 46.) In the ICU, circulatory assist devices are used to manage patients with worsening HF. The intraaortic balloon pump (IABP) is a device that increases coronary blood flow to the heart muscle and decreases the heart's workload through a process called counterpulsation. The IABP is useful in hemodynamically unstable patients because it decreases pulmonary artery pressures and systemic vascular resistance (SVR), leading to improved CO. Ventricular assist devices (VADs) can be used to maintain the pumping action of a heart that cannot effectively pump. A VAD is a mechanical pump that is surgically implanted. (IABPs and VADs are discussed in Chapter 65.) Once the patient is more stable, determination of the cause of ADHF is important. Diagnosis of systolic or diastolic HF will then direct further treatment protocols.

Chronic HF Ambulatory Care

Explain to patient and caregiver physiologic changes that have occurred Assist patient to adapt to both physiologic and psychologic changes Include patient and caregiver(s) in overall care plan HF is a chronic illness. When a patient is diagnosed with HF, care should focus on slowing the progression of the disease. Your important nursing responsibilities include (1) teaching the patient about the physiologic changes that have occurred, (2) assisting the patient to adapt to both the physiologic and psychologic changes, and (3) including the patient and the caregiver in the overall care plan.

Chronic HF Nursing Diagnoses

Impaired gas exchange Decreased cardiac output Excess fluid volume Activity intolerance Nursing diagnoses for the patient with HF include, but are not limited to, the following: Impaired gas exchange related to increased preload and alveolar-capillary membrane changes Decreased cardiac output related to altered contractility, altered preload, and/or altered stroke volume Excess fluid volume related to increased venous pressure and decreased renal perfusion secondary to heart failure Activity intolerance related to imbalance between O2 supply and demand secondary to cardiac insufficiency and pulmonary congestion.

Heart Failure

Inability of the heart muscle to pump effectively Unable to maintain adequate circulation to meet tissue needs. - Involves diastolic or systolic dysfunction - Ejection fraction (EF) is amount of blood pumped by LV with each heart beat Heart failure (HF) is a complex clinical syndrome that results in the inability of the heart to provide sufficient blood to meet the oxygen needs of tissues and organs. It is a major health problem in the United States. A defect in either ventricular filling (diastolic dysfunction) or ventricular ejection (systolic dysfunction) are the key manifestations of HF. The amount of blood pumped by the left ventricle with each heart beat is called the ejection fraction (EF). The American Academy of Cardiology Foundation (ACCF) has adopted the terms heart failure with reduced EF (HFrEF) and heart failure with preserved EF (HFpEF) to describe systolic and diastolic HF. The ineffectiveness to pump results in: - Inadequate Cardiac Output - Myocardial Hypertrophy - Pulmonary/Systemic Congestion Associated with CVDs - Systemic Hypertension - Coronary Artery Disease - Myocardial Infarction - Pulmonary Hypertension - Dysrhythmias - Valvular Heart Disease - Pericarditis - Cardiomyopathy Most common cause for hospital admission in adults over age 65 HF is associated with numerous types of cardiovascular diseases (CVDs), particularly long-standing hypertension, coronary artery disease (CAD), and myocardial infarction (MI). In contrast to other CVDs, HF is increasing in incidence and prevalence. This is due in part to better survival after cardiac events and the aging population. HF is primarily a disease of older adults. The incidence is similar in men and women. The American Heart Association (AHA) estimates that over 650,000 new cases are diagnosed each year. HF is the most common reason for hospital admission in adults over the age of 65. This places a significant economic burden on the health care system. The complex, progressive nature of HF often results in poor outcomes, the most costly being hospital readmissions. Approximately 25% of patients discharged with a primary diagnosis of HF are readmitted within 30 days. The total cost of HF care in the United States exceeds $40 billion annually, with over half of these costs spent on hospitalizations.

Chronic HF Evaluation

Monitoring to assess outcomes and prevent/ limit future hospitalizations - Vital signs - Weight - Pulse oximetry - Dyspnea Home health nurses can be essential Can use electronic monitoring Managing HF patients out of the hospital is a priority. Effective home health care can prevent or limit future hospitalizations by providing ongoing assessments (e.g., monitoring vital signs and weight, evaluating response to therapies). Many agencies offer specialized programs dedicated to managing HF patients at home. For example, these programs may include the use of telehealth monitoring technology (e.g., electronic scale, BP cuff, pulse oximeter) to collect physiologic data. The technology may also be able to audibly ask the patient questions such as, "Are you short of breath today?" Results are transmitted telephonically or by computer to the home care agency. Once received, the data are reviewed. Based on the findings, the patient may be called to further assess the situation or a visit may be scheduled. Home health nurses frequently work with protocols set up with the patient's health care team. The protocols enable you and the patient to identify problems, such as an increase in weight or dyspnea as evidence of worsening HF. Interventions can be started to prevent hospitalization. These may include changing drugs and restricting fluids. Home health nursing care of HF patients is vital in reducing the number of hospitalizations, increasing functional capacity, and increasing the quality of life.

Counterregulatory Mechanisms

Natriuretic peptides - Atrial natriuretic peptide (ANP), b-type natriuretic peptide (BNP) - Released in response to increased blood volume in heart - Causes diuresis, vasodilation, and lowered BP - Counteracts effects of SNS and RAAS The body's ability to try to maintain balance is demonstrated by several counterregulatory processes. Natriuretic peptides (atrial natriuretic peptide [ANP] and brain [b-type] natriuretic peptide [BNP]) are hormones produced by the heart muscle. ANP is released from the atria and BNP is released from the ventricles in response to increased blood volume in the heart. The natriuretic peptides have renal, cardiovascular, and hormonal effects. Renal effects include (1) increased glomerular filtration rate and diuresis, and (2) excretion of sodium (natriuresis). Cardiovascular effects include vasodilation and decreased BP. Hormonal effects include (1) inhibition of aldosterone and renin secretion and (2) interference of ADH release. The combined effects of ANP and BNP help to counter the adverse effects of the SNS and RAAS in patients with HF. Nitric oxide (NO) and prostaglandin - Released from vascular endothelium in response to compensatory mechanisms - NO and prostaglandin relaxes arterial smooth muscle, resulting in vasodilation and decreased afterload Nitric oxide (NO) and prostaglandin are counterregulatory substances released from the vascular endothelium in response to the compensatory mechanisms activated in HF. Like the natriuretic peptides, NO and prostaglandin work to relax the arterial smooth muscle, resulting in vasodilation and decreased afterload. Compensated HF occurs when compensatory mechanisms succeed in maintaining an adequate CO that is needed for tissue perfusion. Decompensated HF occurs when these mechanisms can no longer maintain adequate CO and inadequate tissue perfusion results.

Dilated Heart Chambers

Note the enlarged heart chambers with cardiac dilation.

Hypertrophied Heart Chambers

Note the thickened ventricular walls with hypertrophy.

Chronic HF Planning

Overall Goals - Decrease in symptoms - Decrease in peripheral edema - Increase in exercise tolerance - Compliance with the treatment regimen - No complications related to HF The overall goals for the patient with HF include (1) a decrease in symptoms (e.g., shortness of breath, fatigue), (2) a decrease in peripheral edema, (3) an increase in exercise tolerance, (4) compliance with the treatment regimen, and (5) no complications related to HF.

Pitting Edema

Pitting edema. Note the finger-shaped depressions that do not rapidly refill after an examiner has exerted pressure.

Classification Systems of Heart Failure

The New York Heart Association (NYHA) developed functional guidelines for classifying people with heart disease based on tolerance to physical activity. Because this system only reflected exercise capacity, the American College of Cardiology Foundation/AHA (ACCF/AHA) developed a staging system that identified disease progression and treatment strategies. This system allows for identification of people at risk for developing HF but who do not currently have heart disease. The ACCF/AHA system encourages clinicians to actively address the patient's risk factors and treat any existing conditions to prevent further disease progression. This may help reduce the growing number of HF patients. Patients may move between levels in the NYHA classification system based on worsening or improving symptoms. However, the ACCF/AHA staging system is progressive. Patients can only advance to a higher (worse) stage as the disease progresses.

Pathophysiology Heart Failure in General

Ventricular failure leads to: - Low blood pressure (BP) - Low CO - Poor renal perfusion Abrupt or subtle onset Compensatory mechanisms mobilized to maintain adequate CO The patient with ventricular failure of any type may have low blood pressure (BP), low CO, and poor renal perfusion. HF can have an abrupt onset as with acute MI or it can be a subtle process resulting from slow, progressive changes. The overloaded heart uses compensatory mechanisms to try to maintain adequate CO. The main compensatory mechanisms include (1) neurohormonal responses: renin-angiotensin-aldosterone-system (RAAS) and the sympathetic nervous system (SNS), (2) ventricular dilation, and (3) ventricular hypertrophy.