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(Relates to Chapter 35, “Nursing Management: Heart Failure,” in the textbook) Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. An abnormal condition involving impaired cardiac pumping/filling Heart is unable to produce an adequate cardiac output (CO) to meet metabolic needs. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 2 Characterized by • Ventricular dysfunction • Reduced exercise tolerance • Diminished quality of life • Shortened life expectancy Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 3 Heart failure (HF) is not a disease but a “syndrome” Associated with long-standing hypertension, coronary artery disease (CAD), and myocardial infarction (MI) Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 4 Affects about 5 million people in the United States The most common reason for hospitalization in adults >65 years old Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 5 Primary risk factors • CAD • Advancing age Contributing risk factors • Hypertension • Diabetes • Tobacco use • Obesity • High serum cholesterol Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 6 Causes of HF may be divided into two subgroups: • Primary • Precipitating HF is classified as systolic or diastolic failure (or dysfunction). Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 7 Systolic failure • Hallmark finding: Decrease in the left ventricular ejection fraction (EF) Caused by Impaired contractile function (e.g., MI) Increased afterload (e.g., hypertension) Cardiomyopathy Mechanical abnormalities (e.g., valve disease) Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 8 Diastolic failure • Impaired ability of the ventricles to relax and fill during diastole, resulting in decreased stroke volume and CO • Diagnosis based on the presence of pulmonary congestion, pulmonary hypertension, ventricular hypertrophy, and normal EF Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 9 Diastolic failure (cont’d) • Caused by Left ventricular hypertrophy from chronic hypertension Aortic stenosis Hypertrophic cardiomyopathy Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 10 Mixed systolic and diastolic failure • Seen in disease states such as dilated cardiomyopathy (DCM) • Poor EFs (<35%) • High pulmonary pressures • Biventricular failure Both ventricles may be dilated and have poor filling and emptying capacity. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 11 Compensatory mechanisms are activated to maintain adequate CO. • Sympathetic nervous system (SNS) activation: First and least effective mechanism Release of catecholamines (epinephrine and norepinephrine) Increased heart rate (HR) Increased myocardial contractility Peripheral vasoconstriction Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 12 Compensatory mechanisms (cont’d) • Sympathetic nervous system (SNS) activation Over a period of time these mechanisms are detrimental as they increase the workload of the failing myocardium and the need for O2. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 13 Compensatory mechanisms (cont’d) • Neurohormonal responses: Kidneys release renin Renin converts angiotensinogen to angiotensin I. Angiotensin I is converted to angiotensin II by a converting enzyme made in the lungs. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 14 Compensatory mechanisms (cont’d) • Neurohormonal responses (cont’d) Angiotensin II causes Adrenal cortex to release aldosterone (sodium and water retention) Increased peripheral vasoconstriction (increases BP) Response is known as the reninangiotensin-aldosterone system (RAAS). Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 15 Compensatory mechanisms (cont’d) • Neurohormonal responses (cont’d) Low CO causes a decrease in cerebral perfusion pressure. Antidiuretic hormone (ADH) is secreted and causes Increased water reabsorption in the renal tubules, leading to water retention and increased blood volume Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 16 Compensatory mechanisms (cont’d) • Neurohormonal responses (cont’d) Endothelin is stimulated by ADH, catecholamines, and angiotensin II, causing Arterial vasoconstriction Increase in cardiac contractility Hypertrophy Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 17 Compensatory mechanisms (cont’d) • Neurohormonal responses (cont’d) Proinflammatory cytokines (e.g., tumor necrosis factor): Released by cardiac myocytes in response to cardiac injury Depress cardiac function by causing cardiac hypertrophy, contractile dysfunction, and death of myocytes Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 18 Compensatory mechanisms (cont’d) • Neurohormonal responses (cont’d) Over time, a systemic inflammatory response is mounted and results in Cardiac wasting Muscle myopathy Fatigue Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 19 Consequences of compensatory mechanisms • Dilation Enlargement of the chambers of the heart that occurs when pressure in the left ventricle is elevated Initially an adaptive mechanism Eventually this mechanism becomes inadequate, and CO decreases. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 20 Fig. 35-1. A, Dilated heart chambers. B, Hypertrophied heart chambers. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 21 Consequences of compensatory mechanisms • Hypertrophy Increase in muscle mass and cardiac wall thickness in response to chronic dilation, resulting in Poor contractility Higher O2 needs Poor coronary artery circulation Risk for ventricular dysrhythmias Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 22 Counter regulatory processes • Natriuretic peptides: Atrial natriuretic peptide (ANP), b-type natriuretic peptide (BNP) Released in response to increase in atrial volume and ventricular pressure Promote venous and arterial vasodilation, reducing preload and afterload Chronic HF leads to a depletion of these factors . 23 Counter regulatory processes (cont’d) • Natriuretic peptides are endothelin and aldosterone antagonists. Enhance diuresis Block effects of the RAAS • Natriuretic peptides inhibit the development of cardiac hypertrophy and may have antiinflammatory effects. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 24 Counter regulatory processes (cont’d) • Nitric oxide (NO) Released from the vascular endothelium in response to compensatory mechanisms NO relaxes arterial smooth muscle, resulting in vasodilation and decreased afterload. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 25 Left-sided HF (most common) from left ventricular dysfunction (e.g., MI hypertension, CAD, cardiomyopathy) • Backup of blood into the left atrium and pulmonary veins Pulmonary congestion Pulmonary edema Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 26 Fig. 35-2. Pathophysiology of heart failure. Elevated systemic vascular resistance results in left-sided heart failure that leads to right-sided heart failure. Systemic vascular resistance and preload are exacerbated by the renin-angiotensin-aldosterone system. ADH, Antidiuretic hormone; LA, left atrium; LV, left ventricle; LVEDP, left ventricular end-diastolic pressure; RV, right ventricle. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 27 Right-sided HF from left-sided HF, cor pulmonale, right ventricular MI • Backup of blood into the right atrium and venous systemic circulation Jugular venous distention Hepatomegaly, splenomegaly Vascular congestion of GI tract Peripheral edema Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 28 Pulmonary edema, often lifethreatening • Early Increase in the respiratory rate Decrease in PaO2 • Later Tachypnea Respiratory acidemia Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 29 Fig. 35-3. 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. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 30 Physical findings • Orthopnea • Dyspnea, tachypnea • Use of accessory muscles • Cyanosis • Cool and clammy skin Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 31 Physical findings • Cough with frothy, blood-tinged sputum • Breath sounds: Crackles, wheezes, rhonchi • Tachycardia • Hypotension or hypertension Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 32 . 33 Fatigue Dyspnea, orthopnea, paroxysmal nocturnal dyspnea Persistent, dry cough, unrelieved with position change or over-the-counter cough suppressants Tachycardia Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 34 Dependent edema • Edema may be pitting in nature • Sudden weight gain of >3 lb (1.4 kg) in 2 days may indicate an exacerbation of HF. 35 Nocturia Skin • Dusky, cool, damp to touch • Lower extremities: Shiny and swollen, diminished or absent hair growth, pigment changes 36 Restlessness, confusion, decreased memory Chest pain (angina) Weight changes • Anorexia, nausea • Fluid retention Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 37 Pleural effusion Atrial fibrillation (most common dysrhythmia) • Promotes thrombus/embolus formation, increasing risk for stroke • Treatment can include rate control, cardioversion, antidysrhythmics, and/or systemic anticoagulation. . 38 High risk of fatal dysrhythmias (e.g., sudden cardiac death, ventricular tachycardia) with HF and an EF <35% HF can lead to severe hepatomegaly, especially with RV failure. • Fibrosis and cirrhosis can develop over time. Renal insufficiency or failure . 39 Primary goal: Determine and treat underlying cause • History and physical examination • Chest x-ray • ECG • Lab studies (e.g., cardiac enzymes, BNP) 40 Primary goal: Determine and treat underlying cause • Hemodynamic assessment (pressures within the heart) • Echocardiogram • Stress testing • Cardiac catheterization • Ejection fraction 41 New York Heart Association Functional Classification of HF • Classes I to IV ACC/AHA Stages of HF • Stages A to D Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 42 Overall goals of therapy for ADHF and Chronic HF • Decrease patient symptoms. • Improve LV function. • Reverse ventricular remodeling. • Improve quality of life. • Decrease mortality and morbidity. 43 High Fowler’s position Supplemental oxygen Continuous ECG monitoring Ultrafiltration: Option for patients with volume overload Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 44 Circulatory assist devices are used to treat patients with deteriorating HF. Coexisting psychologic disorders should be addressed. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 45 Decrease intravascular volume • Reduces venous return and preload Loop diuretics (e.g., furosemide [Lasix]) Ultrafiltration or aquapheresis Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 46 Decrease venous return (preload) • Reduces the amount of volume returned to the LV during diastole High-Fowler’s position IV nitroglycerin Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 47 Decrease afterload • Improves CO and decreases pulmonary congestion IV sodium nitroprusside (Nipride) Morphine sulfate Nesiritide (Natrecor) Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 48 Improve gas exchange and oxygenation • Supplemental oxygen • Morphine sulfate • Noninvasive ventilatory support (BiPAP) Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 49 Improve cardiac function • For patients who do not respond to conventional pharmacotherapy (e.g., diuretics, vasodilators, morphine sulfate) Inotropic therapy Digitalis -Adrenergic agonists (e.g., dopamine) Phosphodiesterase inhibitors (e.g., milrinone) Hemodynamic monitoring Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 50 Reduce anxiety • Distraction, imagery • Sedative medications (e.g., morphine sulfate, benzodiazepines) Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 51 Main treatment goals • Treat the underlying cause and contributing factors • Maximize CO • Provide treatment to alleviate symptoms • Improve ventricular function • Improve quality of life • Preserve target organ function • Improve mortality and morbidity . 52 Oxygen administration Physical and emotional rest Non-pharmacologic therapies • Cardiac resynchronization therapy (CRT) or biventricular pacing • Cardiac transplantation Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 53 Nonpharmacologic therapies (cont’d) • Intraaortic balloon pump (IABP) therapy • Ventricular assist devices (VADs) • Destination therapy—Permanent, implantable VAD Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 54 Therapeutic goals for drug therapy • Identification of type of HF and causes • Correction of sodium and water retention and volume overload • Reduction of cardiac workload • Improvement of myocardial contractility • Control of precipitating and complicating factors Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 55 Drug therapy • Diuretics Thiazide Loop Spironolactone . 56 Drug therapy (cont’d) • ACE inhibitors • Angiotensin II receptor blockers • Aldosterone antagonists • Nitrates • -Adrenergic blockers 57 Drug therapy (cont’d) • Positive inotropic (contractility)agents Digitalis Calcium sensitizers • BiDil (combination drug containing isosorbide dinitrate and hydralazine) 58 Nutritional therapy • Diet and weight reduction: Individualize recommendations and consider cultural background • Recommend Dietary Approaches to Stop Hypertension (DASH) diet. • Sodium is usually restricted to 2.5 g per day. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 59 Nutritional therapy • Fluid restriction not generally required • Daily weights are 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 health care provider. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 60 Assessment • Subjective data Past health history Functional health patterns Medications • Objective data Physical examination Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 61 Nursing diagnoses • Activity intolerance • Fluid volume excess • Impaired gas exchange • Anxiety • Deficient knowledge Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 62 Planning: Overall goals • Decrease in symptoms (e.g., shortness of breath, fatigue) • Decrease in peripheral edema • Increase in exercise tolerance • Compliance with the medical regimen • No complications related to HF Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 63 Health promotion • Treatment or control of underlying heart disease key to preventing HF and episodes of ADHF (e.g., valve replacement, control of hypertension, coronary revasculariztion) • Early detection of worsening HF may prevent future hospitalizations. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 64 Health promotion • Patient/caregiver teaching: Medications, diet, and exercise regimens Exercise training (e.g., cardiac rehabilitation) improves symptoms but is often underprescribed. • Home nursing care may be required for follow-up and to monitor patient’s response to treatment. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 65 Acute intervention • HF is a progressive disease—Treatment plans are established with quality-of-life goals. • Symptom management is controlled with the use of self-management tools (e.g., daily weights). Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 66 Acute intervention • Salt must be restricted. • Energy must be conserved. • Support systems are essential to the success of the entire treatment plan. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 67 Ambulatory and home care • Explain to patient and caregiver physiologic changes that have occurred. • Assist patient to adapt to both the physiologic and psychologic changes. • Integrate patient and caregiver(s) or support system into the overall care plan. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 68 Implementation: Patient education • Medications (lifelong) • Taking pulse rate Know when drugs (e.g., digitalis, adrenergic blockers) should be withheld and reported to health care provider. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 69 Implementation: Patient and caregiver education • Home BP monitoring • Signs of hypokalemia and hyperkalemia if taking diuretics that deplete or spare potassium • Instruct patient in energy-conserving and energy-efficient behaviors. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 70 Evaluation • Respiratory status • Fluid balance • Activity tolerance • Anxiety control • Knowledge of disease process 71 Treatment of choice for patients with refractory end-stage HF, inoperable CAD, and cardiomyopathy • Goal of the transplant evaluation process is to identify patients who would most benefit from a new heart. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 72 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. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 73 Bridge to transplantation devices Surgery involves removing the recipient’s heart, except for the posterior right and left atrial walls and their venous connections. Recipient’s heart is replaced with the donor heart. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 74 Donor sinoatrial (SA) node is preserved so that a sinus rhythm may be achieved postoperatively. Immunosuppressive therapy usually begins in the operating room. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 75 Infection is the primary complication, followed by acute rejection, in the first year after transplantation. Malignancy (especially lymphoma) and coronary artery vasculopathy are major causes of death after the first year. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 76 Endomyocardial biopsies are obtained from the right ventricle weekly for the first month, monthly for the following 6 months, and yearly thereafter to detect rejection. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 77 Nursing care focuses on • Promoting patient adaptation to the transplant process • Monitoring cardiac function • Managing lifestyle changes • Providing relevant teaching Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 78 68-year-old woman is admitted to the hospital for shortness of breath. She was diagnosed 4 years ago with HF after failing to follow the recommended medical regimen for an MI she suffered 6 years ago. 79 States she was taking a diuretic but ran out 4 days ago; has not been able to refill her prescription States she noticed some swelling in her feet that seemed worse than usual 80 Physical examination • Alert and oriented to person, place, and time • Fine crackles bilateral lower lobes • Shortness of breath on minimal exertion 81 Physical examination (cont’d) • O2 saturation 89%, room air • S1 and S2 without murmur or extra heart sounds • Capillary refill sluggish in lower extremities, normal in upper extremities • 2+ edema bilateral lower extremities 82 1. What is the priority of care for her? 2. How would you evaluate whether your nursing actions were successful? 3. What teaching measures would you use to prevent a reoccurrence of ADHF? 83