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Chapter 35: Heart Failure = abnormal clinical condition involving impaired cardiac pumping - will see fluid retention and vasoconstriction - not all pts will have pulmonary congestion - not a disease - associated with long-standing HTN,CAD,MI - characterized by ventricular dysfunction, reduced exercise tolerance, diminished quality of life, shortened life expectancy - HF is the most common reason for hospital admission in adults older than 65 years Etiology + Pathophysiology: - CAD and advancing age = Primary risk factors - Others: HTN,DM, cig smoking, obesity, high serum choles. - HTN increases risk 3x - Systolic and diastolic HTN equally predicts risk - DM is more like to predispose women than men CO depends on: 1. preload 2. afterload 3. myocardial contractility 4. HR 5. metabolic state of individual 6. (any alteration in there can lead to decreased ventricular function) Pathology of Ventricular Failure: Systolic Failure: the most common cause of HF, results from inability of the heart to pump bld. - Defect of the ventricles ability to contract - Over time the LV becomes thin walled, dilated, hypertrophied - * decrease in LV EF - normal EF= >55% of ventricular volume - SF is caused by impaired contractile function, increased afterload, cardiomyopathy, mechanical abnormalities.

Diastolic Failure: impaired ability of ventricles to relax and fill - Results in decreased SV and CO

2 Characterized by high filling pressures d/t stiff or noncompliant ventricles and results in venous engorgement of both pulmonary and systemic vascular systems Diagnosed based on presence of pulmonary congestion, pulm HTN, ventricular hypertrophy and normal EF Usually result of LV hypertrophy from chronic systemic HTN, aortic stenosis, or hypertrophic cardiomyopathy Commonly seen in older adults esp. women, as a result of myocardial fibrosis and HTN. (see pg 823 for gender differences) Less common is isolated right ventricular diastolic failure. o Results from pulm HTN and causes reduced R ventricular emptying, resulting in low left ventricular filling pressure and reduced CO

Mixed Systolic and Diastolic Failure: seen in dialated cardiomyopathy (DCM) - DCM condition which poor systolic function is further compromised by dilated LV walls that are unable to relax. - Pt will have extremely poor EF(less than 35%) - High pulmonary pressures - Biventricular failure - Pt with ventricular failure of any type has low systemic arterial BP, low CO, poor renal perfusion, poor exercise tolerance and ventricular dysrrhythmias - Bodys response to low CO is to mobilize its compensatory mechanisms to maintain CO and BP Compensatory Mechanisms: Sympathetic NS activation: is often the first mech triggered in low CO states (least effective) - Activation results in increased release of catecholamine - Results in increased HR and myocardial contractility, and peripheral vasoconstriction. - The vasoconstriction causes an immediate increase in preload. An increase in venous return to a heart which is already volume overloaded, worsens ventricular performance.

Neurohormonal Response: as the CO falls, bld flow to the kidneys decreases. - Kidneys respond but releasing rennin. -> RAAS

3 A decrease in cerebral perfusion pressure-> leads to ADH release: causes water retention and therefore increased BP The production of endothelin is $ by ADH, catecholamines, and angiotensin II. Endothelin results in further arterial vasoconstriction and in an increase in cardiac contractility and hypertrophy Locally, proinflammatory cytokines are released by cardioac myocytes in response to various forms of cardiac injury o 2 cytokines: tumor necrosis factor (TNF) and interleukin1(IL-1), further depress cardiac function by causing cardiac hypertrophy, contractile dysfun, and myocyte death

Together, these factors result in an increase in cardiac workload, myocardial dysfunction, and ventricular remodeling. Remodeling involves hypertrophy of cardiac myocytes, resulting in large, abnormally shaped contractile cells. Eventually leads to an increased ventricular mass, changes in ventricular shape, and impaired contractility. Ventricles because less effective although larger Dilation: enlargement of the chambers of the heart - When pressure in the heart chambers (usually the LV) is elevated overtime. - The degree of stretch is directly r/t Frank-Sterlings law. Hypertrophy: in CHF, increase in muscle mass and cardiac wall thickness in response to overwork and strain. - Generally follows persistent or chronic dilation and thus further increases the contractile power. - Will lead to an increase in CO and maintenance of tissue perfusion. - Risk for ischemia and ventricular dysfunction.

Counterregulatory Mechanisms: - Naturetic peptides are endothelin and aldosterone antagonist and enhance diuresis by increasing GFR and blocking affects of RAAS

4 Inhibit the development of cardiac hypertrophy and may have anti-inflammatory effects. APN is primarily triggered by an increase in volume BPN is primarily increased by increased pressure. NO also works to relax the arterial smooth muscle, resulting in vasodia, and increased afterload. Cardiac Compensation occurs when compen. Mechanisms succeed in maintaining adequate CO that is needed for tissue perfusion. Cardiac Decomposition: occurs when these mechanisms can no longer maintain adequate CO and inadequate tissue perfusion results.

Types of Heart Failure: Usually manifested by biventricular failure, although one ventricle may precede the other in dysfunction. Left Sided Failure: *most common form of HF - Results from LV dysf. - Increased pulmonary pressure leads to pulmonary congestion and edema. Right-Sided Failure: - Causes a back up of blood into the RA and venous circulation. - Venous congestion leads to jugular vein distention, hepatomegaly, splenomegaly, vascular congestion of the GI, peripheral edema. - *the primary cause of RHF is LHF - Cor pulmonale can also cause Clinical Manifestations of Acute Decompensate Heart Failure (ADHF): *typically manifests as Pulmonary Edema. - The most common cause of PE is acute Left ventricular failure, 2ndary to CAD. - An increase in the pulmonary venous pressure caused by a decreased efficiency of the LV. - Lungs become less compliant and increased resistance in the small airways. - Early on it is associated with increased RR and a decrease in PaO2 - When the lymphatic drain, will see interstitial edema. > tachypnea develops. - Alveolar edema develops when fluid with RBCs moves into the alveoli

5 Airways can become flooded with fluid and will see worsening of ABGs S/S: anxious, pale and possibly cyanotic. Cold clammy skin from vasoconstriction The pt has severe dyspnea AEB the use of accessory muscles of respiration, a RR >30bpm, orthpnea. May be wheezing, cough with blood tinged sputum. Crackles, wheezes, ronchi throughout the lungs Rapid HR BP may be elevating or decreasing dependent on the severity of the HF

Clinical Manifestations of Chronic Heart Failure: Fatigue: one of the earliest symptoms. Caused by decrease in CO, impaired perfusion to vital organs, decreased oxygenation of the tissues, anemia. Anemia can result from malnutrition, renal disease, or drug therapy. Dyspnea (SOB) is common. Caused by an increased pulmonary pressures 2ndary to interstial and alveolar edema. o May also have PND o Careful questioning of the pt along with what adaptive behaviors they use is important to ask. Tachycardia: early clinical sign. Pts who take a blockers may not show increased HR Edema Nocturia Skin Changes: bc tissue capillary O2 extraction is increased, the skin may appear dusky. Cool, damp to touch, swollen Behavioral Changes: r/t impaired cerebral circulation, or from poor gas exchange. Chest pain Weight changes: eating habits and edema

Complications of Heart Failure: - Pleural Effusion: from increasing pressure in the pleural capillaries - Dysrhythmias: r/t the enlargements of the chambers of the heart. o Pts with HF and EF less than 35% have a high chance of suffering from fatal dysrhythmias. - Left Ventricular Thrombus: with ADHF or CHF, the enlarged LV and decreased CO combine to increase the chance of thrombus formation.

6 o Once thrombus has formed, it may also decrease left ventricular contractility, decrease CO, and further worsens pts perfusion. o Also places pt at risk for a stroke. Hepatomegaly: *especially in pt with Right sided HF Leads to impaired liver function. Renal Failure: r/t decreased CO

Classification of HF: the New York Heart Association has produced guidelines. See chart on 826. Diagnostic Studies: - Hx and Physical exam - Serum chemistries, cardiac enzymes, BNP levels, liver function test - CXR - 12 lead ECG - echocardiography - exercise stress testing - nuclear imaging - hemodynamic monitoring - Cardiac cath. Nursing and Collaboritive Management: ADHF and Pulmonary Edema: Tx of ADHF is very complex and important. The use of diuretics, vasoactive drugs, ultrafiltration - ADHERE indicate that pt receiving early tx with IV diuretic and vasoactive drugs will have better and shorter stays in the hospital. - Diuretics work to decrease the preload and improving the pts S/S - ADHERE is currently reconsidering tx approach - Treatment strategies should include: o Improving LV function by decreasing intravascular volume, decreasing venous return(preload), decreasing afterload, controlling HR and rhythm, improving gas exchange and oxygenation, increasing CO, reducing anxiety, preserving target organ function, decreasing progression of the disease. Decreasing Intravascular Volume: The use of diuretics to decrease venous return. This increases left ventricular function, decreases pulmonary vascular pressures, improves gas exchange.

7 The use of IV loop diuretics have been associated with increased risk for fatal dysrhythmias, aggravated renal dysfun. And enhanced activation of RAAS and SNS. Overall the effects of lop diuretics actually increase SVR (afterload), decrease preload and cause electrolyte imbalances. Ultrafiltration or aquapheresis is an option for pt with fluid volume overload. Done thru dialysis or central venous access.may be appropriate adjuctive therapy for pts with HF and renal failure. Decreasing Venous Return: - Reduces the amount of volume returned to the LV during diastole. - Place pt in high Fowlers, with feet horizontal in bed or dangling at the side (helps decrease venous return because of pooling of blood in the extremities. It also increases thoracic capacity.) - IV NTG= vasodilator. (tx for ADHF) reduces preload, slightly reduces afterload and increases myocardial O2 supply. {monitor BP Q5-10Mins) Decreasing Afterload: Afterload: resistance against which the LV must pump. - SVS is a determinant of afterload - IV sodium nitroprusside (Nipride) is a potent vasodia. That reduces preload and afterload. *drug of choice for ADHF o Complications: Hypotention Thiocyanate toxicity (48Hrs after use) Monitor BP Q5-10Mins - Morphine Sulfate: reduces preload and afterload. o Used in pt with ADHF and pulmonary edema o Dialates both the pulmonary and systemic blood vessels o Reduces anxiety and may assist in reducing dyspnea Nesiritide ( Natrecor) is an IV vasoactive therapy for ADHF. Recombinant form of BPN and cause both venous and arterial dilation. o Main effects: 1. reduction in pulmonary artery wedge pressure (PAWP) and 2. an increase in CO w/o increasing myocardial O2 consumption or the occurrence of dysrhymias. o Adverse Effect: Hypotension (monitor BP)

Improving Gas Exchange:

8 IV morphine sulfate Administration of O2

Improving Cardiac Function: In addition to the above, Inotropic therapy may be warranted, as well as the initiation of hemodynamic monitoring to evaluate effectiveness of interventions. - Digitalis is a positive inotrope that improves LV function. Increases contractility and also increase hearts Oz consumption. Because it requires a loading dose and time to accomplish hemodynamic improvemtns it not recommended for the initial tx of ADHF - Other positive inotropes : adrenergic agonist (used short term), EPI, NE o Potentials problems of long term tx with adrenergic agonist: tolerance, increased ventricular irritability, increased need for O2. Only available by IV. - Inamrinone (Inocor) and milrinone (Primacor) are 2 phosphodiesterase inhibitors that have been called inodialators because they increase myocardial contractility. They increase CO and reduce arterial pressure o Adverse effects: dysrhy, thrombocytopenia, and hepatoxicity Reducing Anxiety: - Use of sedative medications - Continual physical assessment, hemodynamic monitoring, and evaluating the pts response to treatment Collaborative Care: Chronic Heart Failure: - Want to treat underlying cause and contributing factors, maximize CO, provide tx to alleviate symptoms, improve ventricular function, improve quality of life, preserve target organ function, improve mortality and morbidity. - O2 therapy: helps relieve dyspnea and fatigue. - Physical and emotional rest - Cardiac resynchronization therapy (CRT) coordinates R and LV contractility through biventricular pacing. Allows pt to increase their physical activity. (improves quality of life) - if pt has ischemic- induced HF and an EF of <35%, the implementation and use of implantable cardioverter defibrillator (ICD) with CRT may be warranted.

9 Cardiac transplantation Intraaortic Balloon pump (IABP): may be done in the setting of MI or perioperativly during cardiac surgery. Can be used in a hemodynamically unstable pt. Ventricular assist device (VAD): provide long term support for up to 2 years. Used as a bridge to transplantation, effectively increasing cardiac function until donor becomes available.

Drug Therapy: Chronic Heart Failure: General therapeutic objective for drug management include: 1. identification of the type of HF and underlying causes 2. correction of Na and H2O retention and volume overload 3. reduction of cardiac workload 4. improvement of myocardial contractility 5. control of precipitating factors Aim of the treatment is: Improve symptoms Minimize side effects of treatment Decrease morbidity Improve quality of life Prolong survival Diuretics: used to mobilize edematous fluid, reduce pulmonary venous pressure and reduce preload. - Loop diuretics ex. Lasix - Spironolactone (Aldactone): inexpensive, K+ sparing; also addsd benefits to ACE inhibitors Vasodialators: >Goals: - Increasing venous capacity - Improving EF through improved ventricular contraction - Slowing the process of ventricular dysfunction - Decrease heart size - Avoiding $ of neurohormonal responses initiated by compensatory mechanisms of HF - Enhancing neurohormonal blockade. ACE: beneficial at all stages of HF. - first line therapy for pt with chronic HF - used in combination with diuretic therapy - Major Side Effects: hypotention, intractable cough, hyperK+, angioedema, renal insufficiency. Nitrates: cause vasodilation by acting directly on smooth muscle of the vessel wall. - increasing venous capacitance

10 dilating the pulmonary vasculature Improving arterial compliance.

Nesiritide: synthetic form of BPN - When used in conjunction with lifestyle modifications proves to be effective. - Important treatment for pt with ADHF Adrenergic Blockers: Metoprolol - Reccomended that they be used along with other therapies (ex ACE) - Major adverse SE: edema, worsening of HF, hypotention, fatigue, bradycardia Positive Inotropes: directed at improving cardiac contractility to increase CO, decrease LV diastolic pressure, and decrease SVR. Digitalis Glycosides: mainstay treatment for HF o Toxicity: anorexia, N/V, yellow vision o hypoK+, hyperK+ (increase chance of dysrhythmias) o electrolyte imbalances o diseases of the liver or kidney are more at risk for toxicity o Withhold drug if toxic. B- Adrenergic Agonist: primarily used for short term treatment of ADHF and are controversial in the long term use in CHF Calcium Sensitizers: they improve cardiac performance by ineracting directly with contractile proteins without affecting Ca++ concentrations or increasing myocardial O2 demand. Angiotensin II Receptor Blockers: for pt who is unable to tolerate ACE inhibitors bc of angioedema or intractable cough. - Prevents the vasoconstrictor and aldosterone- secreting effects of Angio II. BiDil: used for the treatment of HF in African Americans who are already being treated with standard therapy.

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Nutritional Therapy: Chronic Heart Failure: - Diet education and wt management are critical to the pts control of chronic HF. The nurse or dietitian should obtains a detailed hx of what and when the pt eats along with any sociocultural value of food to the pt. - The edema of chronic HF is often treated by dietary restriction of Na+. Important to teach pts about these foods. - DASH diet is effective as a first line therapy for many individuals with isolated systolic HTN - For pt with mild HF= 2.5 g Na+ - Na+ restricted to 500-1000mg - Pt and family should be instructed how to read labels for Na+ content - Instruct pt to weight themselves daily and the same time and preferable before breakfast wearing the same type of clothing. - If the pt gains 3lbs ober 2 days or 3-5lbs in a week, pt should see prmary care provider. Nursing Management: Chronic Heart Failure: Assessment: subjective and objective data should be collected. Diagnosis: see page 836: Planning: the overall goals include: 1. decrease in symptoms 2. decrease in peripheral edema 3. an increase in exercise tolerance 4. compliance with the medical regimen 5. no complications r/t HF Implementation: - Health Promotion: nutritional therapy is important. o Counsel pts to get vaccines against flu and pneumonia o Education on medications, diet, exercise o Do they need home care? - Acute Intervention: care depends on many important priciples o HF is a progressive disease and treatment plans are established with quality of life goals o Symptom management controlled by the pt with selfmanagements tools. o Salt and water must be restricted o Energy must be conserved o Support systems are essential to the success of the entire treatment plan.

12 Ambulatory or Home Care: HF is a chronic illness for most persons. Important nursing responsibilities: o Teaching the pt about the physiologic changes that have occurred o Assisting the pt to adapt to both the physiologic and psychologic changes o Integrating the pt and the pts family or support system in the overall care plan. o Keep in mind these pts are at high risk for depression and anxiety r/t their illness. Need to encourage thease pts that a normal life is achievable if they are willing to make the adaptation o HF pts are usually required to take meds for the rest of their life. It must be stressed that their disease is chronic and med compliance is essential. o Teach about the medications action, side effects and interactions. Also want to teach them about S/S of toxicity o Teach pt how to take pulse and that it should be taken for a full minute o A pulse lower than 50 beats/min and be a contraindication to taking dig and B-andren blocker o Home BP monitoring should be done esp. if they have HTN o Teach symptoms of hyper and hypoK+ o If on a loop diuretic they will prob supplement K+ o PT,RN,OT can instruct pt on energy conserving and energy efficient behaviors o Grant pt the permission to take a rest.. The hard-driven person may need a prescription for rest so they do not feel lazy o A home health RN is essential in the care of the HF pt and family o Frequent physical assessments, VS, weight are extremely important o The home health RN is paramount to reducing the number of hospital visits, increasing functional capacity, increasing quality of life

Evaluation: see 837 Cardiac Transplantation: treatment of choice for pt with refractory endstage HF, cardiomyopathy, and inoperable CAD. - evaluate pts who will benefit the greatest from the new heart - pt has a complete physical exam and diagnostic workshop - pt and family undergo a comprehensive psychological profile: coping skills, family support systems, motivation to follow

13 rigorous regimen that is essential following transplantation. (teaching guide pg 838) pt is then placed on transplant list matching is based on body and heart size and by ABO type negative lymphocyte crossmatch (ch 14) want to avoid transplantation from cytomegalovirus(CMV)positive donor to a CMV negative recipient pt is prepared for surgery and cardiopulmonary bypass is used special care given to the donor hearts SA node immunosuppressive therapy begins in OR Usually involve azathioprine, corticosteroids and cyclosporine(C & C usually used together). Tacrolimus want to avoid rejection endomyocardial biopsies are typically obtained from the RV on a weekly basis for the first month, monthly the following 6 months, and yearly if no signs of rejection Heartbreath test: measures methylated alkanes. Used the first year following transplant. Greatest use is to recognize less serious vs serious organ damage. In the first year after transplant the major causes of death are acute rejection or infection Post-op, RN needs to continue teaching pt about lifestyle changes, monitoring cardiac function Devices used as a bridge to transplant: VAD, circulatory support system and BVS 5000

Artificial Heart: the lack of available hearts is leading to more hearts being artifical 1. CardioWest Total Artificial heart 2. AbioCor Implantable Replacement heart - An electronic package in the abd monitors the systems: adjusting HR based on activity - Requires no immunosuppression and may hold promise for short term survival in pts with end-stage HF Ongoing Research: the use of embryotic stem cells to replace myocardial cells damaged from heart disease and to establish new blood vessels to supply the regenerated heart muscle is gaining attention. - directed at getting stems cells to become new cardiomyocytes., vascular endothelia cells, smooth muscle cells.

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