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

The vasoconstriction causes an immediate increase in preload. Neurohormonal Response: as the CO falls. low CO.Pt will have extremely poor EF(less than 35%) . . -> RAAS . or hypertrophic cardiomyopathy Commonly seen in older adults esp.Biventricular failure .Pt with ventricular failure of any type has low systemic arterial BP. poor renal perfusion. .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. poor exercise tolerance and ventricular dysrrhythmias . . pulm HTN.DCM condition which poor systolic function is further compromised by dilated LV walls that are unable to relax.Results in increased HR and myocardial contractility.Body’s 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) . women. o Results from pulm HTN and causes reduced R ventricular emptying.Activation results in increased release of catecholamine . resulting in low left ventricular filling pressure and reduced CO Mixed Systolic and Diastolic Failure: seen in dialated cardiomyopathy (DCM) .High pulmonary pressures . An increase in venous return to a heart which is already volume overloaded. bld flow to the kidneys decreases. (see pg 823 for gender differences) Less common is isolated right ventricular diastolic failure. and peripheral vasoconstriction. worsens ventricular performance.Kidneys respond but releasing rennin. aortic stenosis. as a result of myocardial fibrosis and HTN. ventricular hypertrophy and normal EF Usually result of LV hypertrophy from chronic systemic HTN.

Risk for ischemia and ventricular dysfunction.The degree of stretch is directly r/t Frank-Sterlings law. these factors result in an increase in cardiac workload.Naturetic peptides are endothelin and aldosterone antagonist and enhance diuresis by increasing GFR and blocking affects of RAAS . 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. and myocyte death Together. Eventually leads to an increased ventricular mass. and angiotensin II. increase in muscle mass and cardiac wall thickness in response to overwork and strain. .Will lead to an increase in CO and maintenance of tissue perfusion. catecholamines. and impaired contractility. changes in ventricular shape.When pressure in the heart chambers (usually the LV) is elevated overtime. abnormally shaped contractile cells. . and ventricular remodeling. contractile dysfun. Remodeling involves hypertrophy of cardiac myocytes.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. Endothelin results in further arterial vasoconstriction and in an increase in cardiac contractility and hypertrophy Locally.Generally follows persistent or chronic dilation and thus further increases the contractile power. Hypertrophy: in CHF. Ventricles because less effective although larger Dilation: enlargement of the chambers of the heart . . . Counterregulatory Mechanisms: . myocardial dysfunction. resulting in large.

. vascular congestion of the GI. splenomegaly.Lungs become less compliant and increased resistance in the small airways. . Right-Sided Failure: . APN is primarily triggered by an increase in volume BPN is primarily increased by increased pressure.Early on it is associated with increased RR and a decrease in PaO2 . Mechanisms succeed in maintaining adequate CO that is needed for tissue perfusion. .The most common cause of PE is acute Left ventricular failure. . Types of Heart Failure: Usually manifested by biventricular failure. Cardiac Decomposition: occurs when these mechanisms can no longer maintain adequate CO and inadequate tissue perfusion results.An increase in the pulmonary venous pressure caused by a decreased efficiency of the LV. . NO also works to relax the arterial smooth muscle.Increased pulmonary pressure leads to pulmonary congestion and edema.Cor pulmonale can also cause Clinical Manifestations of Acute Decompensate Heart Failure (ADHF): *typically manifests as Pulmonary Edema. .*the primary cause of RHF is LHF .4 Inhibit the development of cardiac hypertrophy and may have anti-inflammatory effects. .Alveolar edema develops when fluid with RBCs moves into the alveoli . resulting in vasodia. and increased afterload. 2ndary to CAD.When the lymphatic drain.Results from LV dysf. > tachypnea develops. will see interstitial edema. peripheral edema. . Left Sided Failure: *most common form of HF . hepatomegaly.Causes a back up of blood into the RA and venous circulation. although one ventricle may precede the other in dysfunction.Venous congestion leads to jugular vein distention. Cardiac Compensation occurs when compen.

Dysrhythmias: r/t the enlargements of the chambers of the heart. damp to touch. renal disease. Dyspnea (SOB) is common. a RR >30bpm. 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.Left Ventricular Thrombus: with ADHF or CHF. pale and possibly cyanotic. Cold clammy skin from vasoconstriction The pt has severe dyspnea AEB the use of accessory muscles of respiration. cough with blood tinged sputum. . the skin may appear dusky. anemia. Anemia can result from malnutrition. swollen Behavioral Changes: r/t impaired cerebral circulation. 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. wheezes. Caused by decrease in CO. or from poor gas exchange. Tachycardia: early clinical sign.5 Airways can become flooded with fluid and will see worsening of ABGs S/S: anxious. Chest pain Weight changes: eating habits and edema - - Complications of Heart Failure: . Crackles. the enlarged LV and decreased CO combine to increase the chance of thrombus formation. or drug therapy. . Pts who take a β blockers may not show increased HR Edema Nocturia Skin Changes: bc tissue capillary O2 extraction is increased.Pleural Effusion: from increasing pressure in the pleural capillaries . Cool. decreased oxygenation of the tissues. impaired perfusion to vital organs. May be wheezing. orthpnea. o Pts with HF and EF less than 35% have a high chance of suffering from fatal dysrhythmias.

ADHERE indicate that pt receiving early tx with IV diuretic and vasoactive drugs will have better and shorter stays in the hospital.ADHERE is currently reconsidering tx approach . improving gas exchange and oxygenation. Nursing and Collaboritive Management: ADHF and Pulmonary Edema: Tx of ADHF is very complex and important.6 o Once thrombus has formed. decreasing venous return(preload). See chart on 826. preserving target organ function.Treatment strategies should include: o Improving LV function by decreasing intravascular volume. o Also places pt at risk for a stroke. cardiac enzymes. BNP levels.Cardiac cath.nuclear imaging . Renal Failure: r/t decreased CO - Classification of HF: the New York Heart Association has produced guidelines.hemodynamic monitoring .Diuretics work to decrease the preload and improving the pts S/S . controlling HR and rhythm. decreases pulmonary vascular pressures. ultrafiltration . liver function test .Hx and Physical exam . reducing anxiety. . decreasing progression of the disease. The use of diuretics. Hepatomegaly: *especially in pt with Right sided HF Leads to impaired liver function. improves gas exchange. decreasing afterload.CXR . Decreasing Intravascular Volume: The use of diuretics to decrease venous return. decrease CO. increasing CO.echocardiography .exercise stress testing . and further worsens pts perfusion. vasoactive drugs. This increases left ventricular function. .Serum chemistries. Diagnostic Studies: .12 lead ECG . it may also decrease left ventricular contractility.

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

Inamrinone (Inocor) and milrinone (Primacor) are 2 phosphodiesterase inhibitors that have been called inodialators because they increase myocardial contractility. . maximize CO.Want to treat underlying cause and contributing factors. thrombocytopenia. .Cardiac resynchronization therapy (CRT) coordinates R and LV contractility through biventricular pacing.Digitalis is a positive inotrope that improves LV function.if pt has ischemic. Because it requires a loading dose and time to accomplish hemodynamic improvemtns it not recommended for the initial tx of ADHF . improve mortality and morbidity. . EPI. as well as the initiation of hemodynamic monitoring to evaluate effectiveness of interventions.Physical and emotional rest . (improves quality of life) . Allows pt to increase their physical activity. hemodynamic monitoring. and hepatoxicity Reducing Anxiety: .Use of sedative medications . Inotropic therapy may be warranted.Other positive inotropes : β adrenergic agonist (used short term). increased need for O2. . and evaluating the pts response to treatment Collaborative Care: Chronic Heart Failure: .8 IV morphine sulfate Administration of O2 Improving Cardiac Function: In addition to the above. preserve target organ function.Continual physical assessment. increased ventricular irritability. Only available by IV. provide tx to alleviate symptoms. . improve quality of life.O2 therapy: helps relieve dyspnea and fatigue. the implementation and use of implantable cardioverter defibrillator (ICD) with CRT may be warranted. They increase CO and reduce arterial pressure o Adverse effects: dysrhy. improve ventricular function. Increases contractility and also increase hearts Oz consumption.induced HF and an EF of <35%. NE o Potentials problems of long term tx with β adrenergic agonist: tolerance.

Loop diuretics ex. Nitrates: cause vasodilation by acting directly on smooth muscle of the vessel wall.Increasing venous capacity .Avoiding $ of neurohormonal responses initiated by compensatory mechanisms of HF . ACE: beneficial at all stages of HF. hyperK+. . Drug Therapy: Chronic Heart Failure: General therapeutic objective for drug management include: 1.Enhancing neurohormonal blockade. renal insufficiency. . K+ sparing. also addsd benefits to ACE inhibitors Vasodialators: >Goals: . identification of the type of HF and underlying causes 2. reduction of cardiac workload 4. angioedema.used in combination with diuretic therapy . intractable cough.Improving EF through improved ventricular contraction . Can be used in a hemodynamically unstable pt.Decrease heart size .Slowing the process of ventricular dysfunction . Ventricular assist device (VAD): provide long term support for up to 2 years. reduce pulmonary venous pressure and reduce preload.increasing venous capacitance .Spironolactone (Aldactone): inexpensive.Major Side Effects: hypotention. improvement of myocardial contractility 5. .9 Cardiac transplantation Intraaortic Balloon pump (IABP): may be done in the setting of MI or perioperativly during cardiac surgery. correction of Na and H2O retention and volume overload 3. Lasix .first line therapy for pt with chronic HF . effectively increasing cardiac function until donor becomes available. 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. Used as a bridge to transplantation.

.When used in conjunction with lifestyle modifications proves to be effective. and decrease SVR. .10 dilating the pulmonary vasculature Improving arterial compliance.  Digitalis Glycosides: mainstay treatment for HF o Toxicity: anorexia.Prevents the vasoconstrictor and aldosterone.Reccomended that they be used along with other therapies (ex ACE) . 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. Angiotensin II Receptor Blockers: for pt who is unable to tolerate ACE inhibitors bc of angioedema or intractable cough.secreting effects of Angio II. bradycardia Positive Inotropes: directed at improving cardiac contractility to increase CO. BiDil: used for the treatment of HF in African Americans who are already being treated with standard therapy. worsening of HF. fatigue. . Nesiritide: synthetic form of BPN .Major adverse SE: edema. decrease LV diastolic pressure. “yellow vision” o hypoK+. N/V. hypotention.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. B.Important treatment for pt with ADHF β Adrenergic Blockers: Metoprolol .

Na+ restricted to 500-1000mg . .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. .Instruct pt to weight themselves daily and the same time and preferable before breakfast wearing the same type of clothing. decrease in symptoms 2. . Nursing Management: Chronic Heart Failure: Assessment: subjective and objective data should be collected. Important to teach pts about these foods.Diet education and wt management are critical to the pts control of chronic HF.11 Nutritional Therapy: Chronic Heart Failure: . an increase in exercise tolerance 4.The edema of chronic HF is often treated by dietary restriction of Na+.For pt with mild HF= 2. no complications r/t HF Implementation: . o Counsel pts to get vaccines against flu and pneumonia o Education on medications.DASH diet is effective as a first line therapy for many individuals with isolated systolic HTN . decrease in peripheral edema 3. . 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.Pt and family should be instructed how to read labels for Na+ content . exercise o Do they need home care? . diet.5 g Na+ .If the pt gains 3lbs ober 2 days or 3-5lbs in a week. 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. Diagnosis: see page 836: Planning: the overall goals include: 1. compliance with the medical regimen 5. pt should see prmary care provider.Health Promotion: nutritional therapy is important.

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. increasing quality of life Evaluation: see 837 Cardiac Transplantation: treatment of choice for pt with refractory endstage HF. 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.pt and family undergo a comprehensive psychological profile: coping skills. 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. . and inoperable CAD. 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.12 Ambulatory or Home Care: HF is a chronic illness for most persons. motivation to follow . It must be stressed that their disease is chronic and med compliance is essential.evaluate pts who will benefit the greatest from the new heart . o Teach about the medications action.pt has a complete physical exam and diagnostic workshop . family support systems. cardiomyopathy.. VS.OT can instruct pt on energy conserving and energy efficient behaviors o Grant pt the “permission” to take a rest. 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. side effects and interactions. increasing functional capacity. weight are extremely important o The home health RN is paramount to reducing the number of hospital visits. o Keep in mind these pts are at high risk for depression and anxiety r/t their illness.

smooth muscle cells. vascular endothelia cells. Used the first year following transplant.. corticosteroids and cyclosporine(C & C usually used together). circulatory support system and BVS 5000 - Artificial Heart: the lack of available hearts is leading to more hearts being artifical 1. .directed at getting stems cells to become new cardiomyocytes. CardioWest Total Artificial heart 2. (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. RN needs to continue teaching pt about lifestyle changes. Greatest use is to recognize less serious vs serious organ damage. .An electronic package in the abd monitors the systems: adjusting HR based on activity . In the first year after transplant the major causes of death are acute rejection or infection Post-op. Tacrolimus want to avoid rejection endomyocardial biopsies are typically obtained from the RV on a weekly basis for the first month. monitoring cardiac function Devices used as a bridge to transplant: VAD. AbioCor Implantable Replacement heart . and yearly if no signs of rejection Heartbreath test: measures methylated alkanes. monthly the following 6 months.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.13 rigorous regimen that is essential following transplantation.

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