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Transcript
HEART FAILURE by Nancy Jenkins The most common reason for hospitalization in adults >65 years old. 1 in 100 adults has HF heart failure Heart Failure- Clinical syndrome that can result from any structural or functional cardiac disorder that impairs ability of ventricle to fill with or eject blood 5 million Americans have heart failure •500,000 new cases every year • 25-50 billion dollars a year to care for people with Heart Failure •6,500,000 hospital days / year •300,000 deaths/year Heart Failure Mild Mild Cardiogenic shock Cardiomyopathy Uncompensated Heart Failure Pulmonary Edema-ADHF Severe End Stage Irreversible Control With Drugs Diet Fluid Restriction /Same as Mild with Morphine Sulfate Needs new ventricle VAD IABP Heart Transplant Heart Failure Pneumonic U Upright Position N Nitrates L Lasix O Oxygen A Amiodorone, ACE, ARBs D Dig, Dobutamine M Morphine Sulfate E Extremities Up or Down Definition Of Heart Failure • CO=SVxHR is insufficient to meet the metabolic needs of the body • SV is determined by preload, afterload and myocardial contractility • Systolic failure- dec. contractility • Diastolic failure- dec. filling • EF< 40% Heart Failure- Types Systolic versus Diastolic • Systolic failure is the most common cause –”poor pump” – **Hallmark finding: Decrease in the left ventricular ejection fraction (EF) < 40% • Caused by – Impaired contractility (e.g., MI) – Increased afterload (e.g., hypertension) – Cardiomyopathy – Mechanical abnormalities (e.g., valve disease) http://coursewareobjects.elsevier.com/objects/mccance5e_v1/McCance/Module15/Part02/M15L04S41a.html??hostType=undefined& authorName=Mccance&prodType=undefined hypokinesis EF- the % of total ventricular filling volume that is ejected during systole. EF- 55-65 normal Heart Failure Diastolic • Diastolic failure-”poor filling” stiff ventricles – 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, normal ejection fraction (EF) diastolic failure Heart Failure • 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) Your patient has a normal EF but shows signs of heart failure. Your patient most likely has: 1. Decreased cardiac output 2. Systolic failure 3. Diastolic failure 4. LV hypertrophy How the Body Responds: • Remember, a decrease in stroke volume leads to a decrease in cardiac output. • Body attempts to increase cardiac output: 1. 2. 3. 4. 5. Sympathetic Nervous System Neurohormonal Response Dilation of chambers of the heart Hypertrophy Natriuretic peptides The Body’s Response: Sympathetic Nervous System: – Release of catecholamines • (epinephrine and norepinephrine) – Causes increased heart rate & increased contractility – What does this do to the workload on heart? – What does this do to O2 need of the heart? – What meds could we give to decrease this release? The Body Responds (Cont’d): Neurohormonal Response: – As CO decreases, blood flow to kidneys __________: • Causes activation of (RAAS) • RAAS causes _____ & _______ retention, peripheral vasoconstriction, increased BP – Low CO decreases cerebral perfusion pressure: • Posterior pituitary secretes more antidiuretic hormone (ADH) • ADH causes more retention of _______ & production of endothelin. • Endothelin causes arterial vasocontriction & increased contractility of heart muscle The Body Responds (Cont’d): Neurohormal Response (Cont’d): – Due to various types of cardiac injury (ie. MI), proinflammatory cytokines are released. • Cause cardiac hypertrophy, pumping dysfunction, and death of cells in the heart muscle • Over time, this process can lead to a systemic inflammatory response that further damages the heart The Body Responds (Cont’d): Hypertrophy: – Increase in ___________ of heart – Increases contractility at first – However, hypertrophic muscle doesn’t work as well, needs more _________, greater risk for rhythm problems, and has poor circulation The Body Responds (Cont’d): Dilation: – Chambers of the heart get larger – Increase in stretch of muscle fibers due to increase in blood volume – The greater the stretch, the greater the force of contraction (_____________ Law) – Initially, causes increase in cardiac output. After time, muscle fibers are overstretched and contraction decreases .CHF The Body Responds • Counter regulatory processes- these help protect the heart – Natriuretic peptides: atrial natriuretic peptide (ANP) released with cardiac muscle stretch and b-type natriuretic peptide (BNP) released with increased pressure of LV • Released in response to increases in atrial volume and ventricular pressure • Act opposite of RAAS and block effect • Promote venous and arterial vasodilation, reducing preload and afterload • Increase GFR • Prolonged HF leads to a depletion of these factorsNatrecor can be used for same effects Which of the following are compensatory mechanisms for HF? 1. 2. 3. 4. Tachycardia Hypotension RAAS LV hypertrophy Pathophysiology Structural Changes • • • • Decreased contractility Increased preload (volume) Increased afterload (resistance) Ventricular remodeling(ACE inhibitors can prevent this) – Ventricular hypertrophy – Ventricular dilation END RESULT FLUID OVERLOAD AND EDEMA Heart Failure Classification Systems • New York Heart Association Functional Classification of HF – Classes I to IV • ACC/AHA Stages of HF – Stages A to D NYHA Classificationbased on activity Class Patient Symptoms Class I (Mild) No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, or dyspnea (shortness of breath). Class II (Mild) Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in fatigue, palpitation, or dyspnea. Class III (Moderate) Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes fatigue, palpitation, or dyspnea. Class IV (Severe) Unable to carry out any physical activity without discomfort. Symptoms of cardiac insufficiency at rest. If any physical activity is undertaken, discomfort is increased. Stage A Stage B Stage C Those at high risk for developing heart failure. Includes people with: •Hypertension •Diabetes mellitus •Coronary artery disease (including heart attack) •History of cardiotoxic drug therapy •History of alcohol abuse •History of rheumatic fever •Family history of CMP Those diagnosed with “systolic” heart failure but have never had symptoms of heart failure (usually by finding an ejection fraction of less than 40% on echocardiogram). Patients with known heart failure with current or prior symptoms. Symptoms include: •Shortness of breath •Fatigue •Reduced exercise intolerance. •Exercise regularly •Quit smoking •Treat hypertension •Treat lipid disorders •Discourage alcohol or illicit drug use •If previous heart attack or current diabetes mellitus or hypertension angiotensin converting enzyme inhibitor (ACE-I) •Care measures in Stage A + •All patients should be on ACE-I •Beta-blockers should be added •Surgical consultation for coronary artery revascularization and valve repair/replacement (as appropriate) In this group, care measures from Stage A apply, ACE-I and beta-blockers should be used + •Diuretics (water pills) •Digoxin •Dietary sodium (salt) restriction •Weight monitoring •Fluid restriction (as appropriate) •Withdrawal of drugs that worsen the condition •Spironolactone when symptoms remain severe with other therapies AHA Newer Heart FailureStaging A-D Stage D Presence of advanced symptoms, after assuring optimized medical care All therapies under Stages A, B and C + evaluation for: •Cardiac transplantation •Ventricular assist devices •Surgical options •Research therapies •Continuous intravenous inotropic infusions •End-of-life care Heart Failure Risk Factors • Primary risk factors – Coronary artery disease (CAD) (MI) – Advancing age • Contributing risk factors – – – – – – – – Hypertension Diabetes Tobacco use Obesity High serum cholesterol African American descent Valvular heart disease Hypervolemia Which of the following are risk factors for Heart Failure 1. Hypertension 2. Myocardial Infarction 3. Diabetes 4. Valvular Disease Classifications • Systolic versus diastolic – Systolic- loss of contractility get dec. CO – Diastolic- decreased filling or preload • Left-sided versus right –sided – Left- lungs – Right-peripheral • High output- hypermetabolic state- pregnancy • Acute versus chronic – Acute- MI – Chronic-cardiomyopathy Symptoms Left Ventricular Failure • Signs and symptoms – – – – – dyspnea orthopnea PND fatigue Anxiety rales – NOTE L FOR LEFT AND L FOR LUNGS Which of the following is associated with left sided failure? 1. 2. 3. 4. crackles hypoxemia tachypnea Peripheral edema ??????? • WHY DOES THIS OCCUR? ADHF-Clinical Manifestations • Acute decompensated heart failure (ADHF) • When PA WEDGE pressure is approx 30mmHg Physical findings (like ARDS) pulmonary edema • • • • • • • Orthopnea, dyspnea, tachypnea Crackles, wheezes, rhonchi Use of accessory muscles Cool and clammy skin Hypoxemia, Cyanosis 4.s3 gallop The Auscultation Assistant - Rubs and Gallops *Cough with frothy, blood-tinged sputum-why??? (later sign) Person literally drowning in secretions Immediate Action Needed Goals of Treatment for ADHF • MAD DOG • Improve gas exchange (much like ARDS) – – – – O2 intubate elevate HOB BIPAP Right Heart Failure • Signs and Symptoms – fatigue, weakness, lethargy – wt. gain, inc. abd. girth, anorexia,RUQ pain – elevated neck veins – Hepatomegaly +HJR – may not see signs of LVF- why?? Can Have RVF Without LVF • What is this called and what causes it? Cor Pulmonale “Blue Bloater” This results from pulmonary hypertension. How does this affect afterload? Heart Failure- Complications • Pleural effusion • Dysrhythmias-Atrial fibrillation (most common dysrhythmia) – **High risk of fatal dysrhythmias (e.g., sudden cardiac death, ventricular tachycardia) with HF and an EF <35% (Use of ICDs and CRT) – Loss of the atrial contraction (kick) can reduce CO by 20% – Promotes thrombus/embolus formation increasing risk for stroke Heart Failure- Complications Cont. • Hepatomegaly – Fibrosis and cirrhosis can develop over time – can store 10 L • Renal insufficiency or failure • Cardiogenic shock • Why and what would you monitor? Heart Failure Diagnostic Studies • Primary goal is to determine underlying cause – – – – History and physical examination( dyspnea) Chest x-ray 12 lead ECG Lab studies (e.g., cardiac enzymes, BNP) electrolytes, CBC, liver function tests, PT/INR – EF Heart Failure Diagnostic Studies – Hemodynamic assessment-Hemodynamic Monitoring-CVP- (right side) and SG(left and right side) – Echocardiogram-TEE best (EF) also have TTE – Stress testing- exercise or medicine – Cardiac catheterization- determine heart pressures ( inc.PAW ) Nursing Assessment • • • • • • • Vital signs PA readings Urine output --------------------------------------------------------------- Nursing Diagnosis – Activity intolerance – Decreased cardiac output – Fluid volume excess – Impaired gas exchange – Anxiety – Deficient knowledge Decreased cardiac output • • • • Plan frequent rest periods Monitor VS and O2 sat at rest and during activity Take apical pulse Review lab results and hemodynamic monitoring results • Fluid restriction- keep accurate I and O • Elevate legs when sitting • Teach relaxation and ROM exercises Activity Intolerance • • • • • • Provide O2 as needed practice deep breathing exercises teach energy saving techniques prevent interruptions at night monitor progression of activity offer 4-6 meals a day Fluid Volume Excess • • • • • • • Give diuretics and provide BSC Teach side effects of meds Teach fluid restriction Teach low sodium diet Monitor I and O and daily weights Position in semi or high fowlers Listen to BS frequently Knowledge deficit • • • • • Low Na diet Fluid restriction Daily weight When to call Dr. Medications 3 Main Goals- in acute as well as chronic HF • Decrease preload • Decrease afterload • Increase contractility How to Achieve Goals • Decrease preload by : – Dec. intravascular volume-diuretics, natrecor – Dec venous return • Fowlers • MSO4 and Ntg • Decrease afterload– – – – – ACE (pril or ril), ARB (sartans), Vasodilators, beta blockers (al or ol) BiDil (combination drug containing isosorbide dinitrate and hydralazine) approved only for the treatment of HF in African Americans Increase Contractility • 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, dobutamine) – Phosphodiesterase inhibitors (e.g., milrinone) – Question use of calcium channel blockers – New calcium sensitizer-(levosimendan) – CRT Other • Balance supply and demand of oxygen – Inc. O2- O2, intubate, HOB up,Legs down, mech vent with PEEP – Dec. demand-beta blockers, rest, dec B/P Manage symptoms Collaborative Care: • • • • • • • • • • Treat underlying cause (if possible) Oxygen therapy PRN Cardiac rehab Daily weights Drug therapy education Sodium restriction Strict Input/ output Symptom education Home health Specialty clinics Heart Failure- Chronic • Overall long term 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 PATIENT TEACHING Joint Commission has mandated 6 areas of discharge teaching Discharge Teaching 6 areas • • • • • • Weight Monitoring Medications Activity Diet What to do if symptoms worsen Follow-up Weight Monitoring • Weight reduction recommendations must be individualized and culturally sensitive • Same scale every day at same time • Preferably in the morning after voiding • Report weight gain of 3 or more pounds in two days or 3-5 or more in 1 week. Activity • Instruct patient in energy-conserving and energyefficient behaviors • Improves symptoms but often not prescribed • Cardiac Rehab program • Goal is 150 minutes per week • Walking, biking, swimming or a combo is recommended • Nutritional therapy Diet – Diet and weight reduction recommendations must be individualized and culturally sensitive – Dietary Approaches to Stop Hypertension (DASH) diet is recommended • Avoid fats such as butter and margarine • Avoid fried foods • Read labels for hidden sodium – Sodium is usually restricted to 2.5 g per day • Avoid any food with more than 400mg of sodium – Alcohol- limit women 1 drink, men 2 drinks – Fluid restriction may or may not be required Medications – Medications (lifelong) diuretics, vasodilators, positive inotropics • Diuretics- loop, thiazides, spirinolactone (aldactone) • Vasodilators- Ntg, • Postive inotropics- digoxin – Taking pulse rate • Know when drugs (e.g., digitalis, -adrenergic blockers) should be withheld and reported to health care provider • Home BP monitoring – Signs of hypo- and hyperkalemia if taking diuretics that deplete or spare potassium Drug Therapy: Diuretics: – PO or IV, loop - _____________ – PO, potassium sparing - _____________ – When extra diuresis necessary – Metolazone (Zaroxolyn) or Bumex – reduce preload • Ace-Inhibitors: – – – – – – Name some: ______________ first line therapy in chronic HF block conversion of angiotensin I to angiotensin II, decrease aldosterone decrease afterload increase cardiac output Drug Therapy (Cont’d): Vasodilators: – Nitrates • Name some: _____________ • directly dilate vessels, decrease preload, vasodilate coronary arteries. – Nitroprusside (Nipride)- reduces preload and afterload – Nesiritide (Natrecor)- arterial and venous dilation B- Blockers: – Name some:__________________ • Block negative effects of SNS system (such as HR) • Can reduce myocardial contractility • Improve patient survival Drug Therapy (Cont’d): Positive Inotropes: – Increase contractility – Digoxin- increases contractility, decreases HR – Monitor which electrolyte? – Reduces symptoms, but not shown to prolong life – Dopamine Dobutamine Milrinone (Primacor) Angiotensin II Receptor Blockers (ARBs): – Name some: ______________ – Mostly for patients unable to tolerate ACE Inhibitors – Similar effects to Ace Inhibitors Isosorbide dinitrate and hydralazine (BiDil): – for African Americans with HF When to call Dr. • Symptoms worsen – – – – – Shortness of breath Edema Weight gain Side effects of medications Chest pain 4 Core Measures for Heart Failure • Discharge instructions- weight, activity, medications, follow up and when to call dr. • LV function is documented (EF) • If EF less than 40% on ACE or ARB • Smoking Cessation Follow-up • Frequent follow-up with physician • Heart Failure Clinics • Home health care may be needed – Monitor symptoms – Effects of medications and side effects – Blood draws for potassium • Other – Stop smoking – Flu and pneumonia vaccines – Refer to local support group Chronic HF- Devices to increase CO • Ways to achieve goals: (inc. CO) – CRT – Intraaortic balloon pump (IABP) therapy – Ventricular assist devices (VADs) • Destination therapy—permanent, implantable VAD Artificial Heart Cardiomyoplasty-wrap latissimus dorsi around heart Ventricular reduction surgery-ventricular wall is resected CRT-Cardiac Resynchronization Therapy 1.Utilizes biventricular pacing 2.Coordinates right and left ventricle contractility 3.Normal electrical conduction increases CO 4.For patients with Class III and IV HF Patients with HF caused by ischemia and EF <35% may need implantable cardiac defibrillator (ICD) as well due to risk of dysrhythmias Intraaortic Balloon Pump (IABP) • Provides temporary circulatory assistance Used for cardiac shock – –Allows heart to rest – ↓ Afterload – Augments aortic diastolic pressure • Outcomes – Improved coronary blood flow – Improved perfusion of vital organs YouTube - IABP Intraaortic Ballon Pump Ventricular Assist Devices (VADs) • Indications for VAD therapy – Patients with New York Heart Association Classification IV who have failed medical therapy – Bridge to transplant – Destination therapy Ventricular Assist Devices (VAD): • Circulatory device that provides cardiac output in addition to that of native heart • Usually takes blood from left ventricle then pumps to the aorta • Many different types, primarily Heartmate II and PVAD https://www.youtube.com/watch?v=alTp5_p-dmA • Heartmate II much easier to transport, continous flow to put blood out to body • VAD Patient Video • Heartmate II Thoratec Video (2 min 45 sec) Heart Transplantation • • • • First performed in 1967 Over 2000 each year in US Long wait time, not enough hearts From harvest to transplantation there is a 46 hour maximum time limit Who receives a heart? • Absolute indications – – – – Cardiogenic shock On IV inotropes (dobutamine) Severe cardiac ischemia –not treatable Life threatening dysrhythmias- VT Cardiac Transplantation Nursing Management • Treatment of choice for patients with refractory end-stage HF, inoperable CAD and cardiomyopathy • 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 – The overall waiting period for a transplant is long, and many patients die while waiting for a transplant – Goal of the transplant evaluation process is to identify patients who would most benefit from a new heart Cardiac Transplantation • 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 • Donor sinoatrial (SA) node is preserved so that a sinus rhythm may be achieved postoperatively • Immunosuppressive therapy usually begins in the operating room • Infection is the primary complication followed by acute rejection in the first year after transplantation • Beyond the first year, malignancy (especially lymphoma) and coronary artery vasculopathy are major causes of death • One year survival rate is 85-90% • 3 year survival rate is 79% Cardiac Transplantation • 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. Endomyocardial Biopsy Video • Peripheral blood T lymphocyte monitoring to assess the recipient’s immune status • Care focuses on – – – – Promoting patient adaptation to the transplant process Monitoring cardiac function Managing lifestyle changes Providing relevant teaching Blackboard Learning System™ (Release 6) CHF case 4 Congestive Heart Failure: Overview Practice Game http://www.quia.com/cb/107511.html Angiotensin-converting enzyme inhibitors , such as captopril and enalapril, block the conversion of angiotensin I to angiotensin II, a vasoconstrictor that can raise BP. These drugs alleviate heart failure symptoms by causing vasodilation and decreasing myocardial workload. Beta-adrenergic blockers , such as bisoprolol, metoprolol, and carvedilol, reduce heart rate, peripheral vasoconstriction, and myocardial ischemia. Diuretics prompt the kidneys to excrete sodium, chloride, and water, reducing fluid volume. Loop diuretics such as furosemide, bumetanide, and torsemide are the preferred first-line diuretics because of their efficacy in patients with and without renal impairment. Low-dose spironolactone may be added to a patient's regimen if he has recent or recurrent symptoms at rest despite therapy with ACE inhibitors, betablockers, digoxin, and diuretics. Digoxin increases the heart's ability to contract and improves heart failure symptoms and exercise tolerance in patients with mild to moderate heart failure. Other drug options include nesiritide (Natrecor), a preparation of human BNP that mimics the action of endogenous BNP, causing diuresis and vasodilation, reducing BP, and improving cardiac output. Intravenous (I.V.) positive inotropes such as dobutamine, dopamine, and milrinone, as well as vasodilators such as nitroglycerin or nitroprusside, are used for patients who continue to have heart failure symptoms despite oral medications. Although these drugs act in different ways, all are given to try to improve cardiac function and promote diuresis and clinical stability.