HEART FAILUREby Nancy Jenkins

The most common reason for hospitalization in adults >65 years old.

Heart Failure Click here!

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 Failure6,500,000 hospital days / year300,000 deaths/year

MildMildDrugsDiet Fluid RestrictionHeart FailureUncompensated Heart FailurePulmonary EdemaSevere End Stage

Cardiogenic shockCardiomyopathy

Irreversible

Needs new ventricle

VADIABP

VADIABPHeart TransplantControl With/Same as Mild with Morphine Sulfate

Heart Failure PneumonicUUpright PositionNNitratesLLasixOOxygenAAmiodorone, ACE, ARBsDDig, DobutamineMMorphine SulfateEExtremities Up or Down

DefinitionCO=SVxHR is insufficient to meet the metabolic needs of the bodySV is determined by preload, afterload and myocardial contractilitySystolic failure- dec. contractilityDiastolic failure- dec. fillingEF< 40%

Heart Failure Etiology and PathophysiologySystolic failure is the most common cause Hallmark finding: Decrease in the left ventricular ejection fraction (EF)Caused byImpaired contractile function (e.g., MI)Increased afterload (e.g., hypertension)CardiomyopathyMechanical abnormalities (e.g., valve disease)

Systolic Failurehypokinesis

90/140= 64% EF- 55-65 normal

Heart Failure Etiology and PathophysiologyDiastolic failureImpaired ability of the ventricles to relax and fill during diastole resulting in decreased stroke volume and CODiagnosis based on the presence of pulmonary congestion, pulmonary hypertension, ventricular hypertrophy, normal ejection fraction (EF)

Heart Failure Etiology and PathophysiologyDiastolic failureCaused by Left ventricular hypertrophy from chronic hypertensionAortic stenosisHypertrophic cardiomyopathyIsolated right ventricular diastolic failure from pulmonary hypertension

Heart Failure Etiology and PathophysiologyMixed systolic and diastolic failureSeen in disease states such as dilated cardiomyopathy (DCM)Poor EFs (

PreloadVolume of blood in ventricles at end diastole.Depends on venous returnDepends on compliance

Afterload

Force needed to eject the blood into the circulationArterial B/P, pulmonary artery pressureValvular disease increases afterload

CHFPathophysiologyA. Cardiac compensatory mechanisms1.tachycardia2.ventricular dilation-Starlings law3.myocardial hypertrophyHypoxia leads to dec. contractility http://www.heartsite.CHF/html/chf_3.html

cont.B.Homeostatic compensatory mechanismsSympathetic Nervous System-(beta blockers block this)1.vascular system- norepinephrine- vasoconstriction(What effect on afterload?)2.kidneys-A. dec. CO and B/P cause renin angiotensin release.(ACE)B. Aldosterone release causes Na and H2O retentionInc. Na causes release of ADH(diuretics)Release of atrial natriuretic factor- promotes Na and H20 excretion and prevents severe cardiac decompensation3.liver- stores venous volume(ascites, +HJR,Hepatamegaly- can store 10 L. check enzymes

Heart Failure Etiology and PathophysiologyCompensatory mechanisms are activated to maintain adequate CONeurohormonal responses: Endothelin is stimulated by ADH, catecholamines, and angiotensin II and causesArterial vasoconstrictionIncrease in cardiac contractilityHypertrophy

Heart Failure Etiology and PathophysiologyCompensatory mechanisms are activated to maintain adequate CONeurohormonal responses: 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 myocyte cell death

Heart Failure Etiology and PathophysiologyCompensatory mechanisms are activated to maintain adequate CONeurohormonal responses: Over time, a systemic inflammatory response is mounted resulting inCardiac wastingMuscle myopathyFatigue

Heart Failure Etiology and PathophysiologyCounter regulatory processesNatriuretic peptides: atrial natriuretic peptide (ANP) and b-type natriuretic peptide (BNP)Released in response to increases in atrial volume and ventricular pressurePromote venous and arterial vasodilation, reducing preload and afterload Prolonged HF leads to a depletion of these factors

Heart Failure Etiology and PathophysiologyCounter regulatory processesNatriuretic 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

Result of Compensatory MechanismsHeart Failure

PathophysiologyStructural ChangesDecreased contractilityIncreased preload (volume)Increased afterload (resistance)Ventricular remodeling(ACE inhibitors can prevent this)Ventricular hypertrophyVentricular dilation

Heart Failure- Hypertrophy

Ventricular remodeling

END RESULTFLUID OVERLOAD AND EDEMA

Heart FailureClassification Systems New York Heart Association Functional Classification of HFClasses I to IVACC/AHA Stages of HFStages A to D

AHA Newer Classifications of Heart Failure- Staging

Cleveland Clinic Foundation Health Information Center, revised 4/02

Heart Failure Etiology and PathophysiologyPrimary risk factorsCoronary artery disease (CAD)Advancing ageContributing risk factors HypertensionDiabetesTobacco useObesityHigh serum cholesterolAfrican American descentValvular heart diseaseHypervolemia

ClassificationsSystolic versus diastolicSystolic- loss of contractility get dec. CODiastolic- decreased filling or preloadLeft-sided versus right sidedLeft- lungsRight-peripheralHigh output- hypermetabolic stateAcute versus chronicAcute- MIChronic-cardiomyopathy

Symptoms

Left Ventricular FailureSigns and symptomsdyspneaorthopnea PNDCheyne Stokesfatigue Anxietyrales

NOTE L FOR LEFT AND L FOR LUNGS

Left-sided Heart FailureFig. 35-1

???????WHY DOES THIS OCCUR?

Heart FailureClinical ManifestationsAcute decompensated heart failure (ADHF)Pulmonary edema, often life-threatening Early Increase in the respiratory rate Decrease in PaO2 Later Tachypnea Respiratory acidemia

Heart FailureClinical ManifestationsAcute decompensated heart failure (ADHF)Physical findingsOrthopneaDyspnea, tachypneaUse of accessory musclesCyanosisCool and clammy skin

Heart FailureClinical ManifestationsAcute decompensated heart failure (ADHF)Physical findings*Cough with frothy, blood-tinged sputumBreath sounds: Crackles, wheezes, rhonchi TachycardiaHypotension or hypertension

Pulmonary Edema(advanced L side HF)When PA WEDGE pressure is approx 30mmHgSigns and symptoms1.wheezing2.pallor, cyanosis3.Inc. HR and BP4.s3 gallopThe Auscultation Assistant - Rubs and Gallops5.rales,copious pink, frothy sputum

Person literally drowning in secretionsImmediate Action Needed

http://www.biovisuals.com/alveolus.html

Goals of TreatmentMAD DOGImprove gas exchangeO2intubateelevate HOBBIPAP

Right Heart FailureSigns and Symptomsfatigue, weakness, lethargywt. gain, inc. abd. girth, anorexia,RUQ painelevated neck veinsHepatomegaly +HJRmay not see signs of LVF

Can Have RVF Without LVFWhat is this called?

COR PULMONALEThis results from pulmonary hypertension.How does this affect afterload?

Heart FailureComplicationsPleural effusionAtrial fibrillation (most common dysrhythmia) Loss of the atrial contraction (kick) can reduce CO by 10% to 20% Promotes thrombus/embolus formation increasing risk for strokeTreatment may include cardioversion, antidysrhythmics, and/or anticoagulants

Heart FailureComplicationsHigh risk of fatal dysrhythmias (e.g., sudden cardiac death, ventricular tachycardia) with HF and an EF

Heart FailureDiagnostic StudiesPrimary goal is to determine underlying causeHistory and physical examination( dyspnea)Chest x-rayECGLab studies (e.g., cardiac enzymes, BNP) electrolytesEF

Heart FailureDiagnostic StudiesPrimary goal is to determine underlying causeHemodynamic assessment-Hemodynamic Monitoring-CVP and SGEchocardiogram-TEE bestStress testing- exercise or medicineCardiac catheterization- determine heart pressures ( inc.PAW )Ejection fraction (EF)

Transesophageal echocardiogram TEE

Nursing AssessmentVital signsPA readingsUrine output------------------------------------------------------------------

Chronic HF Nursing Management Nursing diagnosesActivity intoleranceFluid volume excessImpaired gas exchangeAnxietyDeficient knowledge

Decreased cardiac outputPlan frequent rest periodsMonitor VS and O2 sat at rest and during activityTake apical pulseReview lab results and hemodynamic monitoring resultsFluid restriction- keep accurate I and OElevate legs when sittingTeach relaxation and ROM exercises

Activity IntoleranceProvide O2 as neededpractice deep breathing exercisesteach energy saving techniquesprevent interruptions at nightmonitor progression of activityoffer 4-6 meals a day

Fluid Volume ExcessGive diuretics and provide BSCTeach side effects of medsTeach fluid restrictionTeach low sodium dietMonitor I and O and daily weightsPosition in semi or high fowlersListen to BS frequently

Knowledge deficitLow Na dietFluid restrictionDaily weightWhen to call Dr.Medications

Heart Failure Nursing and Collaborative Management Overall goals of therapy for ADHF and chronic HF Decrease patient symptomsImprove LV functionReverse ventricular remodelingImprove quality of lifeDecrease mortality and morbidity

Chronic HF Nursing Management Planning: Overall GoalsDecrease in symptoms (e.g., shortness of breath, fatigue)Decrease in peripheral edemaIncrease in exercise toleranceCompliance with the medical regimenNo complications related to HF

Chronic HF Nursing Management Health PromotionTreatment or control of underlying heart disease key to preventing HF and episodes of ADHF (e.g., valve replacement, control of hypertension) Antidysrhythmic agents or pacemakers for patients with serious dysrhythmias or conduction disturbances Flu and pneumonia vaccinations

Chronic HF Nursing Management Health PromotionPatient teaching: medications, diet, and exercise regimens Exercise training (e.g., cardiac rehabilitation) improves symptoms but often underprescribedHome nursing care for follow-up and to monitor patients response to treatment may be required

GOALSDecrease preloadDec. intravascular volume Dec venous returnFowlersMSO4 and NtgDecrease afterloadInc. cardiac performance(contractility)CRTBalance supply and demand of oxygenInc. O2- O2, intubate, HOB up,Legs down, mech vent with PEEPDec. demand-beta blockers, rest, dec B/PManage symptoms

ADHF Nursing and Collaborative Management 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) Dont give calcium channel blockersHemodynamic monitoring

Chronic HF Collaborative Management Main treatment goalsTreat the underlying cause and contributing factorsMaximize COProvide treatment to alleviate symptomsImprove ventricular functionImprove quality of lifePreserve target organ functionImprove mortality and morbidity

Chronic HF Collaborative Management Oxygen administrationPhysical and emotional restNonpharmacologic therapies Cardiac resynchronization therapy (CRT) or biventricular pacingCardiac transplantation

CRT-Cardiac Resynchronization TherapyHOW IT WORKS:Standard implanted pacemakers are equipped with two wires (or "leads") that conduct pacing signals to specific regions of the heart (usually at positions A and C). The biventricular pacing devices have added a third lead (to position B) that is designed to conduct signals directly into the left ventricle. The combination of all three leads creates a synchronized pumping of the ventricles, increasing the efficiency of each beat and pumping more blood on the whole.

Chronic HF Collaborative Management Therapeutic objectives for drug therapy Identification of the type of HF and underlying causesCorrection of sodium and water retention and volume overloadReduction of cardiac workloadImprovement of myocardial contractilityControl of precipitating and complicating factors

Chronic HF Collaborative Management Drug therapyDiureticsThiazide LoopSpironolactone

Chronic HF Collaborative Management Drug therapy (contd)VasodilatorsACE inhibitors- pril or ril Angiotensin II receptor blockers Nitrates -Adrenergic blockers- al or ol Nesiritide- Natrecor

Chronic HF Collaborative Management Drug therapy (contd)Positive inotropic agents DigitalisCalcium sensitizersBiDil (combination drug containing isosorbide dinitrate and hydralazine) approved only for the treatment of HF in African Americans

Chronic HF Collaborative Management Nutritional therapyDiet and weight reduction recommendations must be individualized and culturally sensitiveDietary Approaches to Stop Hypertension (DASH) diet is recommended Sodium is usually restricted to 2.5 g per day

Chronic HF Collaborative Management Nutritional therapyFluid restriction may or may not be not requiredDaily weights are importantSame 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

Chronic HF Collaborative Management Nonpharmacologic therapies (contd)Intraaortic balloon pump (IABP) therapy Ventricular assist devices (VADs)Destination therapypermanent, implantable VAD

Surgical InterventionsIntraaortic balloon pump (IABP)Used for cardiogenic shockAllows heart to restVentricular assist device (VAD)Takes over pumping for the ventriclesUsed as a bridge to transplantArtificial HeartCardiomyoplasty-wrap latissimus dorsi around heartVentricular reduction surgery-ventricular wall is resected

Intraaortic Balloon Pump (IABP)Provides temporary circulatory assistance AfterloadAugments aortic diastolic pressureOutcomesImproved coronary blood flowImproved perfusion of vital organs

IABPFig. 66-14

IABP MachineFig. 66-13

Enhanced External Counterpulsation-EECPPumps during diastole- increasing O2 supply to coronary arteries. Like IABP but not invasive.The Cardiology Group, P.A.

Copyright 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.

Ventricular Assist Devices (VADs)

Indications for VAD therapyExtension of cardiopulmonary bypass Failure to weanPostcardiotomy cardiogenic shock Bridge to recovery or cardiac transplantation

Ventricular Assist Devices (VADs)Indications for VAD therapy (contd)Patients with New York Heart Association Classification IV who have failed medical therapy

Schematic Diagram of Left VAD Fig. 66-16

VAD

LVADVAD

New Heartmate

http://www.clevelandclinic.org/heartcenter/pub/guide/disease/heartfailure/lvad_devices.htm

Cardiomyoplasty technique: the left latissimus dorsi muscle (LDM) is transposed into the chest through a window created by resecting the anterior segment of the 2nd rib (5 cm). The LDM is then wrapped arround both ventricles. Sensing and pacing electrodes are connected to an implantable cardiomyostimulator

Cardiac Transplantation Nursing Management Treatment of choice for patients with refractory end-stage HF, inoperable CAD and cardiomyopathyGoal of the transplant evaluation process is to identify patients who would most benefit from a new heart

Cardiac Transplantation Nursing Management 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 therapyThe overall waiting period for a transplant is long, and many patients die while waiting for a transplant

Cardiac Transplantation Nursing Management Surgery involves removing the recipients heart, except for the posterior right and left atrial walls and their venous connectionsRecipients heart is replaced with the donor heart Donor sinoatrial (SA) node is preserved so that a sinus rhythm may be achieved postoperativelyImmunosuppressive therapy usually begins in the operating room

Cardiac Transplantation Nursing Management Infection is the primary complication followed by acute rejection in the first year after transplantationBeyond the first year, malignancy (especially lymphoma) and coronary artery vasculopathy are major causes of death

Cardiac Transplantation Nursing Management 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 Heartsbreath test is used along with endomyocardial biopsy to assess organ rejection

Cardiac Transplantation Nursing Management Peripheral blood T lymphocyte monitoring to assess the recipients immune statusCare focuses on Promoting patient adaptation to the transplant processMonitoring cardiac functionManaging lifestyle changesProviding relevant teaching

Blackboard Learning System (Release 6)

PATIENT TEACHING

Chronic HF Nursing Management 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

Chronic HF Nursing Management Acute Intervention HF is a progressive diseasetreatment plans are established with quality-of-life goalsSymptom management is controlled with self-management tools (e.g., daily weights)Salt must be restrictedEnergy must be conservedSupport systems are essential to the success of the entire treatment plan

Chronic HF Nursing Management Ambulatory and Home Care Explain physiologic changes that have occurred to patient Assist patient to adapt to both the physiologic and psychologic changesIntegrate patient and patients family or support system in the overall care plan

Chronic HF Nursing Management Implementation: Patient EducationHome BP monitoringSigns of hypo- and hyperkalemia if taking diuretics that deplete or spare potassiumInstruct patient in energy-conserving and energy-efficient behaviors

Whats New in Heart Failure?(myoblasts)Heart Failure Center - Information on congestive heart failure symptoms and treatment information

The 10 Commandments of Heart Failure Treatment Maintain patient on 2- to 3-g sodium diet. Follow daily weight. Monitor standing blood pressures in the office, as these patients are prone to orthostasis. Determine target/ideal weight, which is not the dry weight. In order to prevent worsening azotemia, some patients will need to have some edema. Achieving target weight should mean no orthopnea or paroxysmal nocturnal dyspnea. Consider home health teaching. Avoid all nonsteroidal anti-inflammatory drugs because they block the effect of ACE inhibitors and diuretics. The only proven safe calcium channel blocker in heart failure is amlodipine (Lotrel). Use ACE inhibitors in all heart failure patients unless they have an absolute contraindication or intolerance. Use doses proven to improve survival and back off if they are orthostatic. In those patients who cannot take an ACE inhibitor, use an angiotensin receptor blocker like irbesartan (Avapro). Use loop diuretics (like furosemide [Lasix]) in most NYHA class II through IV patients in dosages adequate to relieve pulmonary congestive symptoms. Double the dosage (instead of giving twice daily) if there is no response or if the serum creatinine level is > 2.0 mg per dL (180 mol per L). For patients who respond poorly to large dosages of loop diuretics, consider adding 5 to 10 mg of metolazone (Zaroxolyn) one hour before the dose of furosemide once or twice a week as tolerated.

The 10 Commandments of Heart Failure Treatment 6.Consider adding 25 mg spironolactone in most class III or IV patients. Do not start if the serum creatinine level is > 2.5 mg per dL (220 mol per L). 7.Use metoprolol (Lopressor), carvedilol (Coreg) or bisoprolol (Zebeta) (beta blockers) in all class II and III heart failure patients unless there is a contraindication. Start with low doses and work up. Do not start if the patient is decompensated. 8.Use digoxin in most symptomatic heart failure patients. 9.Encourage a graded exercise program. 10.Consider a cardiology consultation in patients who fail to improve. ACE = angiotensin-converting enzyme.

Congestive Heart Failure: OverviewHeart failure case studyCHF case 4http://www.austincc.edu/adnlev4/rnsg2331online/module04/heart_failure_case_study.htm

Practice Gamehttp://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, beta-blockers, 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.

Prioritization and Delegation(22)Two weeks ago, a 63 year old client with heart failure received a new prescription for carvedilol (Coreg) 3.125 mg orally. Upon evaluation in the outpatient clinic these symptoms are found. Which is of most concern?A. Complaints of increased fatigue and dyspnea.B. Weight increase of 0.5kg in 2 weeks.C. Bibasilar crackles audible in the posterior chest.D. Sinus bradycardia, rate 50 as evidenced by the EKG.

#24As the charge nurse in a long-term facility that has RN,LPN and nursing assistant staff members, a plan for ongoing assessment of all residents with a diagnosis of heart failure has been developed. Which activity is most appropriate to delegate to an LVN team leader? A. Weigh all residents with heart failure each morningB. Listen to lung sounds and check for edema weekly.C. Review all heart failure medications with residents every month.D. Update activity plans for residents with heart failure every quarter.

#26A cardiac surgery client is being ambulated when another staff member tells them that the client has developed a supraventricular tachycardia with a rate of 146 beats per minute. In what order will the nurse take these actions?A. Call the clients physician.B. Have the client sit down.C. Check the clients blood pressure.D. Administer oxygen by nasal cannula

#27The echocardiagram indicates a large thrombus in the left atrium of a client admitted with heart failure. During the night, the client complains of severe, sudden onset left foot pain. It is noted that no pulse is palpable in the left foot and that it is cold and pale. Which action should be taken next?A. Lower his left foot below heart level.B. Administer oxygen at 4L per nasal cannula.C. Notify the physician about the assessment data.D. Check the vital signs and pulse oximeter.

#14The nurse is caring for a hospitalized client with heart failure who is receiving captopril (Capoten) and spironolactone (aldactone). Which lab value will be most important to monitor?A. SodiumB. Blood urea nitrogen (BUN)C. PotassiumD. Alkaline phosphatase (ALP)