Heart Failure

Heart Failure

MildMildDrugsDiet Fluid RestrictionHeart Failure-(progression)CDHF(Pulmonary Edema)Severe End Stage

Cardiogenic shockCardiomyopathyIrreversible

Needs new ventricle

VADIABP

VADIABPHeart TransplantControl WithEmergency-Upright, O2, morphine, etc

Heart Failure Click to open !Heart Failure- Clinical syndrome can result from any structural or functional cardiac disorder that impairs ability of ventricle to fill with or eject blood

Impact!

5 million Americans- have heart failure 500,000 new cases every year 25-50 billion dollars a year to care for people with HF 6,500,000 hospital days / year and 300,000 deaths/yearDefinition-Heart Failure (HF)Key ConceptsCO = SV x HR-becomes insufficient to meet metabolic needs of bodySV- determined by preload, afterload and myocardial contractilityEF< 40% (need to understand)*Classifications HFSystolic failure- dec. contractilityDiastolic failure- dec. fillingMixedAn ejection fraction (EF) is one of the measurements used by physicians to assess how well a patients heart is functioning. Ejection refers to the amount of blood that is pumped out of the hearts main pumping chamber during each heartbeat. Fraction refers to the fact that, even in a healthy heart, some blood always remains within this chamber after each heartbeat.Therefore an ejection fraction is a percentage of the blood within the chamber that is pumped out with every heartbeat. An EF of 55 to 75 percent is considered normal. A higher than normal ejection fraction could indicate the presence of certain heart conditions, such as hypertrophic cardiomyopathy. A low ejection fraction could be a sign that the heart is weakened.

90/140= 64% EF- 55-65 (75) normalClick for animated EF

Keys to understanding HF

All organs (liver, lungs, legs, etc.) return blood to heart When heart begins to fail/ weaken> unable to pump blood forward-fluid backs up > Inc. pressure within all organs.Organ responseLUNGS: congested > stiffer , inc effort to breathe; fluid starts to escape into alveoli; fluid interferes with O2 exchange, aggravates shortness of breath.

Shortness of breath during exertion, may be early symptoms > progresses > later require extra pillows at night to breathe > experience "P.N.D." or paroxysmal nocturnal dyspnea . Pulmonary edema Legs, ankles, feet- blood from feet and legs > back-up of fluid and pressure in these areas, heart unable to pump blood as promptly as received > inc. fluid within feet and legs causes fluid to "seep" out of blood vessels ; inc. weight

Heart Failure

Heart Failure (ADHF)Pneumonic(emergency mgt >recall for later!)UUpright PositionNNitrates

LLasixOOxygenAACE, ARBs, Amiodorone DDig, Dobutamine

MMorphine SulfateEExtremities DownHeart Failure Click here for Online Lecture (Interactive) orClick here for Online Lecture (Read)

Heart Failure Etiology and PathophysiologySystolic failure- most common cause Hallmark finding: Dec. in *left ventricular ejection fraction (EF)Due to Impaired contractile function (e.g., MI)Increased afterload (e.g., hypertension)CardiomyopathyMechanical abnormalities (e.g., valve disease)Systolic failure- most common cause*Dec. in left ventricular ejection fraction (EF); Dec. contractility left ventricle; unable to generate enough pressure to eject blood forward through high-pressure aorta*EF- percentage of end-diastolic blood volume that is ejected during systole (reflects left ventricular function) (Lewis p. 757) normal-approx 60%; less than 40% = heart failure (determined by ECHO)

Heart Failure Etiology and PathophysiologyDiastolic failureImpaired ability of ventricles to relax and fill during diastole > dec. stroke volume and CODiagnosis based on presence of pulmonary congestion, pulmonary hypertension, ventricular hypertrophy*normal ejection fraction (EF)- Know why!Diastolic heart failureImpaired ability of ventricles to relax and fill during diastole > dec. stroke volume and CODue to left ventricular hypertrophy from chronic hypertension, aortic stenosis (Lewis, p. 880), hypertrophic cardiomyopathy (Lewis p. 888) or isolated right ventricular diastolic failure from pulmonary hypertension (*recall cor pulmonale- how affect afterload ?)Diagnosis based on presence of pulmonary congestion, pulmonary hypertension, ventricular hypertrophy, *normal EF-not much blood to eject!

Heart Failure Etiology and PathophysiologyMixed systolic and diastolic failureSeen in disease states such as dilated cardiomyopathy (DCM)Poor EFs ( renin angiotensin release. (ACE)B. Aldosterone release > Na and H2O retention3. Liver- stores venous volume (ascites, +HJR, Hepatomegaly- can store 10 L. check enzymesCounter-regulatory-Inc. Na > release of ADH (diuretics)*Release of atrial natriuretic factor > Na and H20 excretion, prevents severe cardiac decompensationWhat is BNP? What drug is synthetic form BNP? BNP belongs to a family of protein hormones called natriuretic peptides, which includes ANP, BNP, CNP, and DNP. Natriuretic peptides are part of the bodys natural defense mechanisms designed to protect the heart from stress and play an important role in regulating circulation. They promote urine excretion, relax blood vessels, lower blood pressure, and reduce the hearts workload. Most scientific study has focused on ANP and BNP.Measurement of BNP helps doctors diagnose and treat congestive heart failure. In this condition, the heart is unable to pump blood efficiently, and the heart chambers swell with blood. As the heart cells stretch, they produce extra BNP, which pours into the bloodstream. By measuring blood levels of BNP, doctors can spot signs of congestive heart failure in its early stages, when it may be hard to distinguish from other disorders. A normal BNP level is about 98% accurate in ruling out heart failure. And, in general, the higher the level, the worse the heart failure. Falling BNP levels indicate that treatment is working.

Heart Failure Etiology and PathophysiologyCompensatory mechanisms- activated to maintain adequate CONeurohormonal responses: Endothelin -stimulated by ADH, catecholamines, and angiotensin II >Arterial vasoconstrictionInc. in cardiac contractilityHypertrophy Heart Failure Etiology and PathophysiologyCompensatory mechanisms- 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 > cardiac hypertrophy, contractile dysfunction, and myocyte cell death

Compensatory Mechanisms (Lewis 823-824) (goal-maintain adequate CO!) *Important to understand-basis of management/controlSympathetic nervous system activation-first line response; least effective, release epinephrine, norepinephrineInc. heart rate (HR), myocardial contractility and peripheral vasoconstriction*Overtime-detrimental- inc. failing myocardiums need for oxygen and workload Neurohormonal responseKidneys- release rennin (Lewis, p. 1139, Fig 45-4) Renin- converts angiotensinogen to angiotensin I; Angiotensin I converted to angiotensin II by converting enzyme made in lungs Angiotensin II- > adrenal cortex > release aldosterone (sodium and water retention), inc. peripheral vasoconstriction (inc. BP); known as reninangiotensinaldosterone system (RAAS) Heart Failure Etiology and PathophysiologyCompensatory mechanisms- activated to maintain adequate CONeurohormonal responses: Over time > systemic inflammatory response > resultsCardiac wastingMuscle myopathyFatigue Renin-angiotensin-aldosterone systemNeurohormonal responses (Low CO >dec. in cerebral perfusion pressure-compensatory mechanisms- maintain CO)Antidiuretic hormone (ADH) secreted >inc. water reabsorption in renal tubules > water retention and inc. blood volumeEndothelin- stimulated by ADH, catecholamines, and angiotensin II > arterial vasoconstriction, inc. in cardiac contractility, cardiac hypertrophy Neurohormonal responses >release proinflammatory cytokines (e.g., tumor necrosis factor) by cardiac myocytes in response to cardiac injury; depress cardiac function > cardiac hypertrophy, contractile dysfunction, and myocyte cell deathNeurohormonal responses: *overtime > systemic inflammatory response > cardiac wasting, muscle myopathy, fatigue *Consequences of compensatory mechanismsVentricular dilation: Enlargement of heart chambers-elevated left ventricular pressure; initially effective adaptive mechanism; then mechanism inadequate, CO dec. * Frank-Starling law- inc. ventricular filling and myocardial stretch eventually results in ineffective contraction (typical inc. venous return inc. force of contraction)Hypertrophy: inc. in muscle mass and cardiac wall thickness in response to chronic dilation; heart muscle-poor contractility, inc. oxygen needs, poor coronary artery circulation, prone to ventricular dysrhythmias (sudden cardiac death)

Heart Failure Etiology and Pathophysiology**Counter regulatory processesNatriuretic peptides: atrial natriuretic peptide (ANP) and b-type natriuretic peptide (BNP)- *also dx test for HF

Released in response to inc. in atrial volume and ventricular pressurePromote venous and arterial vasodilation, reduce preload and afterload Prolonged HF > depletion of these factors

Heart Failure Etiology and PathophysiologyCounter regulatory processesNatriuretic peptides- endothelin and aldosterone antagonists Enhance diuresis Block effects of the RAAS Natriuretic peptides- inhibit development of cardiac hypertrophy; may have antiinflammatory effects Counter-regulatory mechanisms (counteract negative effects)*Natriuretic peptides: atrial natriuretic peptide (ANP) and b-type natriuretic peptide (BNP) (*hormones secreted by heart muscle) *Prolonged HF- depletes these factors. *(*BNP-note measure in CHF-secreted by ventricles due to fluid volume overload) (Lewis p. 752. Tab. 32-7)Released in response to inc. in atrial volume and ventricular pressurePromote venous and arterial vasodilation (reduce preload and afterload) diuresis Natriuretic peptides- endothelin and aldosterone antagonists; Enhance dieresis, block effects of RAAS; inhibit development cardiac hypertrophy, possible antiinflammatory (*What drug has this effect- p. 832)Nitric oxide (NO)- Released from vascular endothelium in response to compensatory mechanisms; relaxes arterial smooth muscle > results in vasodilation and dec. afterload

Result of Compensatory Mechanisms >

Heart FailureHeart Failure Explained

Pathophysiology-Structural Changes with HFDec. contractilityInc. preload (volume)Inc. afterload (resistance)**Ventricular remodeling (ACE inhibitors can prevent this)Ventricular hypertrophyVentricular dilationVentricular remodeling

END RESULTFLUID OVERLOAD > Acute Decompensated Heart Failure (ADHF)/Pulmonary Edema

>Medical Emergency!

Heart FailureClassification Systems New York Heart Association Functional Classification of HFClasses I to IVACC/AHA Stages of HF (newer)Stages A to D

NY ASSN Funct ClassACC/AHA Stages Stage AAt high risk for developing heart failure. Includes people with:Hypertension Diabetes mellitus CAD (including heart attack) History of cardiotoxic drug therapy History of alcohol abuse History of rheumatic fever Family history of CMPExercise regularly Quit smoking Treat hypertension Treat lipid disorders Discourage alcohol or illicit drug use If previous heart attack/ current diabetes mellitus or HTN, use ACE-IStage BThose diagnosed with systolic heart failure- have never had symptoms of heart failure (usually by finding an ejection fraction of less than 40% on echocardiogramCare measures in Stage A + Should be on ACE-I Add beta -blockers Surgical consultation for coronary artery revascularization and valve repair/replacement (as appropriateStage CPatients with known heart failure with current or prior symptoms. Symptoms include: SOB, fatigue Reduced exercise intoleranceAll care measures from Stage A apply, ACE-I and beta-blockers should be used + Diuretics, Digoxin,Dietary sodium restriction Weight monitoring, Fluid restriction Withdrawal drugs that worsen condition Maybe Spironolactone therapyStage DPresence of advanced symptoms, after assuring optimized medical care

All therapies -Stages A, B and C + evaluation for:Cardiac transplantation, VADs, surgical options, research therapies, Continuous intravenous inotropic infusions/ End-of-life care

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

CHF-due to1. Impaired cardiac functionCoronary heart diseaseCardiomyopathiesRheumatic feverEndocarditis2. Increased cardiac workloadHypertensionValvular disordersAnemiasCongenital heart defects3.Acute non-cardiac conditionsVolume overloadHyperthyroid, Fever,infection

Classifications- (how to describe)Systolic versus diastolicSystolic- loss of contractility get dec. CODiastolic- decreased filling or preloadLeft-sided versus right sidedLeft- lungsRight-peripheralHigh output- hypermetabolic stateAcute versus chronicAcute- MIChronic-cardiomyopathySymptoms

Left Ventricular FailureSigns and symptomsdyspneaorthopnea PNDCheyne Stokesfatigue Anxietyrales

NOTE L FOR LEFT AND L FOR LUNGSWhy 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 skinPhysical findings*Cough with frothy, blood-tinged sputum-why??? > (see next slide)Breath sounds: Crackles, wheezes, rhonchi TachycardiaHypotension or hypertension

Complete Case study of Heart Failure in Lewis online resources

Conceptual illustration depicting congestive heart failure. Pulmonary edema begins with an increased filtration through the loose junctions of the pulmonary capillaries. Copyright 1998, Lynne Larson All rights reserved. As the intracapillary pressure increases, normally impermeable (tight) junctions between the alveolar cells open, permitting alveolar flooding to occur.| Services | Profile | Clients | Image Gallery | | Contact Information | Home |

Conceptual illustration depicting congestive heart failure. Pulmonary edema begins with an increased filtration through the loose junctions of the pulmonary capillaries. Copyright 1998, Lynne Larson All rights reserved. As the intracapillary pressure increases, normally impermeable (tight) junctions between the alveolar cells open, permitting alveolar flooding to occur.| Services | Profile | Clients | Image Gallery | | Contact Information | Home |

Pulmonary edema begins with an increased filtration through the loose junctions of the pulmonary capillaries. As the intracapillary pressure increases, normally impermeable (tight) junctions between the alveolar cells open, permitting alveolar flooding to occur. Acute Decompensated Heart Failure (ADHF) Pulmonary EdemaADHF/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

Goals of Treatment-ADHF/Pulmonary Edema)MAD DOGImprove gas exchangeStart O2/elevate HOB/intubateMorphine dec anxiety/afterloadA- (airway/head up/legs down)D- (Drugs) Dig not first now- but drugs as IV nitroglycerin; IV Nipride, NatrecorD- DiureticsO- oxygen /measure sats; Hemodynamics, careful observationG- blood gasesThink physiology

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

What does this show?

What is present in this extremity, common to right sided HF?

Can You Have RVF Without LVF?What is this called?COR PULMONALE

Heart FailureComplicationsPleural effusionAtrial fibrillation (most common dysrhythmia) Loss of atrial contraction (kick) -reduce CO by 10% to 20% Promotes thrombus/embolus formation inc. risk for strokeTreatment may include cardioversion, antidysrhythmics, and/or anticoagulants Heart FailureComplications**High risk of fatal dysrhythmias (e.g., sudden cardiac death, ventricular tachycardia) with HF and an EF synchronized pumping of ventricles, inc. efficiency of each beat and pumping more blood on the whole.

Chronic HF Collaborative Management Therapeutic objectives for drug therapy Identification of type of HF & underlying causesCorrection of Na & H2O retention and volume overloadReduction of cardiac workloadImprovement of myocardial contractilityControl of precipitating and complicating factors Chronic HF-Collaborative Management Drug therapy

DiureticsThiazide LoopSpironolactoneVasodilatorsACE inhibitors- pril or ril *first line heart failureAngiotensin II receptor blockers Nitrates -Adrenergic blockers- al or ol Nesiritide- Natrecor (BNP)

Chronic HF Collaborative Management Drug therapy (contd)Positive inotropic agents DigitalisCalcium sensitizers- (Levosimendan) new under research; cardioprotective, inc. cardiac contractilityBiDil (combination drug containing isosorbide dinitrate and hydralazine) approved only for the treatment of HF in African Americans Chronic HF Collaborative Management Nutritional therapyDiet/weight reduction recommendations-individualized and culturally sensitiveDietary Approaches to Stop Hypertension (DASH) diet recommended Sodium- usually restricted to 2.5 g per dayPotassium encouraged unless on K sparing diuretics (Aldactone) Chronic HF Collaborative Management Nutritional therapyFluid restriction may or may not be requiredDaily weights 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-report to health care provider Chronic HF-End Stage >ADHF Collaborative Management Nonpharmacologic therapies (contd)Intraaortic balloon pump (IABP) therapy Used for cardiogenic shockAllows heart to restVentricular assist devices (VADs)Takes over pumping for the ventriclesUsed as a bridge to transplantDestination therapy-permanent, implantable VADCardiomyoplasty- wrap latissimus dorsi around heartVentricular reduction -ventricular wall resectedTransplant/Artificial Heart Intraaortic Balloon Pump (IABP)Provides temporary circulatory assistance Afterload Augments aortic diastolic pressureOutcomesImproved coronary blood flowImproved perfusion of vital organs

Intraaortic balloon pump

IABP MachineEnhanced External Counterpulsation-EECP

Pumps during diastole- increasing O2 supply to coronary arteries. Like IABP but not invasive.The Cardiology Group, P.A.Ventricular Assist Devices (VADs)

Patients with New York Heart Association Classification IV who have failed medical therapyPatient Teaching-Cleveland Clinic for Heart Failure LVAD devices

Schematic Diagram of Left VAD

Left ventricular assist device

The HeartMate II -one of several new LVAD devices- designed to last longer with simplicity of only one moving part; also much lighter and quieter than its predecessors; major differences is rotary action which creates a constant flow of blood, not pumping action.

HeartMate II

Cardiomyoplasty technique: left latissimus dorsi muscle(LDM) transposed into chest through a window created byresecting the anterior segment of 2nd rib (5 cm). LDM isthen wrapped around both ventricles. Sensing and pacingelectrodes are connected to an implantable cardiomyostimulator

Left Ventricular reduction Surgery-Bautista procedureindicated in some cases

Click here for UTube Artificial Heart animination! Cardiac Transplantation Nursing Management Treatment of choice for patients with refractory end-stage HF, inoperable CAD and cardiomyopathyGoal of transplant evaluation process - identify patients who would most benefit from a new heart Cardiac Transplantation Nursing Management Transplant candidates- placed on a list Stable patients wait at home and receive ongoing medical care Unstable patients -may require hospitalization for more intensive therapyOverall waiting period for a transplant is long; many patients die while waiting for a transplant Cardiac Transplantation Nursing Management Surgery involves removing recipients heart, except for posterior right and left atrial walls and their venous connectionsRecipients heart replaced with donor heart Donor sinoatrial (SA) node is preserved so that a sinus rhythm may be achieved postoperatively**Immunosuppressive therapy usually begins in operating room

Click here to Perform a Heart Transplant(your patient with end stage heart failure may require this!) Cardiac Transplantation Nursing Management Infection- primary complication followed by acute rejection in first year post transplantationAfter first year, malignancy (especially lymphoma) and coronary artery vasculopathy = major causes of death Cardiac Transplantation Nursing Management Endomyocardial biopsies -obtained from right ventricle weekly for first month, monthly for following 6 months, and then yearly to detect rejection Heartsbreath test is used along with endomyocardial biopsy to assess organ rejectionPeripheral blood T lymphocyte monitoring- assess recipients immune statusCare focuses: Promoting patient adaptation to transplant processMonitoring cardiac function & lifestyle changesProviding relevant teaching

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 -progressive diseasetreatment plans established with quality-of-life goalsSymptom management controlled with self-management tools (e.g., daily weights)Salt -restrictedEnergy- conservedSupport systems - essential to success of entire treatment plan Chronic HF- Nursing Management Ambulatory and Home Care Explain physiologic changes that have occurred Assist patient to adapt to physiologic and psychologic changesIntegrate patient and patients family or support system in overall care plan Implementation: Patient EducationHome BP monitoringSigns of hypo- and hyperkalemia if taking diuretics that deplete or spare potassiumInstruct in energy-conserving and energy-efficient behaviors

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