CONGESTIVE HEART FAILURE(CHF)

DEFINITIONHeart failure is a broad term that encompasses multiple etiology, pathophysiologic mechanism, and clinical presentation.Heart failure is a clinical syndrome in which structural or functional alterations of the heart lead to secondary phenomena such as exertional dyspnoe and circulatory congestion. Term : istilh

Basic DefinitionHeart failure is a medical term that describes an inability of the heart to keep up its work load of pumping blood to the lungs and to the rest of the body.http://danilhammoudimd_1.tripod.com/cardio1/id57.htmKep up: m lnjutkan

EtiologyIt is a common end point for many diseases of cardiovascular systemIt can be caused by : -Inappropriate work load (volume or pressure overload) -Restricted filling -Myocyte loss

StatisticIt is estimated that as many as two million Americans suffer from congestive heart failure and that up to 29, 000 die annually from this chronic disorder.

Cannobio, Mary. Cardiovascular Disorders. Missouri: C.V. Mosby Company, 1990.

Heart Failure(CHF): EpidemiologyIncidence:

Europe: 0.1-0.5% per year 3-4% >75 years old (Cowie et al, 1997; Cleland, 1997)USA: 300,000 new cases per year (Ho et al, 1997)

Prevalence:Europe: 0.3-2% 3-13%: >75 years (Cleland 1997; ESC 1997) 2-10,000,000 patients (ESC, 1997)USA: 3,000,000 patients (Ho et al, 1997)

Death From Heart Failure1965197019751980198519901995Vital statistics of the USA, National Center for Health Statistics(X 1000)YEAR50

40

30

20

10 0

Heart Failure is Malignant10090807060504030200 1 2 3 4 5 6Breast carcinomaProstate carcinomaHeart failure in womenHeart failure menColon carcinoma in womenColon carcinoma in menYEARS AFTER DIAGNOSISSURVIVAL

Symptoms(involving gravity/exhaustion of heartSwelling of the ankles, legs, and handsOrthopnea, or the shortness of breath when lying flat Shortness of breath during exertion

Grav:k gawtanInvlv m lputi

Symptoms(involving circulation)Cyanosis, or a bluish color that is seen in the lips and fingernails from a lack of oxygenFatigue or weaknessRapid or irregular heart beatChanges of behavior such as restlessness, confusion, and decreased attention span

Span: jangka wkt hdp

Symptoms(involving congestion)Unexplained or unintentional weight gainChronic coughIncreased urinationDistended neck veinsLoss of appetite or indigestionUninten : tdk d sngaja

Congestive heart failure is a syndrome that can be caused by multiple underlying diseases such as:Congenital heart diseaseAtherosclerosisRheumatic feverCardiomyopathyValve disordersVentricular failureLeft or right-sided failureHypertensionProlonged alcohol or drug addictionPrevious heart attackDiabetesChronic rapid heartbeats

Left-sided/Right-sided FailureBlood backs up causing congestion and thus swelling of extremities and internal organsBackup : mnggenangCongest:konjesen

APPROACH TO DIAGNOSE HEART DISEASE1. ANAMNESIS2. PHYSICAL EXAMINATION3. ELECTROCARDIOGRAM4. CHEST X RAY5. ANOTHER SUPPORTING EXAMINATION

ElectrocardiogramOld MI or recent MIArrhythmiaSome forms of Cardiomyopathy are tachycardia related LBBBmay help in management

Chest X-ray

Size and shape of heartEvidence of pulmonary venous congestion (dilated or upper lobe veins perivascular edema)Pleural effusion

Congestive Heart FailureIncreased heart size: cardiothoracic ratio >0.5Large hila with indistinct markingsFluid in interlobar fissuresPleural effusions, alveolar edemaIndsting: kbur

Differential diagnosis

Pericardial diseasesLiver diseasesNephrotic syndromeProtein losing enteropathy(Congestive Heart Failure)

Laboratory Findings AnemiaHyperthyroid Chronic renal insuffiency, electrolytes abnormalityPre-renal azotemia(uremia)Hemochromatosis(primary disorder of iron metabolism)

Progression to Heart Failure from Risk Factors

Heart Failure (HF) is a progressive entity, generally starting with asymptomatic systolic ventricular dysfunction (AVSD) and ending with symptoms which are produced by fluid retention and finally leading to refractory heart failure with systemic hypoperfusion.

Therefore the HF concept has been broadened thus including, on one end of the spectrum; Entty : k satuan yg ada

Progression to Heart Failure from Risk Factors

Coronary disease causes about 60%-70% of HF cases. Other etiologies include: valve disease cardiomyopathy and pressure or volume overload. Setting the cause aside, ventricular dysfunction appears and from that moment on a series of mechanisms will be seen. Aside : d smping

Progression to Heart Failure from Risk FactorsSmokingDyslipidemiaDiabetesHypertension MILVHSystolic dys-functionDiastolic dysfunctionHEART FAILURENormal LV structure and functionLV remodelingSubclinical LV dysfunctionClinical Heart FailureYearsYears/monthsLevy et al. JAMA, 275:1557, 1996

MECHANISM AND EXAMPLES OF CONDITIONS THAT CAUSE LEFT-SIDEDHEART FAILURE

CONDITIONS THAT CAUSE RIGHT HEART FAILURECardiac causes : Left sided heart failurePulmonic valves stenosisRight ventricular infarction

Parenchymal pulmonary disease :Chronic Obstructive Pulmonary DiseaseInterstitial lung diseaseAdult Respiratory Distress SyndromeChronic lung infection or bronchiectasis

Pulmonary vascular disease

Pulmonary embolismPrimary pulmonary hypertension

Precipitating FactorsIncreased metabolic demandsIncreased circulating volume Conditions that increased afterloadConditions that impaired contractilityFailure to take prescribed heart failure medicationsExcessive slow heart rate

CLASSIFICATION OF HEART FAILURENEW YORK HEART ASSOCIATION FUCTIONAL CLASSIFICATION :

I. Pts with cardiac disease but without resulting limitationII. Pts with cardiac disease resulting slight limitation of physical activity.III. Pts with cardiac disease resulting in marked limitation on physical activity.IV. Pts with cardiac disease resulting in inability to carry on any physical activity without discomfort.

MOST COMMON SYMPTOMS AND PHYSICAL FINDINGS IN HEART FAILURE

SYMPTOMPHYSICAL FINDINGS

LEFT SIDEDDiaphoresisDyspneuTachicardi, tachypneuOrthopneuLoud P2Paroxysmal nocturnal dyspneuS3 gallopFatiqueRIGHT SIDEDJugular venous dystensionPeripheral edemaHepatomegalyRight upper quadrant discomfortPeripheral edema

MANAGEMENTMAIN GOALS OF THERAPY :Identification and correction of the underlying conditionsElimination of the acute precipitating cause of symptoms.Treatment of the acute symptoms of congestive heart failureImprovement in longterm survival.

TreatmentWhen a treatable underlying cause of congestive heart failure exists, correcting the cause may resolve, or at least greatly improve, the degree of heart failure

Diet and Activity

Salt restrictionFluid restrictionDaily weight (tailor therapy)Gradual exertion programs

How much Salt is too much? Limit is 2000 mg of salt per day. This equals 1 teaspoon of salt all day. Stay away from salty snacks- potato chips; salted crackers; pretzels. No salt shaker.

Pot.chip:k ripikKrack : kuePretz kue krng asin

How much can I drink? Do not drink more than 1.5 litres to 2 litres of fluid per day. That equals 6-8 cups of fluid all day.

Daily Weights Weigh yourself daily. Use the same scale, and weigh yourself first thing in the morning before breakfast. Call the clinic if weight increases by two pounds overnight or five pounds in a few days.

DrugsDigitalis-strengthen the hearts contractions increasing blood flowDiuretic-increase the output of salt and water in urineVasodilators-relax blood vessels which lowers the resistance to blood flow. More blood reaches the tissues and the heart works no harder than before.

A: High risk for HFA: High risk for HFNo SHD/HF symptomsNo SHD/HF symptomsHypertensionCADDiabetes OrUsing carcinogensFHx cardiomyopathy

SHD: structural heart diseaseFHx family history*in appropriate patients

SHDTreat hypertensionSmoking cessationTreat lipid disordersEncourage regular exerciseDecrease alcohol intake, illicit /hrmdrug useACE inhibition

HypertensionCADDiabetes OrUsing carcinogensFHx cardiomyopathy

A: High risk for HFA: High risk for HFNo SHD/HF symptomsNo SHD/HF symptomsPrevious MILV systolic dysfunctionAsymptomatic valvular diseaseAll stage A interventionsACE inhibitors*-blockers* (post MI)

B: SHDNo HF symptomsSHD: structural heart diseaseFHx family history*in appropriate patients

SHDTreat hypertensionSmoking cessationTreat lipid disordersEncourage regular exerciseDecrease alcohol intake, illicit drug useACE inhibition

Management of HF in Patients With LV Systolic DysfunctionACE inhibitorsRoutine administration for asymptomatic and symptomatic patients with LVEF(ejeck frcsion) 40% (Strength of Evidence =A)ACE inhibitors should be titrated to doses used in clinical trials (Strength of Evidence =C)Substitute for ACE Intolerant to ACE --->ARB (Strength of Evidence = A)Combination Hydralazine + nitrate (Strength of Evidence = C)Hyper-K with ACEi or ARB ---> Nitrate+hydralazine (Strength of Evidence = C)Executive Summary: HFSA, 2006 Comprehensive Heart Failure Practice Guidelines, J of Cardiac Failure, Feb 2006Evdence fkta

Management of HF in Patients With LV Systolic DysfunctionBeta-Adrenergic Blockers For patients with LVEF 40% (Strength of Evidence = A)For patients with recent decompensation of HF after optimization of diuretics, vasoactive agents includig inotropic support (Strength of Evidence = B)Routine therapy in combination with ACEi for asymptomatic LVD (Post-MI (Strength of Evidence = B; non-post-MI: Strength of Evidence = C)BB in patients with concomitant DM, COPD, PAD: (Strength of Evidence = C)Continued in most patients experiencing exacerbation of HF during chronic maintenance therapy: (Strength of Evidence = C)

BlockersHas been traditionally contraindicated in pts with CHFNow they are the main stay in treatment on CHF & may be the only medication that shows substantial improvement in LV functionIn addition to improved LV function multiple studies show improved survivalThe only contraindication is severe decompensated CHF

Management of HF in Patients With LV Systolic DysfunctionAldosterone AntagonistsNYHA III-IV or HF from LV dysfunction with LVEF 35% (Strength of Evidence = A)Consider in patients after an acute MI with clinical HF signs and symptoms and LVEF

Management of HF in Patients With LV Systolic DysfunctionPolypharmacyIn patients with persistent symptoms or progressive worseningAddition of an ARB (Strength of Evidence = A)Addition of AA(Ald.Antgonist) For severe HF (Strength of Evidence = A)For moderate HF (Strength of Evidence = C)DiureticsTo restore and maintain normal fluid status (Strength of Evidence = A)Loop diuretics rather than thiazides (Strength of Evidence = B)

Diuretic TherapyThe most effective symptomatic reliefMild symptomsHCTZChlorthalidoneMetolazoneBlock Na reabsorbtion in loop of henle and distal convoluted tubulesThiazides are ineffective with GFR < 30 --/min

Diuretics (cont.)More severe heart failure loop diureticsLasix (20 320 mg QD), FurosemideBumex (Bumetanide 1-8mg)Torsemide (20-200mg)Mechanism of action: Inhibit chloride reabsortion in ascending limb of loop of Henle results in natriuresis, kaliuresis and metabolic alkalosisAdverse reaction:pre-renal azotemiaHypokalemiaSkin rashototoxicity

Management of HF in Patients With LV Systolic DysfunctionDigoxinConsider in patients with LVSD EF40% NYHA II-III (Strength of Evidence = A)NYHA IV (Strength of Evidence = B)

Executive Summary: HFSA, 2006 Comprehensive Heart Failure Practice Guidelines, J of Cardiac Failure, Feb 2006

Digitalis Glycosides (Digoxin, Digitoxin)The role of digitalis has declined somewhat because of safety concernRecent studies have shown that digitals does not affect mortality in CHF patients but causes significant Reduction in hospitalizationReduction in symptoms of HF

Management of HF in Patients With LV Systolic DysfunctionAnticoagulants and AntiplateletsAll HF patients with chronic or documented PAFib (Strength of Evidence = A)Ischemic cardiomyopathy (Strength of Evidence = B)History of pulmonary emboli, TIA (Strength of Evidence = C)

C: Prior or current HF symptomsD: Refractory HFD: Refractory HFKnown structural heart diseaseShortness of breath and fatigue, reduced exercise tolerance

Marked symptoms at rest despite maximal medical therapyAll stage in A, B, and CMechanical assist devicesHeart transplantationContinuous IV inotropic infusions for palliationHospice care

All stage B interventionsDrugs for routine use:DiureticsACE inhibitors-blockersDigitalisDietary sodium restrictionModified from Hunt, et al. J Am Coll Cardiol. 2001; 38:2101-2113.Refractory symptoms at rest

Novel CHF StrategiesNeurohumoral blockersDecreasemaladaptiveremodeling

Novel Inotropic AgentsIncrease contractility

Mechanical TherapiesIncreaseefficiency

Gene TherapiesCreate new muscle cellsPig cell transplant

Endothelin, cytokine, vasopressin antagonistsCa++ sensitizers (levo-simendan) growth hormoneresynchronization,/CDs, LVAD, mechanical heart, CPAPGene/cell replacement

Non-PharmacologicalBed restInactivityFluid restriction(Digitalis, diuretics)Pre-1980s1980s1990s2000s2020s PharmacologicalDigitalisDiureticsNeuro-hormonal interventionsPharmacologicalDigitalisDiureticsVasodilatorsInotropes

Device/alt brCRTICDsLVADsOthersCellular/GenesGene therapiesCell implantationXenotransplantationEras of Heart Failure Management

In conclusion, congestive heart failure is often assumed to be a disease when in fact it is a syndrome caused by multiple disorders.THE END

Prof.BarmawiNov 09 2009Prof.BarmawiNov 09 2009Prof.BarmawiNov 09 2009Prof.BarmawiNov 09 2009Prof.BarmawiHeart Failure (HF) is a progressive entity, generally starting with asymptomatic systolic ventricular dysfunction (AVSD) and ending with symptoms which are produced by fluid retention and finally leading to refractory heart failure with systemic hypoperfusion. Therefore the HF concept has been broadened thus including, on one end of the spectrum; patients with volume overload and reduced ejection fraction (EF) and on the other end asymptomatic patients with important systolic and diastolic derrangements.In order to understand the benefit exerted by some of these drugs on this population, it is important to bear in mind some of the pathophysiological characteristics that associate a myocardial insult to symptoms manifestation. Coronary disease causes about 60%-70% of HF cases. Other etiologies include: valve disease cardiomyopathy and pressure or volume overload. Setting the cause aside, ventricular dysfunction appears and from that moment on a series of mechanisms will be seen. They are as follows: neurohormonal and aldosterone-renin-angiotensin system activation, endothelial dysfunction and an interplay between vasodilators and vasoconstrictors substances. This will cause a ventricular remodeling process with a consequent fall in EF, which will lead to a clinical HF phase and will end-up in severe pump failure with arrhythmias and death.Nov 09 2009Prof.BarmawiNov 09 2009Prof.BarmawiNov 09 2009Prof.BarmawiNov 09 2009Prof.BarmawiNov 09 2009Prof.BarmawiNov 09 2009Prof.BarmawiNov 09 2009Prof.BarmawiNov 09 2009Prof.BarmawiNov 09 2009Prof.BarmawiNov 09 2009Prof.BarmawiNov 09 2009Prof.BarmawiNov 09 2009