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Hearth failure. Doc.Dr Emir Fazlibegović,ESC,FESC Prof.Dr Mustafa Hadžiomerović, ESC,FESC 5th International Congress of cardiologysts and angyologysts of Bosnia and Herzegovina,Sarajevo 2010. WHAT IS HEART FAILURE?. - PowerPoint PPT Presentation

Text of Hearth failure

  • Hearth failureDoc.Dr Emir Fazlibegovi,ESC,FESCProf.Dr Mustafa Hadiomerovi, ESC,FESC

    5th International Congress of cardiologysts and angyologysts of Bosnia and Herzegovina,Sarajevo 2010.

  • WHAT IS HEART FAILURE? HF is a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood. The cardinal manifestations of HF are dyspnea and fatigue, which may limit exercise tolerance, and fluid retention, which may lead to pulmonary and peripheral edema.Both abnormalities can impair the functional capacity and quality of life of affected individuals, but they may not necessarily dominate the clinical picture at the same time.Evaluation and Management of Chronic Heart Failure in the AdultA Report of the ACC/AHA Task Force on Practice GuidelinesFebruary 2002

    Supply is less then demand Failure of the heart as a pump

  • Systolic/Diastolic does it matter?Systolic: heart cannot contract normally and cannot pump enough blood into the arteries (EF40%)

  • Left, right, or both?Right Heart FailureResults in increased, systemic venous congestion and peripheral oedema Left Heart FailureResults in pulmonary congestion

  • Different etiology so what?Many causes but clinical manifestations similarCoronary artery disease is the underlying cause of HF in approximately two thirds of patients with ischemic left ventricular systolic dysfunction.

    The remainder have nonischemic causes, e.g. hypertension, valvular disease, myocardial toxins, or myocarditis

    or may have no discernible cause (e.g., idiopathic dilated cardiomyopathy).

  • Compensated phaseSupply temporarily meets the altered demand, no or very mild symtoms and signsDecompensated heart failure:new or worsening symptoms/signs of dyspnoea, fatigue or oedema leading to hospitalisation or unscheduled medical carePHASE

  • Terminology or just semantics?Congestive Heart Failure (CHF) Heart failure with extra fluid in vessels and tissues Acute heart failure (AHF) sudden initial episode of HF, severe symptoms; frequent pulmonary edema Chronic heart failure (CHF) (chronic HF) Slow process of myocardium destruction, often unnoticed, mild to moderate symptoms; frequent peripheral edema, may follow acute insult Acute exacerbation of chronic heart failure Immediate and massive decompensation of the previously existing chronic heart

  • Current indicationAcutely Decompensated Severe Low-output Chronic-24 hours?-Abruptly-SuddenlySymptomaticNYHA III-IVCardiac -EF
  • Acute heart failure:

    sudden onset of symptoms or signs of heart failure in a patient with no history of heart failure and previously normal cardiac function

    ONSET

  • ONSETExacerbation of chronic heart failure:

    patient with established diagnosis of heart failure who develops increasing signs or symptoms of the disease after a period of relative stability

  • Conceptual differences between acute and chronic heart failureChronic heart failure:neurohumoral disease that responds to neurohumoral interventionRemodeling, RAAS, cateholamines, PDEAcute heart failure:haemodynamic disease that responds to haemodynamic interventions

  • Classification and causes of heart failureAcute de novo heart failureMyocardial infarctionArrhythmiasValve destructionMyocarditisHypertensive crisisCardiac surgery

    Decompensated chronic heart failureMyocardial ischaemiaArrhythmiasMalcomplianceInfectionsSalt overloadHypertension

    Pulmonary oedemaLow output heart failure (congestion)Cardiogenic shock

  • Differences between acute heart failure and decompensated Chronic HFHaemodynamics:AHF: RV +/- LV, normovolaemic

    Decompensation of Chronic HF: both RV and LV, increased EDV, hypervolaemic

    Prognosis:AHF: potentially reversible, stunning, sepsis

    Decompensation of Chronic HF: chronic disease

  • DIAGNOSISFramingham CriteriaMajor Criteria

    Parox. Nocturnal dyspneaOrthopnea JVPPulmonary ralesThird heart soundCardiomegalyPulmonary edemaMinor Criteria

    Peripheral edemaNight coughDyspnea on exertionHepatomegalyPleural effusionHeart rate>120/minWight loss > 4.5 kg in 5 days

  • Classification

  • Treatment of Decompensated CHFDecompensatedHF PatientEdema (+)Warm ExtremitiesSBP > 90 mm HgDecompensatedHF PatientEdema (+)Cold ExtremitiesSBP > 90 mm HgDecompensatedHF PatientEdema (-)Cold ExtremitiesSBP > 90 mm HgOptimization of therapy:Increase ACEI dosesIV diureticsOther PO or IV vasodilators (nitroprusside)LevosimendanDecompensatedHF PatientEdema (+) or (-)Cold ExtremitiesSBP < 90 mm HgDobutamine/Dopamine/NorepinephrineAdd Levo?67%20%5%8%Inadequate response: Increasing BUN Persisting edema Persisting dyspneaLow-output HFCardio shockHigh output

  • Calcium-Induced Conformational Changes in Troponin Complex

    ActinActinTnTTnTcTnCTnITmTmTnIcTnCcTnCTnIcTnCTnITmTnTTmActinActinTmTmTnTMyosin headMyosin headCa2+Ca2+Ca2+Ca2+Myosin headMyosin headMyofilament lengthMyofilament length

  • LevosimendanCalcium sensitisation through binding to troponin C

    increases cardiac contractility and efficiency Opening of ATP-sensitive potassium channels in vascular smooth muscles

    pulmonary, coronary, systemic vasodilation

  • Calcium Sensitization by LevosimendanNo increase in cAMPNo increase in i/c calciumNo increase in energy consumptionNo arrhythmogenicityNo impairment in relaxationAnti-stunning effectNo antagonism by -blockers

  • Heart FailureLIDO study203 patients with severe HF, levo vs. dobutCASINO study299 patients low-output HF, levo vs. dobut vs. placebo.REVIVE-2 study600 patients. Levo vs placebo. Higher early mortality, but no difference at 90 days.SURVIVE trial1327 patients, levo vs. dobutamine: No mortality difference at 180 days.

  • IHD and Cardiac surgeryRUSSLAN study504 patients with recent MI, levo vs. placebo. Trend to lower mortality at 180 days.Small studies in cardiac surgery show levosimendan increases cardiac output and lowers SVR

  • Mostar study in 20 patients NYHA III-IVaged 43-84, average 69All patients treated with ACE inhibitors, diuretic, beta blockers, aldosterone blockers, statins, and cardiotonics (digoxin chronically and dobutamin, dopamine in the shortly crisis period). on follow-up 1-3 day after infusion and 3 and 6 month, and 1-2-3 year after.

  • Levosimendan and NYHA

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    NYHA kl.

    Sheet1

    ImePrezimeIme Prezimegoditedatum pregledaRtg p(cEFNYHA kl.EndLVDebljina ZZIVSLAAODVFSCRPTr IhipotenzijafrekvencijaAP ZZEfekat ThKomorbiditetEKGIshod

    IbrahimHasi1193517.01.07.1,7217%47.31.715.83.52.97%98,449,590/601100.65HOPB,IM,Aneurizma,Edem pluaBDGH,W u I,II,dobar

    IbrahimHasi1193507.05.07.1,7448%37.71.10.95.13.80.925%62,9100/70900.95"""

    IbrahimHasi1193509.10.07.2,0672%25.61.21.45.93.11.942%20,5100/70801.15"""

    IbrahimHasi1193502.02.10.1,6464%26.11.11.263.32.340%110/70761.15"""

    StankoPjevac2195416.02.07.1,8927%46.81.11.33.93.3213%3,7105/60720.85DCM post myocarditidem,Sy.metabolicumdobar

    StankoPjevac2195427.02.07.35%36.91.20.843.21.317%631.13"""

    StankoPjevac2195405.04.07.33%36.91.10.93.93.3216%7013"""

    JozoMikuli3194924.04.07.1,7255%35.41.31.46.63.83.129%1,4721.32CM chr.post Commisurotomiam mitralis(1974)et Impl.valv.A-23 Carbomedix et mitralis M-31 Carbomedix(23.05.1991.) et ACBPx1(Cx)FA permanentdobar

    JozoMikuli3194922.05.07.58%35.91.41.66.53.82.431%1.22"""

    JozoMikuli3194904.03.08.1,653%35.61.41.46.73.2228%12"""

    VinkoBuli4193225.04.07.1,638%351.41.45.43.12.718%100/60801.15CM hypertrophica post IM decomp,AS 2,AR,Sy.metabolicum,Atherosclerosis generalisatadobar

    VinkoBuli4193211.05.07.69%25.61.61.74.62.92.339%1.25"""

    MileMlinarevi5192818.04.07.1,445%49.210.85.94.83.223%6,9701.93CM dilatativa,Hydrithorax dex.AS 2-3,St.post IM 1988.va,BLGH,BDGHdobar

    MileMlinarevi5192825.04.07.1,537%47.91.70.96.94.33.420%5,81101.50"FA,BDGHExitus 3.5.07.

    ZejnaKurbegovi6192604.10.07.1,720%45.51.115.32.92.70,9%34,3110/60761.34CM chr.dilatativa et ath. Et diabetica,DM,CCVFA,BDGHdobar

    ZejnaKurbegovi6192609.10.07.1,857%25.21.51.15.12.92.830%110/70801.44""dobar

    MirjanaRozi7193926.12.07.1,332%45.91.30.94.42.41.732%76,5650.74CM ischemica decomp.post op ACBPx3,AIM,Insuff.renalis,VF,Syncopa,APdobar

    MirjanaRozi7193926.01.08.1,845%25.71.21.24.52.42.335%120/80701.45"""

    MirjanaRozi7193924.02.08.DM,Cardiac arrest,UroinfectioCardiac arrestExitus letalis 24.02.08.

    IvanBeli8193813.03.08.1,841%35.81.61.43.93.62.121%16,4901.45St.post IM anterolateralis,ACBPx3(LADLIMA,OM1,PDA),Sy. MetabolicumAIMdobar

    IvanBeli8193827.03.08.82%25.91.21.35.22.92.551%2,86015"IMdobar

    IvicaDujmovi9195020.03.08.1,220%49.81.71.15.44.21.611%110/70801.63CM dilatativa decomp,post Impl.valv.mitralis et anuloplasticam tricuspidalis(2004.),Sy.metabolicumBLGH,sinus ritam 70/mindobar

    IvicaDujmovi9195017.04.08.1,343%39.21.30.943.8222%701.44"""

    JureJuri10195818.07.08.1,517%47.91.20.64.43.41.813%110/70900.94CM chr.ath.et isch.post IM anterolateralis,Aneurisma apicalis,Hiatus hernia,Ulcus b.d.PLH,BLGH,ST elevacijadobar

    JureJuri10195820.07.08.1,627%371.10.943.32.313%701.24""Exitus letalis 22.12.08.Cardiac arest

    LjubaRezo11193930.07.08.1,857%36.61.114.93.11.831%5,31001.15CM chr.thyreotoxica dilatativa decomp,FA permanent,BLGH,APFA,BLGHdobar

    LjubaRezo11193931.0

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