Congestive Heart Failure

1. CongestiveHeartFailure Doç. Dr. Elif Eroğlu Büyüköner Yeditepe Üniversite Hastanesi Kardiyoloji ABD 2012-2013

2. DEFINITION of HF • Heart Failure is the clinical syndrome that can result from anystructural or functional cardiac disorder thatimpairs the ability of the ventricle to fill with or eject blood, or the ability to do this by increasing the end-diastolic pressure to pathologic levels • Kalp yetmezliği kardiyak fonksiyonlardaki bozulma nedeni ile vücudun metabolik ihtiyacı olan kanı pompalayamaması ya da bu ihtiyacı, ventrikülün diyastol sonu basıncını normalin üstünde arttırarak yerine getirebilmesi durumudur.

5. PRELOAD/ÖNYÜK Amount of force stretching the myofibrile before contraction • Maximizing preload results in  • Maximized stroke volume • Maximized contractility  • FRANK-STARLING’S LAW!!!

7. FRANK-STARLING’S LAW

8. AFTERLOAD/ARTYÜK • Tension on heart wall during contraction • Clinically, it is the pressure the heart must pump against to eject blood • Afterload reduction reduces cardiac work • Determined by peripheral vascular resistance and the cardiac chamber size

9. LAPLACE’S LAW

16. KY’DE NÖROHUMORAL DENGE • Neurohumoralresponsesincludeactivation of sympatheticnervesandtherenin-angiotensinsystem, andincreasedrelease of antidiuretichormone (vasopressin) andnatriureticpeptides. • The net effect of theseneurohumoralresponses is toproducearterialvasoconstriction (tohelpmaintainarterialpressure), venousconstriction (toincreasevenouspressure), andincreasedbloodvolume. • In general, theseneurohumoralresponses can be viewed as compensatorymechanisms, but they can alsoaggravateheartfailurebyincreasingventricularafterload (depressesstrokevolume) andincreasingpreloadtothepointwherepulmonaryorsystemiccongestionandedemaoccur.

22. RAAS AKTİVASYONU

23. Başlangıç Adaptif Mekanizmalar ve Sonuçları

24. DEFINITION

25. CLASSIFICATION of HF • Acute/Chronic HF • Left/rightsided HF • Forward/backward HF • High/lowoutput HF

26. ETIOLOGY of HF

27. Afterload: arterielhypertension, aortic stenosis • Preload: Volume overload, AR, MR • Pump failure: CAD, cardiomyopathies, arrhythmia, increased workload (infection, high-output states)

28. DEFINITIONS in HF • A patientwho has neverexhibitedthetypicalsignsorsymptoms of HF is described as havingasymptomatic LV systolicdysfunction • Patientswhohave had HF forsome time areoftensaidtohave ‘chronic HF’. • A treatedpatientwithsymptomsandsigns, whichhaveremainedgenerallyunchangedfor at least a month, is saidto be ‘stable’. • Ifchronicstable HF deteriorates, thepatientmay be described as ‘decompensated’ andthismayhappensuddenly, i.e. ‘acutely’, usuallyleadingtohospitaladmission • New (‘de novo’) HF maypresentacutely, forexample as a consequence of acutemyocardialinfarction

29. DEFINITIONS of FUNCTIONAL CLASSIFICATION

30. DIAGNOSIS of HEART FAILURE

32. DIAGNOSTİC TESTS in HF Transthoracicechocardiography is recommendedtoevaluatecardiacstructureandfunction, includingdiastolicfunctionandtomeasure LVEF tomakethediagnosis of HF, assist in planningandmonitoring of treatment, andtoobtainprognosticinformation. A 12-lead ECG is recommendedtodetermineheartrhythm, heart rate, QRS morphology, and QRS duration, andtodetectotherrelevantabnormalities. Thisinformationalsoassists in planningtreatmentand is of prognosticimportance. A completely normal ECG makessystolic HF unlikely (but stillpossible!) Measurement of bloodchemistry (includingsodium, potassium, calcium, urea/bloodureanitrogen, creatinine/estimatedglomerularfiltration rate, liverenzymesandbilirubin, ferritin/TIBC) andthyroidfunction is recommendedto: Evaluatepatientsuitabilityfordiuretic, renin–angiotensin–aldosterone antagonist, andanticoagulanttherapy (andmonitortreatment) (ii) Detectreversible/treatablecauses of HF (e.g. hypocalcaemia, thyroiddysfunction) andco-morbidities (e.g. irondeficiency) (iii) Obtainprognosticinformation.

33. DIAGNOSTİC TESTS in HF A completebloodcount is recommendedto: Detect anaemia, whichmay be an alternativecause of thepatient’ssymptomsandsignsandmaycauseworseningof HF (ii) Obtainprognosticinformation. Measurement of natriureticpeptide (BNP, NT-proBNP, or MR-proANP) should be consideredto: Exclude alternativecauses of dyspnoea (ifthelevel is belowtheexclusion cut-point HF is very unlikely) (ii) Obtainprognosticinformation. A chestradiograph (X-ray) should be consideredtodetect/excludecertaintypes of lungdisease, e.g. cancer (does not exclude asthma/ COPD). Itmayalsoidentifypulmonarycongestion/oedemaand is moreuseful in patientswithsuspected HF in theacutesetting.

34. CMR imaging is recommendedtoevaluatecardiacstructureandfunction, tomeasure LVEF, andtocharacterizecardiactissue, especially in subjectswithinadequateechocardiographicimagesorwheretheechocardiographicfindingsareinconclusiveorincomplete (but takingaccount of cautions/contraindicationsto CMR). Coronaryangiographyis recommended in patientswithanginapectoris, whoareconsideredsuitableforcoronaryrevascularization, toevaluatethecoronaryanatomy. Myocardialperfusion/ischaemiaimaging(echocardiography, CMR, SPECT, or PET) should be considered in patientsthoughttohave CAD, andwhoareconsideredsuitableforcoronaryrevascularization, todeterminewhetherthere is reversiblemyocardialischaemiaandviablemyocardium. Leftandrightheartcatheterizationis recommended in patientsbeingevaluatedforhearttransplantationormechanicalcirculatorysupport, toevaluaterightandleftheartfunctionandpulmonaryarterialresistance. Exercisetestingshould be considered: (i) Todetectreversiblemyocardialischaemia (ii) As part of theevaluation of patientsforhearttransplantationandmechanicalcirculatorysupport (iii) Toaid in theprescription of exercisetraining (iv) Toobtainprognosticinformation.

41. Common chest X-ray abnormalities in HF

45. KY EVRELEMESİ (yapısal) • Stage A • KY için yüksek risk/Yapısal kalp hastalığı yok/KY semptomu yok • Stage B • Yapısal Kalp hastalığı + • Kalp yetmezliği bulgusu yok • Stage C • Semptomatik KY • Stage D • Yoğun tedavi gerektiren refrakter KY

46. Classification of HF by structural abnormality,or by symptoms relating to functional Capacity (NYHA)

47. Semptom ve bulgular • Nefes darlığı • Dispne yada nefes nefese kalma hali (hava açlığı hissetme) • KKY nin en erken bulgusudur. • Başlangıçta egzersiz ile, hastalığın ilerlediği durumlarda daha az hareket ile ortaya çıkar • Bu aşamadan sonra Paroksismal nakturnal dipne ortopneistirahate ND • Sol kalp Yetm.sağ kalp Yetm. Nefes darlığı yakınması azalır • Sağ kalp yetmezliğinde ND yakınması nadirdir çünkü pulmoner konjesyon yoktur fakat sağ kalp yetm.  KO, solunum kası hipoperfüzyonu ve hipoksi nedeni ile gelişen asidoz ND yapabilir.

48. Semptom ve bulgular • Paroksismal nokturnal dispne • Bir süre sırt üstü yatıp uyuduktan sonra hasta aniden boğucu karakterde ND ile uyanır oturur yada pencere açarak yada dışarı çıkarak hava açlığını gidermeye çalışır • Ortopneden önce karşılaşılır • Bronkospazm yada wheezing duyulabilir (astım krizi ile karışır) • Yaklaşık 30 dk sürer • Nedeni infratorasik intertisyel sıvının dolaşıma katılması sırt üstü yatmakla pulmoner venöz basınç artışı (özellikle sol ventrikül diyastolik disfonksiyonunda)

49. Semptom ve bulgular • Ortopne • Sırtüstü yatınca oluşan oturunca geçen ND • Ortopneik hasta ancak oturarak uyuyabilir yada yastık sayısını arttırırlar • PND ile benzer mekanizmaya sahiptir fakat daha ileri bir klinik durumu gösterir • Halsizlik yorgunluk • Özellikle ektremitelerde • Düşük kardiyak output, düşük kas perfüzyonu, egzersiz intoleransı • Yemeklerden sonra daha fazla (kan akımı mide bağırsak sistemine yönlenir) • Pulmoner konjesyon olmaksızın görülebilir. • Hiponatremiye bağlı görülebilir

50. Semptom ve bulgular • Nocturi/oliguri • Sık ve KKY nin erken bulgularından • Su ve tuz filtrasyonu ayaktaki hastada azalır • Sırtüstü yatınca venöz dönüş artar ve gün içindeki kazanılmış tuz ve su atılımı böbrek kan akımının artması ile artar idrar oluşumu artar • Oliguri ciddi KKY bulgusudur son aşama klinik tabloda gözlemlenir