1. Stages of Heart Failure At Risk for Heart Failure: STAGE A High risk for developing HF STAGE B Asymptomatic LV dysfunction Heart Failure: STAGE C Past or current symptoms of HF STAGE D End-stage HF

2. Acute heart failure AHF: AHF: The rapid onset of symptoms and signs secondary to abnormal cardiac function. (reduced CO, tissue hypoperfusion + congestion, increase in PCWP) 1.With or without previous cardiac disease. 2.The cardiac dysfunction can be related: a) to systolic or diastolic dysfunction b) to abnormalities in cardiac rhythm c) to preload and afterload mismatch 3.Often life threatening and requires urgent treatment. The Task Force on Acute Heart Failure of the European Society of Cardiology

3. “FORWARD FAILURE” (Low Cardiac Output): Decreased perfusion of the brain (confusion). kidneys (impaired renal function), skin (cyanosis) etc. “ “BACKWARD FAILURE” : Increased pulmonary venous pressure, pulmonary edema Καρδιακή ανεπάρκεια:η Διάγνωση κλινική πρόκληση

4. Nohria A et al: JACC 2003;41:1797-1804. dry: absence of signs of congestion, wet: elevated filling pressures, dry: absence of signs of congestion, wet: elevated filling pressures, warm: adequate systemic perfusion, cold: inadequate systemic perfusion warm: adequate systemic perfusion, cold: inadequate systemic perfusion “ Clinical severity classification”

5. Hemodynamic subsets in “acute” heart failure Normal Pulmonary edema Cardiac index L/min/m 2 2.2 2.0 1.5 1.0 0.5 0 normal blood pressure 51015182025303540 Pulmonary Wedge Pressure Forrester Α et al: Am J Cardiol 1977; 39:137 reduced blood pressure high blood pressure Cardiogenic shock Hypovolaemic shock Mor:2.2% Mor:10.1% Mor:22.4% Mor:55.5%

6. Η οξεία καρδιακή ανεπάρκεια αποτελεί ένα ετερογενές σύνδρομο που καλύπτει ένα μεγάλο κλινικό φάσμα με δι- αφορετικά εκλυτικά αίτια. Η αντιμετώπιση της οξείας καρδιακής ανεπάρκειας πρέ-πει να ικανοποιεί βραχυχρόνιους (συμπτώματα, αιμοδυ- ναμική κατάσταση) και μακροχρόνιους (επιβράδυνση ε- ξέλιξης νόσου, θνητότητα) στόχους.

7. Acute heart failure Epidemiology Increase of pts with CHF (aging of population + improved survival) = increase in the number of hospitalisations for the decompensated heart failure. AMI + SHF: APO: Poor prognosis: AMI + SHF: 30% annual mortality APO: 40% annual mortality 12% in-hospital mortality 1. CAD: 60-70% (particularly in elderly population) 2. Dilated cardiomyopathy, arrhythmia, congenital or VHD or myocarditis: in youmger subjects. The Task Force on Acute Heart Failure of the European Society of Cardiology

8. Acute Heart Failure : Classification  Acute de novo (new onset of AHF in a patient without previously known cardiac dysfunction). or  Acute decompensation of chronic heart failure. The Task Force on Acute Heart Failure of the European Society of Cardiology Can present itself as:

9. Acute Heart Failure : Other Classifications In AHF after AMI, best applied to acute denovo heart failure:  The Killip classification : based on clinical signs and chest X-ray findings (Stage I: No heart failure, Stage II: Heart failure, Stage III: Severe heart failure and Stage IV: Cardiogenic shock).  The Forrester classification : based on clinical signs and haemodynamic cha- racteristics. In a cardiomyopathy service, best applied to chronic decompensated heart failure:  “ Clinical severity classification” : based on observation of the peripheral cir- culation and on auscultation of the lungs for congestion (Class I: dry and warm, Class II: wet and cold, Class III: cold and dry and Class IV: cold and wet). Nohria A et al: JACC 2003;41:1797-1804.

10. Acute Heart Failure : Classification  Acute decompensated heart failure (de novo or as decompensation of CHF) : With mild signs and symptoms of AHF and do not fulfil criteria for cardio-genic shock, pulmonary oedema or hypertensive crisis.  Hypertensive acute heart failure: Signs and symptoms of HF + high BP + preserved LVF + chest radiograph findings APO.  Pulmonary oedema: Verified by chest X-ray, severe respiratory distress, or- thopnoea with SaO 2 <90%.  Cardiogenic shock: Reduced BP (SBP 30mmHg) and/or low urine output ( 60 bpm with or without evidence of organ congestion.  High output failure: High CO + HR, pulmonary congestion, sometimes low BP (arrhythmias, thyrotoxicosis, anaemia, Paget’ disease, iatrogenic etc)  Right heart failure: Low CO + increased jugular venous pressure + increased liver size + hypotension. The Task Force on Acute Heart Failure of the European Society of Cardiology The patient with AHF may present with one of several distinct clinical conditions:

11. Acute Heart Failure : Classification HRSBPCIPCWPCongestion Killip/ Forrester DiuresisHypo- perfusion End organ hypo- perfusion I. Acute decompensated congestive heart failure* +/- Low Normal / High Low normal / High Mild elevation K II / F II ++/-- II Acute heart failure with hypertension/ hypertensive crisis Usually increased High+/->18K II- IV/ FII-III +/- +, with CNS symptoms III Acute heart failure with pulmonary oedema + Low normal Low Eleva ted KIII/ FII ++/-- Cardiogenic shock*: IVa. Low output syndrome + Low normal Low, <2.2>16K III-IV / F I-III low ++ IVb Cardiogenic shock >90<90<1.8>18K IV/ F IVVery low +++ V. High output failure + +/- + KII/FI-II +-- VI. Right sided acute heart failure Usually low Low F I+/-+/-, acute onset +/-

12. Underlying diseases and co-morbidities in acute heart failure  Coronary artery disease  Valvular disease  Prosthetic valve thrombosis  Aortic dissection  AHF and hypertension  Renal failure  Pulmonary diseases and bronchoconstriction  Arrhythmias and AHF  Peri-operative AHF (usually due to myocardial ischaemia)

13. Clinical  symptoms (dyspnea and/or fatigue)  clinical signs  body weight  diuresis  oxygenation Laboratory examinations  BUN and/or creatinine  serum electrolyte normalisation  plasma BNP blood glucose normalisation Haemodynamic  pulmonary wedge pressure to < 18 mm Hg  cardiac output and/or stroke volume Goals of treatment of the patient with acute heart failure The Task Force on Acute Heart Failure of the European Society of Cardiology

14. Goals of treatment of the patient with acute heart failure Outcome  length of stay in the intensive care unit  duration of hospitalization  time to hospital re-admission  mortality Tolerability Low withdrawal rate Low incidence of adverse effects The Task Force on Acute Heart Failure of the European Society of Cardiology

15. Acute Exacerbations May Contribute to the Progression of the Disease Gheorghiade M, Fonarow G, Filippatos G et al. Am J Cardiology 2005 Time Ventricular function Acute event With each event, hemodynamic alterations contribute to progressive ventricular dysfunction.

16. Patient with AHF: immediate treatment goals The Task Force on Acute Heart Failure of the European Society of Cardiology

17. General medical issues in the treatment of acute heart failure The Task Force on Acute Heart Failure of the European Society of Cardiology  Infections (increase in CRP the only sign)  Diabetes (normoglycemia improves survival)  Catabolic state (reduced caloric uptake)  Renal failure (aggravate and influence the outcome)

19. Oxygen in acute heart failure  Target SaO 2 (95 – 98%) Class I, LOE-C  O 2 administration in hypoxaemic patients with acute heart failure Class IIa, LOE-C  No O 2 (or  FiO 2 ) in patients without evidence of hypoxaemia  Hyperoxia causes harm:  coronary blood flow,  cardiac output  blood pressure  systemic vascular resistance  mortality The Task Force on Acute Heart Failure of the European Society of Cardiology

20. Non – invasive ventilation (NIV) and intubation (TI) in acute heart failure  Use of CPAP and NIPPV in acute cardiogenic pulmonary oedema is associated with a significant reduction in the need for endotracheal intubation (TI) and mechanical ventilation [MV, (Class IIa, LOE-A)].  T.I. (MV) use: To reverse induced respiratory muscle fa- tigue (low respiratory rate, hypercapnia, confusion): a) Intervention b) Only if acute respiratory failure does not respond to vasodilators, O 2 and/or CPAP or NIPPV (Target: SaO 2 > 90%, FiO 2 < 0.60) The Task Force on Acute Heart Failure of the European Society of Cardiology

21. Guidelines for pulmonary artery catheter (PAC) use in acute heart failure Insertion of PAC for the diagnosis of acute heart failure is usually unnecessary PAC can be used to distinguish between a cardiogenic and a not cardiogenic mechanism in complex patients with concurrent cardiac and pulmonary disease. PAC is frequently used to estimate hemodynamic variables and guide therapy in the presence of severe diffuse pulmo-nary pathology or ongoing haemodynamic compromise not resolved by initial therapy The Task Force on Acute Heart Failure of the European Society of Cardiology (Class IIb, LOE-C)

23. Medical Treatment  Morphine and its analogues (early stage, dyspnoea, restlessness, 3 mg IV)  Anticoagulation (less evidence,no clinical improvement,less venous thrombosis)  ACE inhibitors (are not indicated in the early stabilisation, role in pt with AMI)  Diuretics  Vasodilators  b-blocking agents  Inotropic agents

24. Medical Treatment Practical use of diuretics Start with individualized dose depending on clinical condition Titrate according to clinical response Reduce dose when fluid retention is controlled Monitor serum K +, Na + and renal function every 1-2 days Replace K + and Mg 2+ loss

25. Medical Treatment Vasodilators Nitrates Sodium Nitroprusside (SNP) Nesiritide

26. Medical Treatment - Vasodilators The Task Force on Acute Heart Failure of the European Society of Cardiology

27. Nitrates in acute heart failure a.Titration to the highest haemodynamically tolerable dose of nitrates with low dose furosemide is superior to high dose diuretic treatment alone. (Class I, LOE-B) b.Be cautious in aortic stenosis, SBP < 90 – 100 mmHg,  MAP 10mmHg c.In acute heart failure caused by acute coronary syndro- mes, are favoured over nitroprusside (may cause corona- ry steal syndrome) The Task Force on Acute Heart Failure of the European Society of Cardiology

28. Beta – blocking agents 1. “Pts on b-blockers admitted to hospital due to worsening heart failure should be continued on this therapy unless inotropic support is needed (reduce dose)”. 2. Pts with acute myocardial infraction who stabilize after acute heart failure, b-blockers should be initiated early. (Class IIa, LOE-B). The Task Force on Acute Heart Failure of the European Society of Cardiology

29. Beta – blocking agents 3.Pts with overt acute heart failure and more than basal pulmonary rales, b-blockers should be used cautiously. If ongoing ischaemia and tachycardia consider I.V. meto- prolol (Class IIb, LOE-C) 4.Pts with congestive heart failure, b-blockers should be initiated when the patient has stabilized after the acute episode (usually after 4 days) (Class I, LOE-A) The Task Force on Acute Heart Failure of the European Society of Cardiology

30. If clinical situation does not improve with vasodilators and diuretics? AHF Vasodilators Diuretics Levosimendan Inotropes Dopamine/adrenaline if shock with low BP Surgery Assist devices

31. Inotropic agents in acute heart failure Dobutamine Dopamine Adrenaline Phosphodiesterase inhibotors Calcium sensitizers Cardiac glycosides The Task Force on Acute Heart Failure of the European Society of Cardiology

32. Cardiac Glycosides “Not recommended in acute heart failure, in particular following acute myocardial infraction. Tachycardia indu- ced heart failure (e.g. atrial fibrillation with insufficient rate-control by other agents) may be an indication” The Task Force on Acute Heart Failure of the European Society of Cardiology

34. Δακτυλίτιδα πρέπει να λαμβάνουν: Οι ασθενείς με κολπική μαρμαρυγή και καρδιακή ανεπάρκεια (ESC) Οι ασθενείς με συστολική καρδιακή ανεπάρκεια και φλεβοκομβικό ρυθμό που παραμένουν συμπτωματικοί παρά τη θεραπεία με α-ΜΕΑ και διουρητικά (ESC), ενώ Οι Αμερικανικές οδηγίες τονίζουν ότι η θεραπεία με δακτυλίτιδα μπορεί να ξεκινήσει στους ασθενείς οποιαδήποτε στιγμή μαζί με τους α-ΜΕΑ και τα διουρητικά (AHA/ACC)

35. Inotropic agents in acute heart failure Haemodynamics vs arrhythmias, ischemia  MVO 2,  mortality Mechanism of action does matter  cAMP,  myocardial cell Ca ++ have the greatest risk Risk benefit ratio favours levosimendan

37. Inotropic agents “are indicated in the presence of peripheral hypoperfusion (hypotension, decreased renal function) with or without congestion or pulmonary oedema refractory to diuretics and vasodilators at optimal doses” (Class Iia, LOE-C) The Task Force on Acute Heart Failure of the European Society of Cardiology

38. Inotropic agents “Dopamine may be used as an inotrope (>2μg/kg/min i.v.) in acute heart failure with hypotension. Infusion of  2-3 μg/kg/min doses may be used to improve diuresis and renal blood flow in decompensated heart failure with hypotension and low urine output.” (Class IIb, LOE-C) The Task Force on Acute Heart Failure of the European Society of Cardiology

39. Type III PDEIs “are indicated when there is evidence of peripheral hypo- perfusion with or without congestion refractory to diuretics and vasodilators at optimal doses, and preserved systemic BP” (Class IIb LOE-C) “may be preferred to dobutamine in pts on concomitant b-b therapy, and/or with an inadequate response to dobutamine” (Class IIa, LOE-C) The Task Force on Acute Heart Failure of the European Society of Cardiology

40. Levosimendan “is indicated in pts with syptomatic low cardial output heart failure secondary to cardiac systolic dysfuntion without severe hypotension” (Class IIa, LOE-B) The Task Force on Acute Heart Failure of the European Society of Cardiology

41. Rationale for inotropic drugs The Task Force on Acute Heart Failure of the European Society of Cardiology

42. Surgical treatment in acute heart failure

43. Surgical treatment in AHF: mechanical assist devices and heart transplantation (algorithm)