Acute Heart Failure Kendra Marsh, MD Clinical Instructor, Cardiology Fellow

1. Acute Heart Failure Kendra Marsh, MD Clinical Instructor, Cardiology Fellow Department of Cardiology University of Illinois at Chicago

2. Objectives • Definitions • Epidemiology • Pathophysiology • Diagnosis • Management • Summary of Guidelines • Recommended Reading

3. Definitions Epidemiology Pathophysiology Diagnosis Management Summary of Guidelines Recommended Reading

4. Acute Heart Failure • Rapid onset of symptoms and signs related to abnormal cardiac function • As a result of Systolic Dysfunction, Diastolic Dysfunction, Arrhythmias, or Preload-After load Mismatch

5. Related Clinical Conditions • De Novo or Chronic Decompensated • Hypertensive • Pulmonary Edema • Cardiogenic Shock • High Output Heart Failure: Arrhythmias, Thyrotoxicosis, Anemia, Paget’s Disease • Right Heart Failure

6. Stage I: No Heart Failure Stage II: Heart Failure S3 gallop, Pulmonary venous Hypertension, Rales <1/2 of the lung fields Stage III: Severe Heart Failure Frank pulmonary Edema, rales through out the lung field Stage IV: Cardiogenic Shock Systemic hypotension, peripheral vasoconstriction, endorgan failure, cyanosis, diaphoresis Killips Classification This classification system uses the clinical exam to determine the degree of cardiomyopathy after an acute MI.

7. Clinical Severity Classification Warm/Dry Warm/Wet Cold/Dry Cold/Wet • PERFUSION • CONGESTION • Auscultation of the lungs

8. Definitions Epidemiology Pathophysiology Diagnosis Management Summary of Guidelines Recommended Reading

9. Epidemiology • We have greatly improved our management of acute myocardial infarctions. • Large component of care is inpatient • Expensive to manage • High mortality in patients status post MI. • The leading cause of hospitalization in patients over 65 • 1 million hospitalizations per year with HF as primary diagnosis • 2.5 million hospitalizations with heart failure as secondary diagnosis

10. Definitions Epidemiology Pathophysiology Diagnosis Management Summary of Guidelines Recommended Reading

11. A Vicious Circle

12. In an effort to maintain adequate tissue perfusion the body has three defenses: increase heart rate, vascular tone and circulating volume.

17. Definitions Epidemiology Pathophysiology Diagnosis Management Summary of Guidelines Recommended Reading

22. Definitions Epidemiology Pathophysiology Diagnosis Management Summary of Guidelines Recommended Reading

23. General Therapeutic Approach

25. Oxygen • Class I, C • Improves oxygen delivery and tissue perfusion • Goal Saturation should be 95-98%, beyond that there is no indication for increased FIO2 • Always consider CPAP first or Non Invasive Positive Pressure Ventilation First • Endotrachial Intubation as a last resort

26. Pharmacotherapy • Morphine • Anticoagulation • Vasodilators • Diuretics • Beta Antagonists • Inotropic Agents

27. Morphine • Class IIb, B • Great Early in management • Venodilation • Mild Arterial Dilation • Slows Heart rate

28. Anticoagulation • No evidence to support anticoagulation for Acute Heart Failure alone • Yes in the case of Atrial Fibrillation • Yes in the case of LV thrombus • Large Placebo Control Trial with Enoxiparin at 40mg SC showed no mortality benefit

29. Nitrates: Class I, B Improves Cardiac Output and decreases PCWP Best with diuretics Low doses, venodilation High doses, arterial dilation Preload and Afteroad Good for 16-24 hours Sodium Nitroprusside: Class I, C Severe Heart Failure with Hypertension Primarily arterial dilation Need for arterial invasive monitoring Stop if active ischemia due to coronary steal phenomenon Vasodilators

30. Niseritide • Recombinant B-type Brain Naturetic Peptide • Venous, Arterial and coronary affects • Enhanced sodium excretion • Suppresses RAAS and sympathetic system

31. Vasodilators in the Management of Acute Heart Failure Trial (VAMC) • No good data to support adverse affects on renal function and niseritide • Retrospective analysis of VMAC showed potential for increased creatinin with increasing niseritide dose.

32. Summary of Vasodilators

33. Diuretics • Class I, B

34. Diuretic Resistance can be associated with increased mortality.

35. RAPID-CHF Trial 40 patients ADHF and Renal Insufficiency (Cr >1.5) Ultrafiltration had significant increase in fluid removal after 24 hours 4650 L vs 2838L UNLOAD Trial 200 patients Renal insufficiency was not a criteria for inclusion Standard care vs ultra filtration 48 Hours 4.6 L vs 3.3L 90 Days fewer rehospitalizations .22 vs .46 and fewer unscheduled clinic visits 21 vs 44 Ultrafiltration Option in the setting of failed diuretic and vasodilator therapy

36. Beta Blockers • No data to support benefits in AHF • Traditionally considered a contra indication • Consider if there is active ischemia and blood pressure tolerates. • Ischemia and Tachycardia, Class IIb, C • Acute MI after stabilization, Class IIa, B • Chronic CHF after stabilization, Class I, A

37. Inotropic Agents • Peripheral Hypoperfusion refractory to vasodilators and diuretics, Class IIa, C • Danger: May increase oxygen demand and calcium loading

38. Dopamine: Vasodilator of Renal, Coronary, splanchnic and Cerebral Vascular beds Hypotensive patients Drawbacks: arrhythmia, increased pulmonary vascular resistance and increased afterload Dobutamine, Class IIa, C Hypotension and low Urine output Beta 1 and 2 agonist At high doses increases SVR Additive effect with Phosphodiesterase inhibitors Draw Backs- arrhythmia, reflex decrease in sympathetic tone Dopamine and Dobutamine

39. Phosphodiesterase Inhibitors • Milrinone and Enoximone • Hypoperfusion despite Diuretics and Vasodilators with good blood pressure. Class IIb, C • Lucitropic, Inotropic, vasodilator • Inhibits degredation of Cyclic AMP • Increase CO, CI, Stroke Volume, • Decrease PAP, PVR and PCWP • Immediate Action • Effect is Distal to Beta receptors, can be used in the setting Beta Blocker therapy. Class IIa, C

40. Outcomes of a Prospective Trial of Intravenous Milrinone For Exacerbations of Congestive Heart FailureOPTIME-CHF JAMA 2002

41. Levosimendan • Calcium ion sensitization • Also Pimobendon • Increases Contractility • A little PDI activity as well • Severe dysfunction with preserved blood pressure • Drawback: very pro-arrhythmogenic

42. LIDO Trial Levosimendan 24 hr infiusionvs Dobutamine 203 Patients Severe Decompensated HF, AHF, HF after CABG Excluded if cardiogenic shock Endpoints, increased CI (35% vs 25%) and reduced PCWP (28% vs 15%) in favor of Levosimendan SURVIVE Trial Levosimendan vs Dobutamine 24 hour therapy 1327 patients Endpoints symptomatic relief and BNP Levosimendan Greater reduction in BNP but no difference in symptomatic relief Clinical Trials

43. Pressors • Vasopressin: Cardiogenic shock in conjunction with inotropic therapy • Epinephrine B1 and B2, • Norepinephrine alpha receptors • Cardiac Glycosides: Inhibit cardiac Na/K ATPase, increases Ca/Na exchange mechanism. Tachycardia induced Cardiomyopathy.

45. Cardiac and Ventricular Assist Devices

46. Temporary Devices • IABP • Tandem Heart • ECMO • Ventricular Assist Devices

47. IABP

48. ECMO • ECMO removes carbon dioxide from and adds oxygen to venous blood via an artificial membrane lung Severe respiratory failure Cardiac Failure with inability to wean off Bypass Bridge to Cardiac Transplant

49. Temporary Devices:Tandem Heart pVAD • Continuous-flow centrifugal assist device placed extracorporeally • Cannula in femoral vein through intraatrial septum into LA • Pump withdraws oxygenated blood from the left atrium, propels it by a magnetically driven impeller through the outflow port • Blood returns into femoral artery via arterial cannula

50. Longer-term implantable devices • Novacor • HeartMate XVE • HeartMate II • Next Generation Devices