Acute Heart Failure Kendra Marsh, MD Clinical Instructor, Cardiology Fellow Department of Cardiology University of Illinois at Chicago Objectives • Definitions • Epidemiology • Pathophysiology • Diagnosis • Management • Summary of Guidelines • Recommended Reading • Definitions • Epidemiology • Pathophysiology • Diagnosis • Management • Summary of Guidelines • Recommended Reading 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 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 Killips Classification This classification system uses the clinical exam to determine the degree of cardiomyopathy after an acute MI. • 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 Clinical Severity Classification Warm/Dry Warm/Wet Cold/Dry Cold/Wet • PERFUSION • CONGESTION – Auscultation of the lungs • Definitions • Epidemiology • Pathophysiology • Diagnosis • Management • Summary of Guidelines • Recommended Reading 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 • Definitions • Epidemiology • Pathophysiology • Diagnosis • Management • Summary of Guidelines • Recommended Reading A Vicious Circle In an effort to maintain adequate tissue perfusion the body has three defenses: increase heart rate, vascular tone and circulating volume. • Definitions • Epidemiology • Pathophysiology • Diagnosis • Management • Summary of Guidelines • Recommended Reading • Definitions • Epidemiology • Pathophysiology • Diagnosis • Management • Summary of Guidelines • Recommended Reading General Therapeutic Approach 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 Pharmacotherapy • Morphine • Anticoagulation • Vasodilators • Diuretics • Beta Antagonists • Inotropic Agents Morphine • Class IIb, B – Great Early in management – Venodilation – Mild Arterial Dilation – Slows Heart rate 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 Vasodilators • 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 Niseritide • Recombinant B-type Brain Naturetic Peptide • Venous, Arterial and coronary affects • Enhanced sodium excretion • Suppresses RAAS and sympathetic system Vasodilators in the Management of Acute Heart Failure Trial (VAMC) Design Enrolled Agents Primary End Point Randomized DoubleBlinded Control Effects at 3 hours 489 Acute CHF PCWP> 20mmHg Niseritide Change in PCWP Bolus 2 micr/kg from baseline Reduced dyspnea compared to Nitroglycerine standard therapy IV alone Outcomes Significant reduction in dyspnea score and PCWP with addition of NIseritide to standard therapy • 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. Summary of Vasodilators Diuretics • Class I, B Diuretic Resistance can be associated with increased mortality. Ultrafiltration • 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 Option in the setting of failed diuretic and vasodilator therapy 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 Inotropic Agents • Peripheral Hypoperfusion refractory to vasodilators and diuretics, Class IIa, C • Danger: May increase oxygen demand and calcium loading Dopamine and Dobutamine • 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 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 Outcomes of a Prospective Trial of Intravenous Milrinone For Exacerbations of Congestive Heart Failure OPTIME-CHF JAMA 2002 Design Randomized, Control, Double Blinded Milrinone versus Placebo Enrolled Broad Population with systolic dysfunction Without low output syndrome 949 patients Primary Endpoints Repeat hospitalization for cardiovascular causes Outcomes No difference in primary end point between Milrinone and placebo. Higher instance of atrial arrhythmia and hypotension with Milrinone. Milrinone is associated a 30% increase in mortality Conclusions Not indicated in routine use with standard medica therapy. within 60 days of discharge. Levosimendan • • • • • Calcium ion sensitization Also Pimobendon Increases Contractility A little PDI activity as well Severe dysfunction with preserved blood pressure • Drawback: very proarrhythmogenic Clinical Trials • 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 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. Cardiac and Ventricular Assist Devices Temporary Devices • IABP • Tandem Heart • ECMO • Ventricular Assist Devices IABP 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 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 Longer-term implantable devices • Novacor • HeartMate XVE • HeartMate II • Next Generation Devices Operative Mortality Prediction Score • Requirement for ventilator support — 4 points • Clinical picture of post-cardiotomy shock — 2 points • Use of temporary LVAD prior to Heart-Mate insertion — 2 points • Central venous pressure >16 mmHg — 1 point • Prothrombin time >16 seconds — 1 point • Scoring – 0-5: Low risk • Mortality 8% – 5-7: Intermediate Risk • Mortality 32% – 8-10: High Risk • Mortality 49% Novacor- Long-term Device Cardiac Replacement Bridge to Transplant Magnetic Actuator Blood Propelled via collapsing bladder and to prosthetic valves One Year Survival No risk factors, 60% 1 Risk factor, 24% 25% risk of Thromboembolic Event Heart-mate • • • • • • Rehabilitation and hospital discharge $70,000 LV apex to ascending aorta Textured surface allows for endotheliazation to reduce need for anticoagulation Improves perfusion: decrease renal failure and pulmonary HTN Complications: infection, bleeding, monomorphic VT, RV failure and Aortic Stenosis HeartMate II Suggested Reading • Randomized evaluation of Mechanical Assistance for • • • • Treatment of Chronic Heart Failure (Rose et al. NEJM 2001) Evaluation and management of patients with acute decompensated heart failure. Journal of Cardiac Failure. Vol.12 No. 1 2006 Medical Management of Advanced Heart Failure. JAMA, February 6,2002- Vol. 27, No. 5 http://www.med.umich.edu/AnesCriticalCare/Documents /Rosenberg_Circulatory_Assist_Devices.pdf http://texasheart.org/Research/Devices/thoratec_heartm ateii.cfm Thank you! • Special Thanks to – Dr. Chad Feldman, Associate Director of Medicine Advocate Christ Hospital – Dr. Ali Zadi, Clinical Instructor, Cardiology Fellow – Dr. Saba Khan, Heart Failure Fellow