acute heart failure kendra marsh, md clinical instructor, cardiology fellow department of cardiology...

Acute Heart Failure

Kendra Marsh, MD

Clinical Instructor, Cardiology Fellow

Department of Cardiology

University of Illinois at Chicago

ObjectivesObjectives

• DefinitionsDefinitions

• EpidemiologyEpidemiology

• Pathophysiology Pathophysiology

• DiagnosisDiagnosis

• Management Management

• Summary of Guidelines Summary of Guidelines

• Recommended ReadingRecommended Reading



• PathophysiologyPathophysiology



• Summary of GuidelinesSummary of Guidelines

• Recommended Reading Recommended Reading

Acute Heart FailureAcute Heart Failure

• Rapid onset of symptoms and signs Rapid onset of symptoms and signs related to abnormal cardiac functionrelated to abnormal cardiac function

• As a result of Systolic Dysfunction, As a result of Systolic Dysfunction, Diastolic Dysfunction, Arrhythmias, Diastolic Dysfunction, Arrhythmias, or Preload-After load Mismatchor Preload-After load Mismatch

Related Clinical ConditionsRelated Clinical Conditions

• De Novo or Chronic Decompensated De Novo or Chronic Decompensated

• Hypertensive Hypertensive

• Pulmonary EdemaPulmonary Edema

• Cardiogenic ShockCardiogenic Shock

• High Output Heart Failure: Arrhythmias, High Output Heart Failure: Arrhythmias, Thyrotoxicosis, Anemia, Paget’s Thyrotoxicosis, Anemia, Paget’s DiseaseDisease

• Right Heart Failure Right Heart Failure

Killips Classification Killips Classification

• Stage I: No Heart FailureStage I: No Heart Failure

• Stage II: Heart FailureStage II: Heart Failure S3 gallop, Pulmonary venous Hypertension, Rales <1/2 of the lung S3 gallop, Pulmonary venous Hypertension, Rales <1/2 of the lung

fields fields

• Stage III: Severe Heart FailureStage III: Severe Heart Failure Frank pulmonary Edema, rales through out the lung fieldFrank pulmonary Edema, rales through out the lung field

• Stage IV: Cardiogenic ShockStage IV: Cardiogenic Shock Systemic hypotension, peripheral vasoconstriction, endorgan Systemic hypotension, peripheral vasoconstriction, endorgan

failure, cyanosis, diaphoresisfailure, cyanosis, diaphoresis

This classification system uses the clinical exam to determine the degree of cardiomyopathy after an acute MI.

Clinical Severity Clinical Severity ClassificationClassification

• PERFUSIONPERFUSION

• CONGESTIONCONGESTION– Auscultation of the lungs Auscultation of the lungs

Warm/Dry

Cold/Dry

Warm/Wet

Cold/Wet

EpidemiologyEpidemiology

• We have greatly improved our We have greatly improved our management of acute management of acute myocardial infarctions.myocardial infarctions.

• Large component of care is Large component of care is inpatientinpatient

• Expensive to manageExpensive to manage• High mortality in patients High mortality in patients

status post MI.status post MI.• The leading cause of The leading cause of

hospitalization in patients hospitalization in patients over 65over 65

• 1 million hospitalizations per 1 million hospitalizations per year with HF as primary year with HF as primary diagnosisdiagnosis

• 2.5 million hospitalizations 2.5 million hospitalizations with heart failure as with heart failure as secondary diagnosissecondary diagnosis

A Vicious Circle

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

General Therapeutic General Therapeutic ApproachApproach

OxygenOxygen

• Class I, CClass I, C– Improves oxygen delivery and tissue Improves oxygen delivery and tissue

perfusionperfusion– Goal Saturation should be 95-98%, beyond Goal Saturation should be 95-98%, beyond

that there is no indication for increased that there is no indication for increased FIO2FIO2

– Always consider CPAP first or Non Invasive Always consider CPAP first or Non Invasive Positive Pressure Ventilation FirstPositive Pressure Ventilation First

– Endotrachial Intubation as a last resortEndotrachial Intubation as a last resort

PharmacotherapyPharmacotherapy

• MorphineMorphine

• AnticoagulationAnticoagulation

• VasodilatorsVasodilators

• DiureticsDiuretics

• Beta AntagonistsBeta Antagonists

• Inotropic AgentsInotropic Agents

Morphine Morphine

• Class IIb, BClass IIb, B– Great Early in managementGreat Early in management– VenodilationVenodilation– Mild Arterial DilationMild Arterial Dilation– Slows Heart rate Slows Heart rate

AnticoagulationAnticoagulation

• No evidence to support No evidence to support anticoagulation for Acute Heart anticoagulation for Acute Heart Failure alone Failure alone

• Yes in the case of Atrial FibrillationYes in the case of Atrial Fibrillation

• Yes in the case of LV thrombus Yes in the case of LV thrombus

• Large Placebo Control Trial with Large Placebo Control Trial with Enoxiparin at 40mg SC showed no Enoxiparin at 40mg SC showed no mortality benefitmortality benefit

Vasodilators Vasodilators

• Nitrates: Class I, BNitrates: Class I, B– Improves Cardiac Improves Cardiac

Output and decreases Output and decreases PCWPPCWP

– Best with diureticsBest with diuretics– Low doses, venodilationLow doses, venodilation– High doses, arterial High doses, arterial

dilationdilation– Preload and AfteroadPreload and Afteroad– Good for 16-24 hours Good for 16-24 hours

• Sodium Nitroprusside: Sodium Nitroprusside: Class I, CClass I, C– Severe Heart Failure Severe Heart Failure

with Hypertensionwith Hypertension– Primarily arterial Primarily arterial

dilationdilation– Need for arterial Need for arterial

invasive monitoring invasive monitoring – Stop if active ischemia Stop if active ischemia

due to coronary steal due to coronary steal phenomenon phenomenon

Niseritide Niseritide

• Recombinant B-type Brain Naturetic Recombinant B-type Brain Naturetic Peptide Peptide

• Venous, Arterial and coronary affectsVenous, Arterial and coronary affects

• Enhanced sodium excretionEnhanced sodium excretion

• Suppresses RAAS and sympathetic Suppresses RAAS and sympathetic systemsystem

Vasodilators in the Vasodilators in the Management of Acute Heart Management of Acute Heart Failure Trial (VAMC)Failure Trial (VAMC)DesignDesign Enrolled Enrolled AgentsAgents Primary End Primary End

PointPointOutcomesOutcomes

RandomizedRandomized

Double-Double-Blinded Blinded

ControlControl

Effects at 3 Effects at 3 hourshours

489 489

Acute CHFAcute CHF

PCWP> PCWP> 20mmHg20mmHg

Niseritide Niseritide

Bolus 2 Bolus 2 micr/kg micr/kg

NitroglycerinNitroglycerine IVe IV

Change in Change in PCWP from PCWP from baselinebaseline

Reduced Reduced dyspnea dyspnea compared to compared to standard standard therapy alonetherapy alone

Significant Significant reduction in reduction in dyspnea score dyspnea score and PCWP with and PCWP with addition of addition of NIseritide to NIseritide to standard standard therapytherapy

• No good data to support adverse affects on renal No good data to support adverse affects on renal function and niseritidefunction and niseritide

• Retrospective analysis of VMAC showed potential for Retrospective analysis of VMAC showed potential for increased creatinin with increasing niseritide dose.increased creatinin with increasing niseritide dose.

Summary of Vasodilators Summary of Vasodilators

DiureticsDiuretics• Class I, BClass I, B

Diuretic Resistance can be associated with increased mortality.

UltrafiltrationUltrafiltration

• RAPID-CHF TrialRAPID-CHF Trial– 40 patients40 patients– ADHF and Renal ADHF and Renal

Insufficiency (Cr >1.5)Insufficiency (Cr >1.5)– Ultrafiltration had Ultrafiltration had

significant increase in significant increase in fluid removal after 24 fluid removal after 24 hourshours

– 4650 L vs 2838L4650 L vs 2838L

• UNLOAD TrialUNLOAD Trial– 200 patients200 patients– Renal insufficiency was Renal insufficiency was

not a criteria for not a criteria for inclusioninclusion

– Standard care vs ultra Standard care vs ultra filtrationfiltration

– 48 Hours 4.6 L vs 3.3L48 Hours 4.6 L vs 3.3L– 90 Days fewer 90 Days fewer

rehospitalizations .22 rehospitalizations .22 vs .46 and fewer vs .46 and fewer unscheduled clinic visits unscheduled clinic visits 21 vs 4421 vs 44Option in the setting of failed diuretic and

vasodilator therapy

Beta Blockers Beta Blockers

• No data to support benefits in AHFNo data to support benefits in AHF

• Traditionally considered a contra Traditionally considered a contra indicationindication

• Consider if there is active ischemia and Consider if there is active ischemia and blood pressure tolerates.blood pressure tolerates.

• Ischemia and Tachycardia, Class IIb, CIschemia and Tachycardia, Class IIb, C

• Acute MI after stabilization, Class IIa, BAcute MI after stabilization, Class IIa, B

• Chronic CHF after stabilization, Class I, AChronic CHF after stabilization, Class I, A

Inotropic Agents Inotropic Agents

• Peripheral Hypoperfusion refractory Peripheral Hypoperfusion refractory to vasodilators and diuretics, Class to vasodilators and diuretics, Class IIa, CIIa, C

• Danger: May increase oxygen Danger: May increase oxygen demand and calcium loading demand and calcium loading

Dopamine and DobutamineDopamine and Dobutamine

• Dopamine: Dopamine: – Vasodilator of Renal, Vasodilator of Renal,

Coronary, splanchnic Coronary, splanchnic and Cerebral Vascular and Cerebral Vascular beds beds

– Hypotensive patientsHypotensive patients– Drawbacks: arrhythmia, Drawbacks: arrhythmia,

increased pulmonary increased pulmonary vascular resistance and vascular resistance and increased afterloadincreased afterload

• Dobutamine, Class IIa, CDobutamine, Class IIa, C– Hypotension and low Hypotension and low

Urine outputUrine output– Beta 1 and 2 agonistBeta 1 and 2 agonist– At high doses increases At high doses increases

SVRSVR– Additive effect with Additive effect with

Phosphodiesterase Phosphodiesterase inhibitors inhibitors

– Draw Backs- arrhythmia, Draw Backs- arrhythmia, reflex decrease in reflex decrease in sympathetic tonesympathetic tone

Phosphodiesterase Phosphodiesterase InhibitorsInhibitors• Milrinone and EnoximoneMilrinone and Enoximone

– Hypoperfusion despite Hypoperfusion despite Diuretics and Vasodilators Diuretics and Vasodilators with good blood pressure. with good blood pressure. Class IIb, CClass IIb, C

– Lucitropic, Inotropic, Lucitropic, Inotropic, vasodilatorvasodilator

– Inhibits degredation of Cyclic Inhibits degredation of Cyclic AMPAMP

– Increase CO, CI, Stroke Increase CO, CI, Stroke Volume, Volume,

– Decrease PAP, PVR and PCWPDecrease PAP, PVR and PCWP– Immediate ActionImmediate Action– Effect is Distal to Beta Effect is Distal to Beta

receptors, can be used in the receptors, can be used in the setting Beta Blocker therapy. setting Beta Blocker therapy. Class IIa, CClass IIa, C

Outcomes of a Prospective Trial of Intravenous Outcomes of a Prospective Trial of Intravenous Milrinone For Exacerbations of Congestive Heart Milrinone For Exacerbations of Congestive Heart FailureFailureOPTIME-CHF OPTIME-CHF JAMA 2002JAMA 2002DesignDesign Randomized, Control, Double BlindedRandomized, Control, Double Blinded

Milrinone versus PlaceboMilrinone versus Placebo

EnrolledEnrolled Broad Population with systolic dysfunction Broad Population with systolic dysfunction

Without low output syndromeWithout low output syndrome

949 patients 949 patients

Primary EndpointsPrimary Endpoints Repeat hospitalization for cardiovascular Repeat hospitalization for cardiovascular

causes within 60 days of dischargecauses within 60 days of discharge..OutcomesOutcomes No difference in primary end point between No difference in primary end point between

Milrinone and placebo.Milrinone and placebo.

Higher instance of atrial arrhythmia and Higher instance of atrial arrhythmia and hypotension with Milrinone.hypotension with Milrinone.

Milrinone is associated a 30% increase in Milrinone is associated a 30% increase in mortalitymortality

ConclusionsConclusions Not indicated in routine use with standard Not indicated in routine use with standard medica therapy.medica therapy.

LevosimendanLevosimendan

• Calcium ion Calcium ion sensitizationsensitization

• Also Pimobendon Also Pimobendon

• Increases ContractilityIncreases Contractility

• A little PDI activity as A little PDI activity as wellwell

• Severe dysfunction with Severe dysfunction with preserved blood preserved blood pressurepressure

• Drawback: very pro-Drawback: very pro-arrhythmogenic arrhythmogenic

Clinical TrialsClinical Trials

• LIDO TrialLIDO Trial– Levosimendan 24 hr Levosimendan 24 hr

infiusionvs Dobutamineinfiusionvs Dobutamine– 203 Patients203 Patients– Severe Decompensated Severe Decompensated

HF, AHF, HF after CABGHF, AHF, HF after CABG– Excluded if cardiogenic Excluded if cardiogenic

shockshock– Endpoints, increased CI Endpoints, increased CI

(35% vs 25%) and (35% vs 25%) and reduced PCWP (28% vs reduced PCWP (28% vs 15%) in favor of 15%) in favor of LevosimendanLevosimendan

• SURVIVE TrialSURVIVE Trial• Levosimendan vs Levosimendan vs

Dobutamine 24 hour Dobutamine 24 hour therapytherapy

• 1327 patients1327 patients• Endpoints symptomatic Endpoints symptomatic

relief and BNPrelief and BNP• Levosimendan Greater Levosimendan Greater

reduction in BNP but reduction in BNP but no difference in no difference in symptomatic reliefsymptomatic relief

PressorsPressors

• VasopressinVasopressin: Cardiogenic shock in : Cardiogenic shock in conjunction with inotropic therapyconjunction with inotropic therapy

• Epinephrine Epinephrine B1 and B2, B1 and B2,

• Norepinephrine alpha receptorsNorepinephrine alpha receptors

• Cardiac GlycosidesCardiac Glycosides: Inhibit cardiac : Inhibit cardiac Na/K ATPase, increases Ca/Na Na/K ATPase, increases Ca/Na exchange mechanism. Tachycardia exchange mechanism. Tachycardia induced Cardiomyopathy. induced Cardiomyopathy.

Cardiac and Ventricular Assist Cardiac and Ventricular Assist Devices Devices

Temporary DevicesTemporary Devices

• IABPIABP

• Tandem HeartTandem Heart

• ECMOECMO

• Ventricular Assist DevicesVentricular Assist Devices

IABPIABP

ECMOECMO

• ECMO removes carbon ECMO removes carbon dioxide from and adds dioxide from and adds oxygen to venous blood via oxygen to venous blood via an artificial membrane an artificial membrane lung lung

Severe respiratory failureCardiac Failure with inability to wean off BypassBridge to Cardiac Transplant

Temporary Devices:Temporary Devices:Tandem Heart pVADTandem Heart pVAD• Continuous-flow centrifugal Continuous-flow centrifugal

assist device placed assist device placed extracorporeallyextracorporeally

• Cannula in femoral vein Cannula in femoral vein through intraatrial septum through intraatrial septum into LAinto LA

• Pump withdraws Pump withdraws oxygenated blood from the oxygenated blood from the left atrium, propels it by a left atrium, propels it by a magnetically driven magnetically driven impeller through the impeller through the outflow portoutflow port

• Blood returns into femoral Blood returns into femoral artery via arterial cannulaartery via arterial cannula

Longer-term implantable Longer-term implantable devicesdevices

• NovacorNovacor

• HeartMate XVEHeartMate XVE

• HeartMate IIHeartMate II

• Next Generation DevicesNext Generation Devices

Operative Mortality Prediction Operative Mortality Prediction ScoreScore• Requirement for ventilator Requirement for ventilator

support — 4 points support — 4 points

• Clinical picture of post-Clinical picture of post-cardiotomy shock — 2 points cardiotomy shock — 2 points

• Use of temporary LVAD prior to Use of temporary LVAD prior to Heart-Mate insertion — 2 points Heart-Mate insertion — 2 points

• Central venous pressure >16 Central venous pressure >16 mmHg — 1 point mmHg — 1 point

• Prothrombin time >16 seconds Prothrombin time >16 seconds — 1 point — 1 point

• ScoringScoring– 0-5: Low risk 0-5: Low risk

• Mortality 8%Mortality 8%– 5-7: Intermediate Risk5-7: Intermediate Risk

• Mortality 32%Mortality 32%– 8-10: High Risk8-10: High Risk

• Mortality 49%Mortality 49%

Novacor- Long-term Device Novacor- Long-term Device

Cardiac ReplacementCardiac ReplacementBridge to TransplantBridge to Transplant

Magnetic ActuatorMagnetic ActuatorBlood Propelled via Blood Propelled via

collapsing bladder and to collapsing bladder and to prosthetic valvesprosthetic valves

One Year Survival One Year Survival No risk factors, 60%No risk factors, 60%1 Risk factor, 24%1 Risk factor, 24%

25% risk of Thromboembolic 25% risk of Thromboembolic EventEvent

Heart-mateHeart-mate

• Rehabilitation and hospital dischargeRehabilitation and hospital discharge• $70,000$70,000• LV apex to ascending aortaLV apex to ascending aorta• Textured surface allows for endotheliazation to reduce need for Textured surface allows for endotheliazation to reduce need for

anticoagulationanticoagulation• Improves perfusion: decrease renal failure and pulmonary HTNImproves perfusion: decrease renal failure and pulmonary HTN• Complications: infection, bleeding, monomorphic VT, RV failure and Aortic Complications: infection, bleeding, monomorphic VT, RV failure and Aortic

Stenosis Stenosis

HeartMate IIHeartMate II

Suggested Reading Suggested Reading

• Randomized evaluation of Mechanical Assistance Randomized evaluation of Mechanical Assistance for Treatment of Chronic Heart Failure (Rose et al. for Treatment of Chronic Heart Failure (Rose et al. NEJM 2001)NEJM 2001)

• Evaluation and management of patients with Evaluation and management of patients with acute decompensated heart failure. Journal of acute decompensated heart failure. Journal of Cardiac Failure. Vol.12 No. 1 2006Cardiac Failure. Vol.12 No. 1 2006

• Medical Management of Advanced Heart Failure. Medical Management of Advanced Heart Failure. JAMA, February 6,2002- Vol. 27, No. 5JAMA, February 6,2002- Vol. 27, No. 5

• http://www.med.umich.edu/AnesCriticalCare/Docuhttp://www.med.umich.edu/AnesCriticalCare/Documents/Rosenberg_Circulatory_Assist_Devices.pdfments/Rosenberg_Circulatory_Assist_Devices.pdf

• http://texasheart.org/Research/Devices/http://texasheart.org/Research/Devices/thoratec_heartmateii.cfmthoratec_heartmateii.cfm

http://www.med.umich.edu/AnesCriticalCare/Documents/Rosenberg_Circulatory_Assist_Devices.pdf

http://www.med.umich.edu/AnesCriticalCare/Documents/Rosenberg_Circulatory_Assist_Devices.pdf

Thank you!Thank you!

• Special Thanks to Special Thanks to – Dr. Chad Feldman, Associate Director of Dr. Chad Feldman, Associate Director of

Medicine Advocate Christ HospitalMedicine Advocate Christ Hospital– Dr. Ali Zadi, Clinical Instructor, Dr. Ali Zadi, Clinical Instructor,

Cardiology FellowCardiology Fellow– Dr. Saba Khan, Heart Failure FellowDr. Saba Khan, Heart Failure Fellow