ACUTE HEART FAILURE

Julie Gorchynski MD, MSc, FACEP, FAAEM

Department of Emergency MedicineEmergency Residency Program

UTHSC, San AntonioTCEP 2014

No disclosures

Objectives

• Overview

• Cases

• Current Therapy

• Risk stratification: phenotypes

• AHF studies

• Future therapeutic agents

Case 1

• 78 yo male c/o SOB

• 187/92 – 32- 88% RA – 98.6F

• PE: JVD, rales, peripheral edema

• A. Diuretic, NTG, CPAP

• B. Diuretic, CPAP

• C. NTG, CPAP

• D. Dobutamine, CPAP

Case 2

• 78 yo male c/o SOB

• 132/67– 32- 88% RA – 98.6F

• PE: JVD, peripheral edema

• A. Diuretic, NTG, CPAP

• B. Diuretic, CPAP

• C. NTG, CPAP

• D. Dobutmaine, CPAP

Case 3

• 78 yo male c/o SOB

• 89/46– 32- 88% RA – 98.6F

• PE: JVD, rales, peripheral edema, ALOC

• A. Diuretic, NTG, CPAP

• B. Diuretic, CPAP

• C. NTG, CPAP

• D. Dobutamine, CPAP

AHF: Epidemic

• Major public health concern

• Hospitalizations• 1 million /year

• 80% via ED

• Cost: $32 billion/year

• Significant M&M

• High recidivism

Hospitalization

• Predicts early death and readmissions

• Mortality rates

• 5-15 x more likely to die first year

• 3 – 6 months mortality 10%-20%

• I year mortality 22%-32%

• Recurrent admissions for decomposition

• 35% readmitted at 60-90 days

Current Therapies

• 40 years• Modestly effective at best • Same medications

• NTG, Diuretics, Inotropes

• Not improve • In-hospital or • Post-discharge survival rates or • Decreased readmissions

• No mitigation in mortality rate

• Unlike ACS and CVA

Acute Heart Failure

• NOT a single disease entity

• Single therapy NOT efficacious

• Individualize therapy

• Not everyone gets

• Diuretic

• Vasodilator

• Inotrope

• Recognize: syndrome

• Heterogeneous

• Numerous co-morbidities

• Emphasis

• Clinical phenotypes

• Therapy

• Clinical findings and

• Initial systolic blood pressure

Current HF Therapies

Chronic LV HF

• Well established guidelines

• ARBs, ACEI, beta-blocker

• Improved outcomes

AD HF

• No improvement in outcomes

• Loop diuretics• Class I recommendation

• Vasodilators

• Inotropes

• Short term feel better

• No long term impact

Acute Heart Failure

• CONGESTION• Majority

• Pulmonary or systemic congestion

• Caused by elevated LV filling pressure

• SOB, JVD, peripheral edema

• EF > 50% : “preserved” LV systolic function

• LOW CARDIAC OUTPUT• Uncommon but high mortality rate

• Circulatory failure

• Fatigue, N/V, ALOC, SOB, reduced exercise capacity

• Severe LV systolic dysfunction

• EF < 20%

Precipitating Factors in AHF

Cardiac

• Afib with RVR

• Ischemia, ACS

• Arrhythmias

• Valvular disease

• Myopathies

• Uncontrolled HTN

Non-cardiac

• COPD, Asthma, Pneumonia

• Noncompliance

• CRI, Anemia

• TH, DM

• CVA

• Surgery

• Alcohol, Drugs

Therapeutic Goals

• Improve signs and symptoms

• ED

• First 6-12 hours

• Improve quality of life

• Short term

• Improve post discharge outcomes

• Long term

Treatment Emphasis

• Initiate early therapy

• Maintain oxygenation

• Prevent intubation

• Improve clinical symptoms

• Prevent infarction

AHF Disease Stratification

• 3 phenotypes

• Based on systolic blood pressure on presentation

• Hypertensive

• Normotensive

• Hypotensive

Target therapy by phenotype

Systolic BP (mmHg)

• Hypertensive > 160

• Normotensive

• Hypotensive < 100

First agent

• Vasodilators

• Loop diuretics

• Inotropes

Hypertensive AHF

• Vascular failure

• Sbp > 160 mm Hg

• Develops over hours

• Preserved EF > 50%

• Increased SVR

• Pulmonary congestion

• respiratory distress,

rales, orthopnea

• O2 saturation < 90%

• Pulmonary edema

• Extreme form

• Agents

• Vasodilators

• First line treatment

• Adjunct therapy

• Loop diuretics

Pharmacological therapy:

HTN AHFNesiritide: rBNP

• VMAC study (+)

• ASCEND-HF trial (+/--)

• Rose study (-)

• Neutral

• Neither unsafe or efficacious

Serelaxin: rHR-2

• RELAX-AHF (+) • Peptide regulates

maternal adaptation to pregnancy

• Reduces signs and symptoms of congestion

• Reduces 180-day CV mortality

• Reduces all cause mortality by 37%

Vasodilators

Serelaxin

• Increases renal function

• Improves vascular compliance

• Improves cardiac output

Relaxin

• Improves dyspnea

• Improves congestion

• No improvement in re-hospitalization rate

• PRE-RELAX-AHF (+)

• RELAX-AHF 2

Serelaxin and Relaxin

• Beneficial effects on dyspnea and post discharge clinical outcomes • Decreased LOS• Decrease in worsening of HF inpatient• Improved signs and symptoms inpatient• Supported by biomarker changes

• Hs-Toponin T, Cystatin C, NT- proBNP

• Given early • Within 16 hours (window of time)

• Prevent end-organ damage

• Long-term end organ protection• No benefit

Normotensive AHF

• Acutely decompensatedsystolic or diastolic CHF

• Normal blood pressure

• Develops over days or weeks

• Chronic HF

• Peripheral edema• Common

• Systemic congestion • Primarily

• Pulmonary congestion• Minimal

• Agents• Loop diuretics • First- line therapy

Hypotensive AHF

• Low cardiac output

• Sbp < 100 mmHg

• EF < 20%

• Decreased renal function• Poor renal blood

flow

• ALOC, lethargy, abdominal pain, muscle aches

• Congestion• Subtle

• Cardiogenic shock• Extreme form

• Agents• Dobutamine• First line treatment

Pharmacological Therapy:

Hypotensive AHF

• Inotrope: mainstay

• Enhance cardiac contractility

• Dobutamine, milrinone, levosimendan (Europe)

• Alleviate symptoms

• Compromised vital organ perfusion and hypotension

• DAD-HF trial and ROSE trial: dopamine (-)

• Milrinone and Levosimendan

• serious adverse effects

• Limited efficacy in improving signs and symptoms

• OMTIME-CHF

• Milrinone : first large scale (-)

• REVIVE-1 and REVIVE-2 trials and SURVIVE study

• Levosimendan : (-)

• Dobutamine (-)

Omecamtiv mecarbil

• Novel inotropic agent

• Cardiac myosin activator

• Direct effects on sarcomere

• Dyspnea response rate improved

• Improved stroke volume

• ESC 2013 (+)

• ATOMIC HF (+)

• (+) Intracellular Ca2+ not increased

• No pro-arrhythmic potential

• COSMIC-HF

• Ongoing

• Oral form

CART analysis and ADHERE data

• Correlation of systolic BP and outcomes for AHF

• Sbp < 115 mmHg

• Worse in-hospital prognosis

• Sbp > 160 mm Hg

• Good myocardial contractile reserve

• Better outcomes

• Pharmacological agents

• Currently initiated

• In-hospital 24 hours

• Implement early

• < 16 hours in ED

Non-invasive ventilation

• CPAP vs BIPAP

• Maintain oxygenation

• Prevent intubation

• Feel better faster• Clinically oriented outcome• Decreases work of breathing• Increases intra-thoracic pressures > cardiac output• Studies

• Neutral but lack of harm

BIOMAKERS

• BNP• Delta

• Fall of 30%

• NT-pro BNP

• Higher levels• Poor prognosis

• Identify high risk patients

• Aggressive therapy

• Disease severity

• Troponin

• Cr and Cystatin C• Renal marker for injury

• ST2 • fibrosis markers

• heart

• Galectin-3 • fibrosis markers

• Heart

• Copeptin: newest

• Vasopressin peptide

• Hormone in HF

• Tailor therapy• Receptor vasopressin

antagonist

Case 1

• 78 yo male c/o SOB

• 187/92 – 32- 88% RA – 98.6F

• PE: JVD, rales, peripheral edema

• A. Diuretic, NTG, CPAP

• B. Diuretic, CPAP

• C. NTG, CPAP

• D. Dobutamine, CPAP

Case 2

• 78 yo male c/o SOB

• 132/67– 32- 88% RA – 98.6F

• PE: JVD, peripheral edema

• A. Diuretic, NTG, CPAP

• B. Diuretic, CPAP

• C. NTG, CPAP

• D. Dobutmaine, CPAP

Case 3

• 78 yo male c/o SOB

• 89/46– 32- 88% RA – 98.6F

• PE: JVD, rales, peripheral edema, ALOC

• A. Diuretic, NTG, CPAP

• B. Diuretic, CPAP

• C. NTG, CPAP

• D. Dobutmaine, CPAP

Overview

• Heterogenous syndrome

• Based on 3 phenotypes • HTN > 160 Vasodilator• Normotensive Loop diuretic• Hypotensive < 100 Inotrope

• Initiate therapy early

• CPAP/ BIPAP

• Future agents• Initiate in ED

Questions