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ACUTE HEART FAILURE
Julie Gorchynski MD, MSc, FACEP, FAAEM
Department of Emergency MedicineEmergency Residency Program
UTHSC, San AntonioTCEP 2014
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