ACUTE HEART FAILURE Julie Gorchynski MD, MSc, FACEP, FAAEM Department of Emergency Medicine Emergency Residency Program UTHSC, San Antonio TCEP 2014
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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 comorbidities 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 AHF Nesiritide: 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 rehospitalization 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 decompensated systolic or diastolic CHF Normal blood pressure Develops over days or weeks Chronic HF Systemic congestion Primarily Pulmonary congestion Minimal Agents Loop diuretics First- line therapy Peripheral edema Common
Hypotensive AHF Low cardiac output Sbp < 100 mmhg EF < 20% Decreased renal function Poor renal blood flow Congestion Subtle Cardiogenic shock Extreme form Agents Dobutamine First line treatment ALOC, lethargy, abdominal pain, muscle aches
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 ESC 2013 (+) ATOMIC HF (+) (+) Intracellular Ca2+ not increased No pro-arrhythmic potential COSMIC-HF Ongoing Oral form Improved stroke volume
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 Normotensive Hypotensive < 100 Vasodilator Loop diuretic Inotrope Initiate therapy early CPAP/ BIPAP Future agents Initiate in ED
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