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Acute Heart Failure. Approach to the Patient in The Emergency Room Gad Cotter MD. Disclosure: Grants from Actelion , Novacardia , Merck, Cytokinetics /Amgen, Cardio3, Bioheart, Nile thera, Corthera, Bioheart, Novartis, Travena, NIH. …The Reality. Higher than COPERNICUS Almost at REMACH…. - PowerPoint PPT Presentation
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Approach to the Patient in The Emergency Room
Gad Cotter MD.Disclosure: Grants from Actelion , Novacardia ,
Merck, Cytokinetics /Amgen, Cardio3, Bioheart, Nile thera, Corthera, Bioheart,
Novartis, Travena, NIH.
…The Reality
Lee DS, Lee DS, Am. J. Med. 2004Am. J. Med. 2004
Higher than COPERNICUS
Almost at REMACH…
Higher than COPERNICUS
Almost at REMACH…
It is really not about weight gain or fluid accumulation….
Classification By Syndrome
Classification to specific Syndromes Acute Heart Failure (Suggested new name: Acute
vascular failure - AVF): Rapidly evolving pulmonary congestion + blood pressure rapid respiratory failure, multi-organ failure and death. (Elderly, female, preserved EF, mild chronic CHF)
Acute Decompensated Heart Failure - ADHF: Slow deterioration in severe chronic heart failure, slowly progressive low cardiovascular perfusion and
pulmonary congestion, accompanied by relatively blood pressure, peripheral edema and weight gain. (Younger, male, low EF, significant background CHF)
Other: Acute coronary syndromes, arrhythmias (mostly A.Fib),High output failure, RV Failure.
How do we tell them apart ?
Acute Acute Vascular Vascular
FailureFailure
Acute Acute CardiacCardiac FailureFailure
• Background Chronic HF 0 / + +++
• Congestion (Chest X-Ray) +++ ++
• Low CVS perfusion + +++
• High BP at admission +++ 0/+
• Neurohormonal/Inflammatory Activation
+++ ++
• Causal factor (Infection)
+++ +
• Weight / Leg edema + +++
•Reduced EF (echo) + +++
M. Metra (Brescia) European Working Group on AHF
Classification to specific Syndromes
Acute “Cardiac” Heart Failure
The “core mechanism” is a deterioration in cardiac contractility (“Cardiac Power”) caused by either acute processes (Ischemia, Arrhythmia) or slow processes (LV remodeling and progressive myocardial cell loss).
Central FluidRedistribution
Acute (Cardiac) Heart Failure
PulmonaryCongestion
Wedge
Forward Failure(Effective Blood Volume )
Renal Impairment /Fluid Accumulation (3-4 Kg)
Inflammatory/
Neurohormonal Activation “Low CVS
perfusion”
Arterial Resistance/ Stiffness
Diastolic Dysfunction
Over Diuresis
Decreasing Cardiac Contractility (Cpo)
Compliance
What is Cardiac Power?
Cardiac Power is the measure of left ventricular systolic contractility power and is calculated by incorporating flow and pressure domains of the CV system; Hence:
Cardiac Power Output = Cardiac Output * Mean Arterial Blood Pressure
Cpo = MAP * CO
What is the Range of Cpo?
Cotter, Tan et.al. Curr. Opinion. Card 2003
Cardiac power for the diagnosis of Acute hemodynamic instability instability
Cotter, Tan et al. Curr Opin Cardiol 2003, 18:215–222
Cardiac Power Output [(Mean Arterial Pressure*Cardiac Output)/451]
Estim
ate
d I
n-h
osp
ita
l P
rop
ort
ion
De
ad
0.2 0.4 0.6 0.8 1.0 1.2 1.4 1.6 1.8 2.0
0.0
0.1
0.2
0.3
0.4
0.5
0.6
0.7
0.8
0.9
1.0
J Am Coll Cardiol 2004;44:340–8
Predicting Recurrent HF and Death:
Cotter, Tan et al. Curr Opin Cardiol 2003, 18:215–222
Chronic Heart Failure
Acute “Vascualr” Heart Failure
The “core mechanism” is an abrupt increase in vascular stiffness/resistance, probably secondary to neurohormonal/inflammatory excessive activation in response to “normal” insults such as minor infections.
Central FluidRedistribution
Acute (Vascular) Heart Failure
PulmonaryCongestion
Wedge
Forward Failure(Effective Blood Volume )
Renal Impairment /Fluid Accumulation (0-2 Kg)
Inflammatory/
Neurohormonal Activation “Low CVS
perfusion”
Arterial Resistance/ Stiffness
Diastolic Dysfunction
Over Diuresis
Low Cardiac Contractility Reserve (Cpo)
“small Tn Release”
First admission Systolic BP in patients admitted for AHF in a “real life” community center
Cotter et al. European Journal of Heart Failure 9 (2007) 178–183
Inflammation and Neurohormonal Activation in AHF:Cause for Arterial Stiffness/Vascular resistance, Decreased Contractility and Diastolic Dysfunction? –
Milo, Cotter, et. al. Am. J. Cardiol. 2003
ET-1 and IL-6 levels in patients admitted with AHF at baseline (0), 2 and 60 days follow-up.
Measuring circulatory and Respiratory Failure
Central FluidRedistribution
PulmonaryCongestion
Forward Failure(Effective Blood Volume )
Renal Impairment /
Inflammatory/
Neurohormonal Activation
Arterial Resistance/ Stiffness
Low Cardiac Contractility Reserve (Cpo)
“Low CVS
perfusion”
Severity of congestion = Admission SO2Recurrent HF/Death Death
Circulatory failure = Admission Sys BPRecurrent HF/Death Death
Combined circulatory and respiratory failure = Admission Sys BP and SO2Recurrent HF/Death Death
Combined SEVRE circulatory and respiratory failure = Admission Need for pressors or mechanical ventilationRecurrent HF/Death Death
Laboratory Evaluation
Central FluidRedistribution
PulmonaryCongestion
Forward Failure(Effective Blood Volume )
Renal Impairment /
Inflammatory/
Neurohormonal Activation
Arterial Resistance/ Stiffness
Low Cardiac Contractility Reserve (Cpo)
“Low CVS
perfusion”
Simple way to measure neurohormoanl activation - Na+ and Glucose
Cotter et al JCF 2006Cotter et al JCF 2006
Cardiology 2010 in Print
Simple way to measure inflammatory activation – Lymphocyte ratio of WBC differential
Other Lab Predictors at admission
Troponin?BNP ?Endothelin ?Others ?
Baseline Model Predicting Time to Death Adding Troponin Levels
Term HazardRatio
95 %Confidence
Interval
Chi-square
P-Value
Troponin T (per 0.1) 1.839 1.361, 2.485 15.74 <.0001
BNP (log) 1.395 1.064, 1.829 5.80 0.0160
Baseline Model Predicting Time to Death or Re-hospitalization Adding Troponin Levels
Term HazardRatio
95 % Confidence
Interval
Chi-Square
P-Value
Troponin T (per 0.1) 1.372 1.165, 1.617 14.27 0.0002
Six-minute-walk (per 100 ft) 0.942 0.885, 1.002 3.58 0.0586
No walk (relative to walkers)
0.937 0.545, 1.611 0.06 0.8131
Ghandi et al, NEJM 2001
Echo - Changes in Ejection Fraction During Recovery from Pulmonary Edema
0.80
0.60
0.40
0.20
0.00
LV
Eje
ctio
n F
ract
ion
Du
ring
Acu
te P
ulm
ona
ry E
de
ma
LV Ejection Fraction After Treatment0.00 0.20 0.40 0.60 0.80
Echocardiographic Changes During Recovery from Pulmonary Edema
Measures of dyastolic dysfunction improved during follow up: E/A ratio (1.3±0.8 to 1.5 ± 1.0) and E-wave declaration (174 ± 62 to 194 ± 62).
The authors concluded that: “... high BP related wedge pressure increase caused diastolic dysfunction in these patients … and …no changes in EF occurred during the acute heart failure episode”.
Choen-Solal et al in a study of patients with AHF: “…LVEF was poorly predictive while the predischarge Doppler mitral pattern was strongly associated with death or re-admission..”
Ghandi et al, NEJM 2001, Choen-Solal et al JACC 2004
ConclusionsONCE AHF IS DIAGNOSED - Evaluation in
the ER should include:Variables related to respiratory and
circulatory failure – mostly oxygen saturation and BP
Lab – Sodium, glucose, kidney function , WBC count with diferencial and possibly BNP and troponin
Echocardiography – to rule out mechanical complications, PE, possibly to evaluate severity of diastolic dysfunction