Download 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…
Lee DS, Am. J. Med. 2004
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
Vascular
Failure
Acute
Cardiac
Failure
• Congestion (Chest X-Ray)
+++
• Background Chronic HF
0/+
++
+++
• High BP at admission
+++
0/+
• Low CVS perfusion
+
+++
• Reduced EF (echo)
+
+++
+
• Weight  / Leg edema
• Neurohormonal/Inflammatory
+++
Activation
• Causal factor
(Infection)
+++
+++
++
+
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).
Acute (Cardiac) Heart Failure
Decreasing Cardiac
Inflammatory/
Contractility (Cpo)
Neurohormonal Activation
“Low CVS
perfusion”
Forward Failure
(Effective Blood Volume )
Over Diuresis
Renal Impairment /
Fluid Accumulation (3-4 Kg)
Wedge 
Compliance
Pulmonary
Congestion
Diastolic
Dysfunction
Arterial Resistance/
Stiffness 
Central Fluid
Redistribution
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
J Am Coll Cardiol 2004;44:340–8
1.0
Estimated In-hospital Proportion Dead
0.9
0.8
0.7
0.6
0.5
0.4
0.3
0.2
0.1
0.0
0.2
0.4
0.6
0.8
1.0
1.2
1.4
1.6
1.8
Cardiac Power Output [(Mean Arterial Pressure*Cardiac Output)/451]
2.0
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.
Acute (Vascular) Heart Failure
Low Cardiac Contractility
Inflammatory/
Reserve (Cpo)
Neurohormonal Activation
“Low CVS
“small Tn Release”
perfusion”
Forward Failure
(Effective Blood Volume )
Over Diuresis
Renal Impairment /
Fluid Accumulation (0-2 Kg)
Arterial Resistance/
Stiffness 
Wedge 
Pulmonary
Congestion
Diastolic
Dysfunction
Central Fluid
Redistribution
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? –
ET-1 and IL-6 levels in patients admitted with AHF at
baseline (0), 2 and 60 days follow-up.
Milo, Cotter, et. al. Am. J. Cardiol. 2003
Evaluation of
AHF Severity in
the ER
Measuring circulatory and
Respiratory Failure
Low Cardiac Contractility
Reserve (Cpo)
“Low CVS
Inflammatory/
Neurohormonal Activation
perfusion”
Forward Failure
(Effective Blood Volume )
Arterial Resistance/
Stiffness 
Renal Impairment /
Pulmonary
Congestion
Central Fluid
Redistribution
Severity of congestion =
Admission SO2
Recurrent HF/Death
Death
Circulatory failure = Admission
Sys BP
Recurrent HF/Death
Death
Combined circulatory and
respiratory failure = Admission
Sys BP and SO2
Recurrent HF/Death
Death
Combined SEVRE circulatory and
respiratory failure = Admission Need
for pressors or mechanical ventilation
Recurrent HF/Death
Death
Laboratory Evaluation
Low Cardiac Contractility
Reserve (Cpo)
“Low CVS
Inflammatory/
Neurohormonal Activation
perfusion”
Forward Failure
(Effective Blood Volume )
Arterial Resistance/
Stiffness 
Renal Impairment /
Pulmonary
Congestion
Central Fluid
Redistribution
Simple way to measure neurohormoanl
activation - Na+ and Glucose
Cotter et al JCF 2006
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
Hazard
Ratio
95 %
Confidence
Interval
Chisquare
PValue
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
Hazard
Ratio
95 %
Confidence
Interval
ChiSquare
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
Echocardiographic
Evaluation
LV Ejection Fraction
During Acute Pulmonary Edema
Echo - Changes in Ejection Fraction
During Recovery from Pulmonary Edema
0.80
0.60
0.40
0.20
0.00
0.00
0.20
0.40
0.60
0.80
LV Ejection Fraction After Treatment
Ghandi et al, NEJM 2001
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
Conclusions
 ONCE 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