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