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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….

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acute heart failure

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
…The Reality

Higher than COPERNICUS

Almost at REMACH…

Lee DS, Am. J. Med. 2004

so what is it about

So what is it about????

Classification By Syndrome

classification to specific syndromes
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
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

acute cardiac heart failure
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).
slide11

Acute (Cardiac) Heart Failure

Decreasing Cardiac Contractility (Cpo)

Inflammatory/

Neurohormonal Activation

“Low CVS

perfusion”

Forward Failure

(Effective Blood Volume )

Over Diuresis

Arterial Resistance/ Stiffness 

Renal Impairment /

Fluid Accumulation (3-4 Kg)

Wedge 

Compliance

Diastolic Dysfunction

Central Fluid

Redistribution

Pulmonary

Congestion

what is cardiac power
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
What is the Range of Cpo?
  • Cotter, Tan et.al. Curr. Opinion. Card 2003
cardiac power for the diagnosis of acute hemodynamic instability instability
Cardiac power for the diagnosis of Acute hemodynamic instability instability

Cotter, Tan et al. Curr Opin Cardiol 2003, 18:215–222

predicting recurrent hf and death
Predicting Recurrent HF and Death:

Cotter, Tan et al. Curr Opin Cardiol 2003, 18:215–222

acute vascualr 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.
slide19

Acute (Vascular) Heart Failure

“small Tn Release”

Low Cardiac Contractility

Reserve (Cpo)

Inflammatory/

Neurohormonal Activation

“Low CVS

perfusion”

Forward Failure

(Effective Blood Volume )

Over Diuresis

Arterial Resistance/ Stiffness 

Renal Impairment /

Fluid Accumulation (0-2 Kg)

Wedge 

Pulmonary

Congestion

Diastolic Dysfunction

Central Fluid

Redistribution

first admission systolic bp in patients admitted for ahf in a real life community center
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

slide21

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

measuring circulatory and respiratory failure
Measuring circulatory and Respiratory Failure

Low Cardiac Contractility

Reserve (Cpo)

Inflammatory/

Neurohormonal Activation

“Low CVS

perfusion”

Forward Failure

(Effective Blood Volume )

Arterial Resistance/ Stiffness 

Renal Impairment /

Pulmonary

Congestion

Central Fluid

Redistribution

combined circulatory and respiratory failure admission sys bp and so2
Combined circulatory and respiratory failure = Admission Sys BP and SO2

Recurrent HF/Death

Death

slide28
Combined SEVRE circulatory and respiratory failure = Admission Need for pressors or mechanical ventilation

Recurrent HF/Death

Death

laboratory evaluation
Laboratory Evaluation

Low Cardiac Contractility

Reserve (Cpo)

Inflammatory/

Neurohormonal Activation

“Low CVS

perfusion”

Forward Failure

(Effective Blood Volume )

Arterial Resistance/ Stiffness 

Renal Impairment /

Pulmonary

Congestion

Central Fluid

Redistribution

slide32

Simple way to measure inflammatory activation – Lymphocyte ratio of WBC differential

  • Cardiology 2010 in Print
other lab predictors at admission
Other Lab Predictors at admission
  • Troponin?
  • BNP ?
  • Endothelin ?
  • Others ?
baseline model predicting time to death or re hospitalization adding troponin levels
Baseline Model Predicting Time to Death or Re-hospitalization Adding Troponin Levels
slide37

Echo - Changes in Ejection Fraction During Recovery from Pulmonary Edema

0.80

0.60

LV Ejection Fraction

During Acute Pulmonary Edema

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
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
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