Working Group of Heart Failure and Cardiac Function
Download
1 / 30

HEART FAILURE: WHAT CAN A PHYSIOLOGIST TELL THE CLINICIANS? Robert Naeije - PowerPoint PPT Presentation


  • 121 Views
  • Uploaded on

Working Group of Heart Failure and Cardiac Function Second Annual Symposium, Woluwe, 14th of October 2006. HEART FAILURE: WHAT CAN A PHYSIOLOGIST TELL THE CLINICIANS? Robert Naeije Erasme University Hospital, Brussels, Belgium. What is heart failure

loader
I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
capcha
Download Presentation

PowerPoint Slideshow about ' HEART FAILURE: WHAT CAN A PHYSIOLOGIST TELL THE CLINICIANS? Robert Naeije' - nuala


An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.


- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
Working Group of Heart Failure and Cardiac FunctionSecond Annual Symposium, Woluwe, 14th of October 2006

HEART FAILURE: WHAT CAN A PHYSIOLOGIST TELL THE CLINICIANS?

Robert Naeije

Erasme University Hospital, Brussels, Belgium


What is heart failure

We define heart failure as a state in which the heart is unable to meet the demands for blood flow without excessive use of the Frank-Starling mechanism, that is the increase in stroke volume associated with increased preload

Sagawa, Maughan, Suga, Sunagawa.

Cardiac Contraction and the Pressure-Volume Relationship. Oxford University Press, 1988


Definition of heart failure
Definition of Heart Failure

  • Excessive use of the Frank-Starling mechanism: dilated cardiomyopathy and congestion – adaptation vs maladaptation or decompensation

  • Inability to meet peripheral demand: decreased aerobic exercise capacity – decreased VO2max (or maximum average running speed), because of a limitation in cardiac output


O Frank 1865-1944

Isometric contractions of a frog ventricle at increasing filling pressures O. Frank, Z Biol1895; 32:370


Ventricular PV curves during ejecting vs non-ejecting beats

Isobaric end-systolic PV

relationship positioned to

the right of the isovolumic

end-systolic PV curve

indicating strong history-

dependence of the end-

systolic PV curve – But

in canine and human hearts,

both curves are superposed

Frank O. Die Grundform des arteriellen Pulses

Z Biol 1899; 37:484-526


Frog ventricle

Dog ventricle

Squelettal muscle

Isovolumic diastolic and systolic PV relationships



Sequential P-V loops

Contractility

Emax

Pes/Ves

Afterload = PxV

or: Pes/SV

Pressure

Decreased

venous return

Preload = EDV

Volume

SV




Stroke volume increases with end-diastolic volume preparation - 1910

Patterson et al, J Physiol (London) 1914; 48:357


An increase in preload increases stroke volume preparation - 1910

SV ~ EDV EF = SV / ED increased


Stroke work increases with end-diastolic volume preparation - 1910

Patterson et al, J Physiol (London) 1914; 48:357


An increase in blood pressure decreases stroke volume (1) preparation - 1910

which is restored by a an adaptative increase in EDV (2)

SV is initially

decreased, then

restored with

adaptative  EF

to increased

afterload


A decrease in contractility decreases stroke volume preparation - 1910

1: increased contractility 2: decreased contractility


Starling s law of the heart
Starling ’s law of the heart preparation - 1910

Now here are two conditions in which the work of the heart is increased and in which this organ adapts itself by increasing the chemical changes in its muscle at each contraction to the increased demands made upon it. It is evident that there is one factor which is common to both cases, and that is the increased volume of the heart when it begins to contract. So we may make the following general statement. Within physiological limits, the larger the volume of the heart, the greater are the energy of its contraction and the amount of chemical change at each contraction.

EH Starling. The Linacre lecture on the law of the heart. London: Longmans, Green, 1918


Heterometric vs homeometric autoregulation of the heart preparation - 1910

After 60 s of increased loading conditions, return to initial state is

associated with decreased EDV and ESV, suggesting increased

contractility Patterson et al, J Physiol (London) 1914; 48:357


Heterometric vs homeometric autoregulation of the heart preparation - 1910

Source: Rosenblueth et al. Arch Int Physiol 1959; 67: 358


Limitations to starling s law of the heart
Limitations to Starling’s law of the heart preparation - 1910

  • Frank-Starling’s law of the heart states that ventricular stroke work increases as a function of end diastolic volume

  • This is valid for the rapid adaptation of flow output to changing loading conditions

  • Otherwise, the essence of ventricular adaptation to loading conditions is homeometric (systolic function, Anrep’s relationship) rather than heterometric (change in dimensions, Starling’s relationship)


What is heart failure preparation - 1910

We define heart failure as a state in which the heart is unable to meet the demands for blood flow without excessive use of the Frank-Starling mechanism, that is the increase in stroke volume associated with increased preload

Sagawa, Maughan, Suga, Sunagawa.

Cardiac Contraction and the Pressure-Volume Relationship. Oxford University Press, 1988


Heart failure preparation - 1910

Type 1:

increased loading

Type 2:

altered inotropic state

Type 3

altered lusitropic state

Sagawa, Maughan, Suga, Sunagawa.

Cardiac Contraction and the Pressure-Volume Relationship. Oxford University Press, 1988


Definition of heart failure1
Definition of Heart Failure preparation - 1910

  • Excessive use of the Frank-Starling mechanism: dilated cardiomyopathy and congestion – adaptation vs maladaptation or decompensation

  • Inability to meet peripheral demand: decreased aerobic exercise capacity – decreased VO2max (or maximum average running speed), because of a limitation in cardiac output


Vo 2 q x cao 2 cvo 2
VO preparation - 19102 = Q x (CaO2 – CvO2)

  • A VO2max is achieved on a bicycle with about half of body’s muscles

  • Minimum CvO2 is constant – cf HbO2 dissociation curve, and chronic disease

    (except sepsis?) does not affect O2 extraction

  • VO2max is determined by maximum O2 delivery, or cardiac output

    VO2max ~ Qmax x CaO2

Fleg et al, AHA advisory Circulation 2000;102:15917


Aerobic exercise capacity is determined by o 2 delivery q x cao 2
Aerobic exercise capacity is determined by O preparation - 19102 delivery Q x CaO2

Source: Saltin and Strange, MSSE 1992; 24: 30-37


Linear increase in VO preparation - 19102 and Q as a function of workload


Exercise testing: linear relationship between VO preparation - 19102 (or cardiac output) and running speed (workload)


VO preparation - 19102max and the Cooper test (12 min run)

Cooper et al, JAMA 1968; 203: 201-4


Six min walk distance and cpet in heart failure
Six-min Walk Distance and CPET in heart failure preparation - 1910

Miyamoto et al, AJRCCM 2000; 161: 487-492

VO2/HR = SV


Rationale for exercise testing to evaluate heart failure
Rationale for exercise testing to evaluate heart failure preparation - 1910

  • Linear relationships between VO2, cardiac output and workload, or average running or walking speed

  • VO2max or 6MWD exclusively determined by maximum cardiac output, - or the ability of systolic function to cope with increased afterload

  • This is why the 6MWD is correlated to functional class, survival, and clinical state, and is sensitive to therapeutic interventions

Fleg et al, AHA advisory Circulation 2000;102:15917


Conclusions
Conclusions preparation - 1910

  • A sound definition of heart failure rests on the notion of changes in loading conditions and/or relative insufficiency of systolic/diastolic adaptation, as a cause of insufficient flow output (O2 delivery, Q x CaO2) to peripheral demand (VO2)

  • Associated changes in ventricular dimensions and diastolic function may be a cause of congestion

  • Heart failure is a continuum, with uncertain significance of clinical notions of compensation or decompensation


ad