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
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
1.
2.
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 Biol 1895; 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 historydependence of the endsystolic 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
Length-tension relationship applied to the intact ventricle
Pressure
Sequential P-V loops
Contractility
Emax
Pes/Ves
Afterload = PxV
or: Pes/SV
Decreased
venous return
Preload = EDV
SV
Volume
EH Starling in his laboratory, at work on his heart-lung preparation - 1910
Patterson et al, J Physiol (London) 1914; 48:357
Stroke volume increases with end-diastolic volume
Patterson et al, J Physiol (London) 1914; 48:357
An increase in preload increases stroke volume
SV ~ EDV
EF = SV / ED increased
Stroke work increases with end-diastolic volume
Patterson et al, J Physiol (London) 1914; 48:357
An increase in blood pressure decreases stroke volume (1)
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
1: increased contractility 2: decreased contractility
Starling ’s law of the heart
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
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
Source: Rosenblueth et al. Arch Int Physiol 1959; 67: 358
Limitations to Starling’s law of the heart
• 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
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
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 Failure
1.
2.
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
VO2 = 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 O2 delivery Q x CaO2
Source: Saltin and Strange, MSSE 1992; 24: 30-37
Linear increase in VO2 and Q as a function of workload
Exercise testing: linear relationship between VO2 (or cardiac
output) and running speed (workload)
VO2max and the Cooper test (12 min run)
Cooper et al, JAMA 1968; 203: 201-4
Six-min Walk Distance and CPET in heart
failure
Miyamoto et al, AJRCCM 2000; 161: 487-492
VO2/HR = SV
Rationale for exercise testing to evaluate
heart failure
- 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
• 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