Transcript The Cardiac Pump

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The Cardiac Cycle
Work Output of the Heart
Preload, Afterload and Contractility
Regulation of Heart Function – The Frank
Starling Mechanism
Measurement of Cardiac Output
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During systole, blood accumulates in the atria.
At end systole, the higher pressure forces open
the AV valves causing rapid ventricular filling.
This lasts about 1/3.
In the middle 1/3, there is minimal flow.
In the last 1/3, the atria contracts to deliver up
to 20% of the total ventricular volume.
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At the start of systole, the intraventricular
pressure rises which closes the AV valves.
For approximately 0.02 to 0.03 seconds, the
pressure continues to rise but is less than that
required to open the semilunar valves.
This is called isovolumic contraction because
the ventricular volume does not change.
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Once the semilunar valves open the ejection
phase begins.
About 70% of the total blood ejected occurs in
the first 1/3.
This is called the rapid ejection period
The final 30% empties in the next 2/3 and is
called the slow ejection period.
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At end-systole, ventricular relaxation begins
suddenly and causes intraventricular pressure
to fall rapidly.
The semilunar valves close once its pressure is
greater than intraventricular pressure.
For 0.03 – 0.06 seconds the muscle continues to
relax, pressure continues to fall but no filling
occurs because the AV valves are still closed.
This is the period of isovolumic relaxation.
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After the aortic valve opens, blood enters the
aorta, stretching it and causes the pressure to
rise to 120 mmHg.
An incisura occurs just before the aortic valve
closes from a short backward flow of blood.
During diastole, the aortic pressure slowly falls
as blood flows out to the venous side.
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The stroke work output of the heart is the
amount of energy converted to work per beat.
Two forms of work output:
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Volume pressure (external) work: moving blood
from the low pressure veins to high pressure
arteries.
Kinetic energy of blood flow: accelerate the blood to
its velocity of ejection.
RV external work is 1/6 of the LV because of
the six fold difference in systolic pressure.
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Understand how the
systolic and diastolic
pressure curves are
derived.
By combining the end
diastolic and systolic
curves, the volumepressure diagram can
be defined.
The area inside the VP
diagram is the EW.
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Preload can be described as the stress
experienced at end-diastole
Preload=(EDP x EDR)/2w
Thus, preload represents all the factors that
contribute to passive ventricular wall stress (or
tension) at end diastole.
This means that EDP (P) or EDV (R) contribute
to, be should not be equated to preload.
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Laplace’s Law can be used to describe afterload
as ventricular stress during systolic ejection.
Therefore, stress=TP x R/2w
Afterload represents all the factors that
contribute to total myocardial wall stress (or
tension) during systolic ejection.
Arterial pressure and TPR contribute to
afterload but should not be equated with
afterload.
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Focusing on wall stress is important
Metabolic cost is related to the wall tension
 The greater the tension, the greater the oxygen
demand.
 Physiological and therapeutic regimens reduce wall
stress and restore oxygen supply and demand.
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The relationship among P, R and w provides a
clear physiological explanation for the different
patterns of hypertrophy and remodelling.
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Contractility is the peak isometric force generated at
a given preload and afterload.
A increase in contractility causes incremental
increases in developed force and velocity of
contraction.
Results from different degrees of binding between
myosin and actin filaments.
This is dependant on the intracellular calcium
concentration.
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The amount of blood pumped by the heart is
determined by the rate of blood flow from the
veins (venous return).
The intrinsic ability of the heart to adapt to
increasing volumes of blood is the FrankStarling mechanism.
With the extra delivery of blood, the cardiac
muscle contracts with greater force because of
improved actin/myosin interaction.
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The ventricular
function curve is a
way of expressing the
Frank-Starling
mechanism.
Increases in atrial
pressure causes an
increase volume and
strength of contraction
which causes an
increase in cardiac
output.
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Suppose blood flow is Q
(ml/s) and q mg of dye is
injected.
If the concentration of dye
is continually measured
farther downstream, a
curve of the dye
concentration, c, is
recorded as a function of
time, t.
The amount of dye at point
B between the time t1 and
t2 will be q = cQ(t2-t1).
Therefore, Q = q/(t2-t1)c
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c is properly defined as an integral with limits of t1
to t2.
Clinically, we use the temperature as the indicator
instead of a dye.
Therefore, we can adjust the equation to:
Q
V  (TB  TI )  K 1  K 2
t2
 TB(t )dt
t1
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What would the curve look like in a high cardiac
output state? Low? What is the effect of tricuspid
regurgitation?
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The Cardiac Cycle
Work Output of the Heart
Preload and Afterload and Contractility
Regulation of Heart Function – The Frank
Starling Mechanism
Measurement of Cardiac Output
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Wall Stress
An increase in wall stress achieved by either increasesd
LV size or intraventricular pressure will increase
myocardial oxygen uptake.
 This is because a greater rate of ATP use is required as the
myofibrils develop greater tension.
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Wall Stress, Preload and Afterload
Preload can now be defined as the wall stress at the end
of diastole and therefore at the resting maximal resting
length of the sarcomere.
 Afterload, being the load on the contracting myocardium,
is also the wall stress during LV ejection.
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Preload
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The stretch of the individual sarcomere regulates the
performance of the heart.
Afterload
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Peak systolic wall stress reflects the three major
components of the afterload-peripheral resistance, arterial
compliance, and peak intraventricular pressure.
This is the force against which muscle contracts.
Contractility
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This is the intrinsic ability of the heart muscle to generate
force and to shorten. It is manifest as the rate of pressure
development and shortening from any preload.
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Ventricular Function Curve
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The dependancy of stroke volume on preload was
described more than 100 years ago by Otto Frank
and E.H. Starling and since then has been called the
Frank-Starling mechanism. Using this relationship
between preload and stroke volume or stroke work,
a ventricular function curve can be consructed by
plotting stroke work at various levels of preload.