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 Back to Book/course Clinical Echocardiography  Left ventricular systolic funct…

Clinical SECTION 4, CHAPTER 3  


Echocardiography

Ventricular Pressure-
Introduction to echocardio… 12 Chapters
Volume Relationship:

Preload, Afterload,
Principles of hemodynamics 5 Chapters
Stroke Volume, Wall

The echocardiographic exa… 3 Chapters


Stress & Frank-

Starling’s law
 Left ventricular systolic fun… 11 Chapters
Chapter contents [ Show ]
 Left Ventricular Function 
Ventricular Pressure-Volume
 Myocardial Mechanics: Structure an… 
Relationship
 Ventricular Pressure-Volume Relatio… 
Left ventricular pressure-volume relationship
 Assessing left ventricular systolic fu…  can be described by a loop diagram with volume
depicted on the x-axis and left ventricular
 Left ventricular mass and volume (si…  pressure on the y-axis. If left ventricular
pressure and volume are measured continuously
 Ejection fraction (EF): Physiology, M…  during a single cardiac cycle, the loop diagram
shown in Figure 1 is obtained.
 Fractional shortening for estimation … 

 Strain, strain rate and speckle tracki… 

 Left Ventricular Segments for Echoc… 

 The Coronary Arteries 

 Regional Myocardial Contractile Fun… 

Left ventricular diastolic fun… 3 Chapters



Figure 1. Left ventricular pressure-volume


relationship during a single cardiac cycle.

In Figure 1 we begin in diastole, when the mitral


valve opens. When the mitral valve opens, blood

flows into the left ventricle. This results in a


rapid increase in left ventricular volume, but only

a small increase in left ventricular pressure. This


is explained by the fact that the left ventricle is
capable of relaxing and expanding rapidly during
diastole. The term complianceis used to
describe the ability of the left ventricle to relax
during diastole. Compliance is fundamental to
diastolic function. High compliance is desireable
and means that the ventricle is capable of filling
rapidly while operating at low end-diastolic
pressure.

EDV (End Diastolic Volume) denotes the


volume in the left ventricle, just before
contraction commences. Left ventricular
pressure increases when the contracting starts,
and when left ventricular pressure exceeds left
atrial pressure, the mitral valve closes. Upon
closing of the mitral valve, left ventricular
pressure increases rapidly while both the aortic
valve and the mitral valve are closed. This phase
is called isovolumetric contraction (IVC;
Figures 1 and 2).

Relationshipbetweenpressure,volumeandECG

Systole Diastole
ejection filling
IVR

ECG

Aorticvalve
;closes

120+ Aorticvalve
opens
Pressure(mmHg)

80 Aorticpressure

40 Mitralvalve Mitralvalve
closes opens Leftventricularpressure

Leftatrialpressure

-EDV Leftventricular
130+ volume
ng
Filli
Eje

90-
Volume

c ti
on

50- ESV

Contraction Relaxation
Filling

Figure 2. Left ventricular pressure-volume


relationship and ECG waveforms during systole
and diastole.

When left ventricular pressure exceeds diastolic


pressure in the aorta, the aortic valve opens and
blood is ejected into the aorta. Left ventricular
volume decreases as the ventricle contracts and
pumps blood into the aorta. After the maximum
pressure is reached, the ventricle relaxes, which
results in diminished left ventricular pressure.
The aortic valve closes when aortic pressure
exceeds left ventricular pressure.

ESV (End Systolic Volume) is defined as left


ventricular volume at the closure of the aortic
valve. Upon aortic valve closure, the ventricle
relaxes and pressure drops rapidly, without any
significant changes in volume. This phase is
referred to as isovolumetric relaxation (IVR;
Figures 1 and 2). When the ventricular pressure
is less than left atrial pressure, the mitral valve
opens and the cycle is repeated.

Stroke volume (SV) and stroke


work (SW)

Stroke volume (SV) is defined as the difference


between ESV and EDV, which is equivalent to the
width of the loop in Figure 1. The area within the
loop is the stroke work (SW), which is
discussed below.

The pressure-volume loop in Figure 1 can be


moved along the black lines called EDPVR and
ESPVR. EDPVR (End-Diastolic Pressure-
Volume Relationship) shows the relationship
between ESV and left ventricular volume. The
EDPVR curve shows that the left ventricle can
withstand large pressure increases but at a
certain threshold, pressure rises rapidly with
further increases in volume. This is explained by
the existence of an upper limit for ventricular
compliance. The greater the left ventricular
compliance, the less steep the slope of the
EDPVR curve, and vice versa.

ESPVR (End-Systolic Pressure-Volume


Relationship) shows how maximum pressure
varies with volume. The smaller the EDV, the
lower the maximum generated pressure, and the
smaller the stroke volume. Thus, low preload
leads to low EDV, which results in lower
generated pressure and ultimately smaller
stroke volume.

Two-dimensional (2D) and three-dimensional


(3D) echocardiography allows for the calculation
of stroke volume. The drawback of stroke
volume as a measure of left ventricular function
is that it ignores the ability of the ventricle to
generate pressure. This is evident from Figure 1,
which demonstrates that stroke volume is the
difference between ESV and EDV, which can be
calculated without considering pressure (the y-
axis). Moreover, stroke volume also ignores the
ability of the ventricle to shorten. These
drawbacks become clear when examining
patients with dilated cardiomyopathy (DCM).
These patients may have normal stroke volumes,
due to their large ventricular volumes, despite
severe impairment of left ventricular function.

The ability to generate pressure can be


calculated by estimating stroke work (SW).

Stroke work (SW)

In physics, work is equivalent to the product of


power (f) and distance (d). The work required to
move an object is the product of the force
needed to move the object and the distance the
object is moved. With regards to the left
ventricle, the object is blood, and the force is the
pressure generated by the left ventricle. Stroke
work is the work performed to move blood from
the ventricle into the aorta.

Stroke work is represented by the area within the


pressure-volume loop in Figure 1. In vivo
measurement of stroke work requires
continuous measurement of ventricular pressure
and volume during the cardiac cycle, which is
not technically feasible. However, stroke work
can be approximated as the product of stroke
volume and mean arterial pressure (MAP). This
does, however, result in an underestimation of
stroke work.

Cardiac work

Cardiac work (CW) is the product of heart rate


(HR) and stroke work (SW):

CW = HR • SW
(SW = SV • MAP)

Frank-Starling's law
(mechanism)

Stroke volume is greater in the supine position,


as compared with an upright position. This is
because venous return increases in the supine
position. More blood flows back to the heart,
leading to increased ventricular filling (EDV). The
left ventricle responds to increased EDV by
automatically increasing stroke volumes. It
follows that the heart can adapt its stroke
volumes to variations in left ventricular filling.
This phenomenon is called Frank-Starling's
mechanism (law).

Figure 3. Frank-Starling's mechanism.

Frank and Starling discovered that an increase in


Left Ventricular End Diastolic Pressure
(LVEDP) leads to stronger contractions and
greater stroke volumes. This mechanism is
independent of neurohumoral stimuli, although
such stimuli can adjust the intensity of the
mechanism. As evident in Figure 3, the Frank-
Starling curve is modified by afterload and
inotropy of the myocardium.

A rather simple cellular mechanism seems to


explain Frank-Starling's mechanism. When
ventricular filling is increased, the myocardial
fibers and their sarcomeres, are stretched. This
results in troponin C becoming more sensitive to
calcium (sensitivity depends on sarcomere
length), which accelerates the interaction
between actin and myosin, and ultimately
produces more force.

The difference between


contractility and contractile
function

There is a discreet difference between


contractility and contractile function.

Contractility describes the intrinsic ability of


the myocardium to contract, regardless of
preload and afterload. Contractility is the ability
of individual muscle fibers to shorten.
Contractility is not studied with
echocardiography.

Contractile function describes the ability of


the myocardium, in a given hemodynamic state
(at certain preload and afterload conditions).
This is synonymous with systolic function and
can be estimated by echocardiography.

Preload

Preload is the force that stretches myocardial


fibers during diastole. Stretching can be
described by end-diastolic pressure, end-
diastolic volume or end-diastolic diameter.
However, neither pressure, volume, nor diameter
is normalized. Therefore, preference should be
given to preload adjusted for the surface area of
the ventricle, which is equivalent to end-
diastolic wall tension (discussed below).

Preload reserve is an important parameter. It


indicates how much reserve there is in preload.
A ventricle with a large preload reserve can
receive a larger volume of blood (i.e increase its
LVDP). In upright position, all healthy individuals
have a large preload reserve, which becomes
useful during physical activity. In the supine
position, however, preload reserve is small. This
is because venous return increases so much in
the supine position, that the ventricle is already
stretched and operates at or close to its reserve.

Afterload

Afterload is the force that the myocardium


generates during systole. Afterload can also be
described in terms of wall tension, which means
that the force is adjusted for surface area.
Afterload depends on the thickness of the
myocardium. Individuals with high blood
pressure (high afterload) often develop a
compensatory hypertrophy, which may
normalize afterload per surface area.

Wall tension

Wall tension is the force applied to the wall of the


ventricle. The force should be adjusted for the
ventricular surface area, resulting in wall tension
per surface area (σ):

σ  = (p·r)/2·t
p = transmural pressure; r = ventricular
radius; t = wall thickness.

Transmural pressure (p) is the pressure in the


left ventricle. It can be approximated; this is
done by approximating p to systolic pressure
(measured as conventional blood pressure).

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