Section 3 Cardiovascular Physiology

Chapter
Cardiac Pressure–Volume Loops

31
Describe the left ventricular pressure–  Ventricular ejection, in which the stroke volume
(SV) is ejected into the aorta.
volume loop  Isovolumetric relaxation, a vertical line
The left ventricular pressure–volume loop provides a representing the fall in intraventricular pressure
useful representation of left ventricular performance without a change in ventricular volume.
through the cardiac cycle (Figure 31.1; see also  Diastolic ventricular filling, in which the ventricle
Chapter 28, Figure 28.1). fills with blood ready for the next contraction.
In a normal left ventricle (LV), the pressure–
volume loop is approximately rectangular and can
be divided into four phases: How does the pressure–volume loop
 Isovolumetric contraction, a vertical line change when preload is increased?
representing the increase in intraventricular Preload can be thought of as the volume of blood
pressure without a change in ventricular volume. within the ventricle prior to contraction (see

Figure 31.1 Pressure–volume loop of the

normal left ventricle (BP = blood pressure).
140 Aortic valve
closes

120
Systolic BP
Left ventricular pressure (mmHg)

Aortic valve opens

100
Diastolic BP
Isovolumetric

80
contraction
Isovolumetric
relaxation

60

40

Mitral valve Mitral valve closes

20 opens
Diastolic filling End-diastolic volume

0
0 20 40 60 80 100 120 140 160
Left ventricular end- Left ventricular volume (mL)
diastolic pressure Stroke volume
End-systolic volume

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 Chapter 31: Cardiac Pressure–Volume Loops

Chapter 29). For the LV, it is the left ventricular end-
diastolic volume (LVEDV). According to Starling’s
law, an increase in preload results in a greater dia-
stolic stretch of the contractile myocardial fibres (see
Chapter 30). The stretched sarcomeres contract more
forcefully, thus increasing SV (Figure 31.2).
Figure 31.2 illustrates a number of important features:
 The width of the pressure–volume loop, which
represents SV, is increased due to the increase in
LVEDV. The left ventricular end-systolic volume
(LVESV) increases slightly due to an increase in
afterload (aortic pressure) caused by the greater
cardiac output.
 The end-diastolic pressure–volume relationship
(EDPVR) line reflects the passive diastolic
compliance of the LV. Beyond a certain preload,
left ventricular end-diastolic pressure (LVEDP)
increases sharply, reflecting the nonlinear
compliance of the left ventricular wall. This is due
to the elastic proteins and connective tissue within
the myocardium reaching their elastic limit.
How does the pressure–volume loop
change when afterload is increased?
Afterload is the stress developed in the left ventricular
wall during ejection, and it reflects the force opposing
the shortening of cardiac myocytes. As afterload
increases (e.g. due to an increase in diastolic aortic
pressure), both the rate and extent of sarcomere
shortening decrease, resulting in a reduction in SV:
 As a reduced volume of blood is ejected from the
LV, the LVESV is increased.
 In turn, the addition of the venous return leads to
an increase in LVEDV.
 According to Starling’s law, an increase in LVEDV
causes an increase in myocardial contractility.
Thus, SV increases, returning LVEDV to near
normal.
Overall, the increase in LVESV is greater than that of
LVEDV. SV is slightly decreased, and the left ven-
tricular pressure–volume loop looks taller and thinner
(Figure 31.3a).
How does an increase in myocardial
contractility alter the pressure–
volume loop?
Myocardial contractility may be altered extrinsically by
the autonomic nervous system, circulating hormones
or positively inotropic drugs. It is therefore independ-
ent of preload and afterload. Graphically, increased
contractility (positive inotropy) increases the gradient

Systolic and diastolic BP increase slightly

140

120
Left ventricular pressure (mmHg)

100

80

60

40 LVEDP
increased EDPVR

20
Higher end-diastolic volume
0
0 20 40 60 80 100 120 140 160 180 200
Left ventricular volume (mL)
Stroke volume increased

Figure 31.2 Effect of increased preload on the pressure–volume loop (BP = blood pressure; EDPVR = end-diastolic pressure–volume
relationship; LVEDP = left ventricular end-diastolic pressure).

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 Section 3: Cardiovascular Physiology

(a) Increased afterload (b) Increased contractility

ESPVR ESPVR

160 160
Increased Increased contractility
systolic and
140 140
diastolic BP
Left ventricular pressure (mmHg)

Left ventricular pressure (mmHg)

120 Increased afterload 120

100 100

80 80

60 60

40 40 LVEDV is
EDPVR
LVESV is lower slightly lower
20 20

0 0
0 20 40 60 80 100 120 140 160 180 200 0 20 40 60 80 100 120 140 160
Stroke volume Left ventricular Stroke volume Left ventricular
is reduced volume (mL) is increased volume (mL)

Figure 31.3 Effect of (a) increased afterload and (b) increased contractility on the pressure–volume loop (BP = blood pressure).

of the end-systolic pressure–volume relationship

(ESPVR) line (Figure 31.3b). ESPVR
140
The increased strength of myocardial contrac- Area =
internal work
tion ejects additional blood, resulting in a lower LVESV.
Left ventricular pressure (mmHg)

120
Following the addition of venous return, LVEDV is
reduced. As positive inotropy decreases LVESV more 100 Area = external work
than LVEDV, overall SV is increased.
80

How is the left ventricular pressure– 60

volume loop related to cardiac work? 40 EDPVR

The mechanical work of the heart can be divided into:
 External work (or stroke work), the kinetic energy 20
expended when blood is ejected under pressure
from the ventricle. The area enclosed by the 0
ventricular pressure–volume loop (i.e. pressure  0 20 40 60 80 100 120 140 160 180 200
Left ventricular volume (mL)
volume) represents the external work done during
a single cardiac cycle (Figure 31.4). Figure 31.4 External and internal work expended during the
cardiac cycle.
 Internal work, the energy expended during
isovolumetric contraction. It is sometimes known
as ‘pressure work’. As myofilament shortening expended is potential energy. The area enclosed
does not occur, the energy expended during within the ESPVR, the EDPVR and the
isovolumetric contraction is converted to heat isovolumetric relaxation lines represents the
energy during diastole; that is, the energy internal work.

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 Chapter 31: Cardiac Pressure–Volume Loops

The total work done – that is, the sum of external and  Increased afterload may not increase external
internal work – is known as the pressure–volume area work significantly, but does increase internal work
(PVA). PVA correlates surprisingly well with the myo- (Figure 31.3a); thus, myocardial O2 demand
cardial O2 consumption for the heart. Note: whilst increases.
mechanical work accounts for most of the heart’s  Increased myocardial contractility may not
energy expenditure, basal metabolism accounts for a increase internal work, but does increase external
small percentage, resulting in a small discrepancy work (Figure 31.3b). Overall, myocardial O2
between PVA and myocardial O2 consumption. consumption is increased.
Looking back at Figures 31.2 and 31.3, it can be
seen that: How does the pressure–volume loop of
 Increased preload leads to increased external work
(Figure 31.2); thus, myocardial O2 demand is higher. the right ventricle compare with that of
the left?
The right ventricular pressure–volume loop has a
characteristic triangular shape (Figure 31.5). Some
Right ventricular pressure (mmHg)

Ejection important points regarding Figure 31.5 are:

30
 The pressure developed within the right ventricle
25 (RV) is significantly lower than that of the LV; the
20 RV must overcome a much lower afterload, as
Ventricular Ventricular
15
pulmonary vascular resistance and thus
relaxation contraction
pulmonary artery pressure are low.
10  Despite pumping the same volume of blood (i.e.
5 the SV), the area enclosed by the right ventricular
Diastolic filling pressure–volume loop (i.e. the stroke work) is
0
0 20 40 60 80 100 120 140 160 only 20–25% that of the left ventricular loop.
Right ventricular volume (mL)  Ejection of blood from the RV begins early in
systole: right ventricular volume starts to fall
Figure 31.5 Right ventricular pressure–volume loop.
shortly after right ventricular pressure increases.

(a) LV systolic failure (b) LV diastolic failure

Reduced
ESPVR unchanged
contractility
140 ESPVR 140

120 120
Left ventricular pressure (mmHg)
Left ventricular pressure (mmHg)

100 100

Increased LVEDP,
80 80 reduced LVEDV

60 60
EDPVR

40 EDPVR 40

20 20 Reduced left
Increased
ventricular
EDV
compliance
0 0
0 20 40 60 80 100 120 140 160 180 200 0 20 40 60 80 100 120 140 160 180 200
Left ventricular Stroke volume Left ventricular
Stroke volume volume (mL) volume (mL)
reduced reduced

Figure 31.6 Left ventricular (a) systolic failure and (b) diastolic failure.

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 Section 3: Cardiovascular Physiology
 In the RV, stroke work makes up a greater
proportion of the total work than the LV does.
The RV is therefore more susceptible to failure
in the presence of pulmonary hypertension
than the LV is in the presence of systemic
hypertension.
How does the left ventricular pressure–
volume loop change in heart failure?
As discussed in Chapter 30, left ventricular failure is
classified as systolic, diastolic or mixed. Left ventricu-
lar systolic failure results in a reduction in myocardial
140
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contractility (reduced gradient of the ESPVR line) and
an increase in LVEDV. A subnormal SV is ejected
from the LV, resulting in a higher than normal
LVESV (Figure 31.6a).
Left ventricular diastolic failure is due to reduced
left ventricular compliance. The EDPVR line follows
a different course, but the contractility of the LV
(the ESPVR line) is unchanged. Overall, SV is reduced
(Figure 31.6b).
Further reading
R. E. Klabunde. Cardiovascular Physiology Concepts, 2nd
edition. Philadelphia, Lippincott Williams & Wilkins, 2011.