FIGURE 4.24 Interdependent effects of changes in preload, afterload, and inotropy on left ventricular
pressure-volume loops. Panel A shows effects of increasing preload (end-diastolic volume) with and with-
out a secondary increase in afterload (aortic pressure). Panel B shows the effects of increasing afterload
with and without a secondary increase in preload. Panel C shows the effects of increasing inotropy with
and without secondary changes in preload and afterload.
CASE 4-3
A patient suddenly goes into sinus tachycardia, which reduces ventricular filling time.
This also causes a fall in arterial pressure. Using left ventricular pressure-volume loops,
describe how the tachycardia and hypotension likely alters ventricular function. Assume
no changes in inotropy.
increasing the inotropy causes an upward
shift in the Frank-Starling curve. The heart
responds hy increasing the SV while, at the
FIGURE 4.25 Frank-Starling curves show-
ing interactions between preload, afterload,
and inotropy. Increased afterload or decreased
inotropy shifts the Frank-Starling curve down and
to the right, whereas the decreased afterload or
increased inotropy shift the curve upward and to
the left. The diagonal arrows show how changes in
afterload and inotropy change both stroke volume
(SV) and preload (
, left ventricular end-
diastolic pressure).
pressure (i.e., there is a diagonal shift in the
operating point between the curves). With
an increase in afterload or a decrease in inot-
ropy, the Frank-Starling curves shifts down-
ward, leading to a fall in SV and a secondary
increase in EDV.
These interactions between changes in pre-
load, afterload, and inotropy will be discussed
further in Chapter 9 in the context of car-
diac disorders such as heart failure and valve
Changes in SV, whether caused by changes in
preload, afterload, or inotropy, alter the oxygen
consumption of the heart. Changes in heart
rate likewise affect myocardial oxygen con-
sumption. The contracting heart consumes a
considerable amount of oxygen because of its
need to regenerate the large amount of ATP
hydrolyzed during contraction and relaxation.
Therefore, any change in myocardial function
previous page 97 Cardiovascular Physiology Concepts  2nd Edition read online next page 99 Cardiovascular Physiology Concepts  2nd Edition read online Home Toggle text on/off