ISOLATED HEART MUSCLE

The three major factors affecting the force, velocity and extent of
isolated heart muscle contraction are preload, contractility and
afterload.

Preload
When the preload or resting cardiac muscle length is increased,
the force of contraction is increased (Starling's law). Increasing
the preload increases the maximum force a muscle develops, but
does not alter the velocity offeree development at a given load.

Contractility
Increasing the inotropic state of cardiac muscle (contractility)
produces an increase in the maximum force a muscle develops and
an increase in the velocity offeree development with no change in
resting muscle length.

Afterload
When the load against which cardiac muscle is contracting is
increased, both the maximum force and the velocity of force
development are decreased.

THE INTACT HEART

Within the intact heart, it is much harder to measure preload,
afterload or force of contraction directly, so alternative measures
are required. Preload is probably best reflected by end-diastolic
volume, but ease of measurement has meant that end-diastolic
pressures have been used much more widely. Afterload is usually
reflected by vascular resistance. For cardiac contractility, many different,
variables have been used, including stroke volume (SV),
speed of contraction, maximum rate of rise of ventricular pressure,
peak ventricular pressure, ejection fraction (SV/end-diastolic volume)
and stroke work (SV x [mean arterial pressure (MAP) mean venous pressure (MVP)]).

Ventricular function curves

By plotting indices of cardiac contractility against indices for preload,
a curve is derived which may give an indication of ventricular
function, and which may be useful clinically in assessing the
response to treatment (Fig. 5.5). A shift of the curve upwards and
to the left indicates improved contractility or reduced vascular
resistance (afterload). A shift downwards and to the right indicates
myocardial depression or increased vascular resistance.
When such curves are plotted using filling pressures rather
than volumes, great care is needed in interpretation, because enddiastolic
pressure does not relate directly to fibre length and enddiastolic
volume. In addition, alterations may occur in ventricular