Figures 9–8 and 9–9). Contraction ends when calcium is
returned to the sarcoplasmic reticulum and extracellular ﬂ
-ATPase pumps and Na
The amount that cytosolic calcium concentration
increases during excitation is a major determinant of the
strength of cardiac muscle contraction. You may recall that
in skeletal muscle, a single action potential releases sufﬁ
calcium to fully saturate the troponin sites that activate con-
traction. By contrast, the amount of calcium released from
the sarcoplasmic reticulum in cardiac muscle during a rest-
ing heartbeat is not usually sufﬁ
cient to saturate all tropo-
nin sites. Therefore, the number of active cross-bridges, and
thus the strength of contraction, can be increased if more
calcium is released from the sarcoplasmic reticulum. The
mechanisms that vary cytosolic calcium concentration will
be discussed later.
Refractory Period of the Heart
Ventricular muscle, unlike skeletal muscle, is incapable of any
signiﬁ cant degree of summation of contractions, and this is
a very good thing. Imagine that cardiac muscle were able to
undergo a prolonged tetanic contraction. During this period,
no ventricular ﬁ lling could occur because ﬁ lling can occur
only when the ventricular muscle is relaxed, and the heart
would therefore cease to function as a pump.
The inability of the heart to generate tetanic contrac-
tions is the result of the long absolute
of cardiac muscle, deﬁ ned as the period during and follow-
ing an action potential when an excitable membrane cannot
be re-excited. As in the case of neurons and skeletal muscle
ﬁ bers, the main mechanism is the inactivation of sodium
channels. The absolute refractory period of skeletal muscle is
much shorter (1 to 2 ms) than the duration of contraction (20
to 100 ms), and a second contraction can therefore be elicited
before the ﬁ
rst is over (summation of contractions). In con-
trast, because of the prolonged, depolarized plateau in the car-
diac muscle action potential, the absolute refractory period of
cardiac muscle lasts almost as long as the contraction (250 ms),
and the muscle cannot be re-excited in time to produce sum-
; also review Figure 9–41).
of the Cardiac Cycle
The orderly process of depolarization described in the previ-
ous sections triggers a recurring
of atrial and
ventricular contractions and relaxations (
we will present an overview of the cycle, naming the phases and
key events. A closer look at the cycle will follow, with a discus-
sion of the pressure and volume changes that cause the events.
The cycle is divided into two major phases, both named
for events in the ventricles: the period of ventricular contrac-
tion and blood ejection called
and the alternating
period of ventricular relaxation and blood ﬁ lling,
a typical heart rate of 72 beats/min, each cardiac cycle lasts
approximately 0.8 s, with 0.3 s in systole and 0.5 s in diastole.
Electrocardiograms from a healthy person and from two people
suffering from atrioventricular block. (a) A normal ECG. (b) Partial
block. Damage to the AV node permits only every-other atrial
impulse to be transmitted to the ventricles. Note that every second
P wave is not followed by a QRS and T. (c) Complete block. There is
no synchrony between atrial and ventricular electrical activities, and
the ventricles are being driven by a very slow pacemaker cell in the
bundle of His.
Some people have a potentially lethal defect of ventricular
muscle, in which the current through voltage-gated K
is delayed and reduced. How could this defect be detected on
their ECG recordings?
Answer can be found at end of chapter.
Relationship between membrane potential changes and contraction
in a ventricular muscle cell. The refractory period lasts almost as
long as the contraction. Tension scale not shown.
Membrane potential (mV)