Maintenance of the Body
Te ability of cardiac muscle to depolarize and contract is in-
trinsic. In other words, it is a property of heart muscle and does
not depend on the nervous system. Even if all nerve connec-
tions to the heart are severed, the heart continues to beat rhyth-
mically, as demonstrated by transplanted hearts. Nevertheless,
the healthy heart is amply supplied with autonomic nerve ﬁbers
that can alter its basic rhythm.
Setting the Basic Rhythm:
The Intrinsic Conduction System
Te independent, but coordinated, activity of the heart is a
function of (1) the presence of gap junctions, and (2) the activ-
ity of the heart’s “in-house” conduction system. Te
cardiac conduction system
consists of noncontractile cardiac
cells specialized to initiate and distribute impulses throughout
the heart, so that it depolarizes and contracts in an orderly, se-
quential manner. Let’s look at how this system works.
Action Potential Initiation by Pacemaker Cells
contractile cells of the heart (and neurons and skeletal muscle
ﬁbers) maintain a stable resting membrane potential. Unlike
cardiac pacemaker cells
making up the intrinsic conduction system have an
that continuously depolarizes, driFing slowly
toward threshold. Tese spontaneously changing membrane
initiate the action potentials that spread throughout the heart
to trigger its rhythmic contractions. Let’s look at the three
parts of an action potential in pacemaker cells as shown in
Te pacemaker potential is due to the
special properties of the ion channels in the sarcolemma. In
these cells, hyperpolarization at the end of an action poten-
tial both closes K
channels and opens slow Na
inﬂux alters the balance between K
loss and Na
entry, and the membrane interior becomes less and less
negative (more positive).
by skeletal muscle activity. Consequently, the real danger of an
inadequate blood supply to the myocardium is not lack of nutri-
ents, but lack of oxygen.
When a region of heart muscle is oxygen-starved (as during a
heart attack), the ischemic cells (ischemic
begin to metabolize anaerobically, producing lactic acid. Te ris-
level that results raises intracellular Ca
, damaging mi-
tochondria and hindering cardiac cells’ ability to produce A±P.
High levels of intracellular H
also cause the gap junc-
tions (which are usually open) to close, isolating the damaged
cells and forcing action potentials to ﬁnd alternate routes to the
cardiac cells beyond them. Tis may lead to fatal arrhythmias.
Check Your Understanding
For each of the following, state whether it applies to skeletal
muscle, cardiac muscle, or both: (a) refractory period is
almost as long as the contraction; (b) source of Ca
SR; (c) AP exhibits a plateau phase; (d) has
troponin; (e) has triads.
Cardiac muscle cannot go into tetany. Why?
For answers, see Appendix H.
Name the components of the conduction system of the
heart, and trace the conduction pathway.
Draw a diagram of a normal electrocardiogram tracing.
Name the individual waves and intervals, and indicate what
Name some abnormalities that can be detected on an ECG
This slow depolarization is
due to both opening of Na
channels and closing of
channels. Notice that the membrane potential is
never a ﬂat line.
The action potential begins when
the pacemaker potential reaches threshold.
Depolarization is due to Ca
inﬂux through Ca
is due to Ca
channels opening. This allows K
brings the membrane potential back to its most
Membrane potential (mV)
Pacemaker and action potentials of pacemaker cells in the heart.