Chapter 33
CARDIAC STRUCTURE
AND FUNCTION
The following material summarizes the key
aspects of the myocardium that were
presented in Chapters 2 and 23, in the
context of heart muscle as an excitable
tissue. The emphasis is now placed on the
function of this highly specialized tissue.
Some of the details provided earlier are
reviewed quickly before they are developed
in relation to the regulation of cardiac
function.
A. Structure of the muscle
Cardiac muscle grossly appears to be
syncytial; however, the cells are
mononucleate but provided with very tight
electrocoupling via gap junctions, within
their multiple intercalated disks. Each cell is
in direct communication with about a dozen
others.
Distinct striations are evident. It can
be assumed at this level of treatment that the
ultimate intracellular mechanisms of
contraction described for skeletal muscle are
broadly applicable to cardiac muscle. That
is, Ca
2+
is needed to couple excitation and
contraction, and the role of regulatory
proteins, the function of crossbridges,
ratchet mechanism for filament sliding, and
adenosine triphosphate (ATP) hydrolysis are
all essentially as described for skeletal
muscle in Chapter 22.
B. Electrophysiology
A major distinction between muscle types is
evident in the form of excitation at the
sarcolemmal level. The nature of
depolarization in cells of the pacemaker and
those of the bulk of the myocardium was
described in detail in Chapter 23.
The
following review items will indicate if the
reader needs to return to the description in
that earlier chapter.
•
Myocardial cells exhibit autorhythmicity
-
even in completely isolated cells that
continue to "beat" in cell culture.
•
The cells forming the sinoatrial (SA)
node (pacemaker), are most obviously
autorhythmic, simply because of the
instability of the recovery potential and
the drift of potential up to threshold.
•
Because the cells are so tightly
electrocoupled, the activity of the cell
population as a whole tends to be
dictated by the pacemaker cells -
those
with the fastest intrinsic rate of firing.
•
The intrinsic activity of the SA node is
subject to influences from the autonomic
nervous system. Most importantly,
parasympathetic, cholinergic innervation
from the vagus provides a means of
slowing down the firing rate of the SA
node.
•
Depolarization in the bulk myocardium
is of very long duration, as is the
refractory period.
This prevents
temporal summation and provides for an
obligatory relaxation phase, needed for
heart filling. Without this protection, a
steady cycle of relaxation and
contraction could not occur and the heart
would be unable to act as a pump.
Although the SA node normally
provides the pacemaker role, if for some
reason any other myocardial area develops
excessive excitability and begins firing more
frequently than the SA node, this new area
can take over the pacemaker function. This
is a well-known aspect of caffeine
intoxication. Some other aspects of
abnormal pacemaker function are noted in
Box 33-1.
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- Fall '08
- BruceCurrie
- heart rate
-
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