C H A P T E R 4 2
Introduction to the cardiovascular system
645
• Phase 1 is the very short period when the sodium ion
concentrations are equal inside and outside the cell.
• Phase 2, or the plateau stage, occurs as the cell
membrane becomes less permeable to sodium.
Calcium slowly enters the cell and potassium begins
to leave the cell. The cell membrane is trying to return
to its resting state, a process called repolarisation.
• Phase 3 is a period of rapid repolarisation as the gates
are closed and potassium rapidly moves out of the cell.
• Phase 4 occurs when the cell comes to rest as the
sodium–potassium pump returns the membrane to
its previous state, with sodium outside and potassium
inside the cell. Spontaneous depolarisation begins
again.
Each area of the heart has an action potential that
appears slightly different from the other action poten
tials, reflecting the complexity of the cells in that
particular area. Because of these differences in the action
potential, each area of the heart has a slightly different
rate or rhythm. The SA node generates an impulse about
90 to 100 times a minute, the AV node about 40 to
50 times a minute and the complex ventricular muscle
cells only about 10 to 20 times a minute (Figure 42.3).
Conductivity
Normally, the SA node sets the pace for the heart rate
because it depolarises faster than any cell in the heart.
However, the other cells in the heart are capable of
generating an impulse if anything happens to the SA
node, which is another protective feature of the heart.
As mentioned earlier, the SA node is said to be the pace
maker of the heart because it acts to stimulate the rest
of the cells to depolarise at its rate. When the SA node
sets the pace for the heart rate, the person is said to be
in sinus rhythm.
The specialised cells of the heart can conduct an
impulse rapidly through the system so that the muscle
cells of the heart are stimulated at approximately the
same time. This property of cardiac cells is called
con
ductivity
. The conduction velocity, or the speed at which
the cells can pass on the impulse, is slowest in the AV
node and fastest in the Purkinje fibres.
A delay in conduction at the AV node, between
the atria and the ventricles, accounts for the fact that
the atria contract a fraction of a second before the
ventricles contract. This allows extra time for the ven
tricles to fill completely before they contract. The
almost simultaneous spread of the impulse through the
Purkinje fibres permits a simultaneous and powerful
contraction of the ventricle muscles, making them an
effective pump.
After a cell membrane has conducted an action
potential, there is a span of time, called the absolute
refractory period, in which it is impossible to stimulate
that area of membrane. The absolute refractory period
is the minimal amount of time that must elapse between
two stimuli applied at one site in the heart for each of
these stimuli to cause an action potential. This time
reflects the responsiveness of the heart cells to stimuli.
Cardiac drugs may affect the refractory period of the
cells to make the heart more or less responsive.
Autonomic influences
The heart can generate action potentials on its own
and could function without connection to the rest of
the body. However, the autonomic nervous system (see
Chapter 29) can influence the heart rate and rhythm
and the strength of contraction. The parasympathetic
nerves—primarily the vagus or tenth cranial nerve—can
slow the heart rate and decrease the speed of conduction
through the AV node. This allows the heart to rest and
conserve its strength. In addition, the parasympathetic
influence on the SA node is the dominant influence
most of the time, keeping the resting heart rate at 70 to
80 beats per minute.
The sympathetic nervous system stimulates the heart
to beat faster, speeds conduction through the AV node
and causes the heart muscle to contract harder. This
action is important during exercise or stress, when the
body’s cells need to have more oxygen delivered.
0
–20
+20
–40
phase 4
phase 4
RMP
A
SA node action potential
B
Ventricular muscle cell action potential
phase 0
phase
0
Stimulation
Resting membrane
potential
phase
1 phase
2
phase 3
phase 3
–60
Membrane potential (mV)
–80
0
–20
+20
–40
–60
Membrane potential (mV)
–80
–100
FIGURE 42.3
Action potentials recorded from a cell in the sinoatrial
(SA) node
(A)
showing diastolic depolarisation in phase 4 and
recorded from a ventricular muscle cell
(B)
. In phase 0, the cell is
stimulated, sodium rushes into the cell, and the cell is depolarised.
In phase 1, sodium levels equalise. In phase 2, the plateau phase,
calcium enters the cell (the slow current), and potassium and sodium
leave. In phase 3, the slow current stops, and sodium and potassium
leave the cell. In phase 4, the resting membrane potential (RMP)
returns and the pacemaker potential begins in the SA node cell.
