The heart is essentially a muscle that contracts
and pumps blood. It consists of specialized muscle cells called
cardiac myocytes. The contraction of these cells is initiated
by electrical impulses, known as action potentials. Unlike skeletal muscles, which have to be
stimulated by the nervous system, the heart generates its own electrical stimulation. In fact, a heart can keep on beating even
when taken out of the body. The nervous system can make the heartbeats
go faster or slower, but cannot generate them. The impulses start from a small group of myocytes
called the pacemaker cells, which constitute the cardiac conduction system. These are modified myocytes that lose the
ability to contract and become specialized for initiating and conducting action potentials. The SA node is the primary pacemaker of the
heart. It initiates all heartbeats and controls heart
rate. If the SA node is damaged, other parts of
the conduction system may take over this role. The cells of the SA node fire spontaneously,
generating action potentials that spread though the contractile myocytes of the atria. The myocytes are connected by gap junctions,
which form channels that allow ions to flow from one cell to another. This enables electrical coupling of neighboring
cells. An action potential in one cell triggers another
action potential in its neighbor and the signals propagate rapidly. The impulses reach the AV node, slow down
a little to allow the atria to contract, then follow the conduction pathway and spread though
the ventricular myocytes. Action potential generation and conduction
are essential for all myocytes to act in synchrony. Pacemaker cells and contractile myocytes exhibit
different forms of action potentials. Cells are polarized, meaning there is an electrical
voltage across the cell membrane. In a resting cell, the membrane voltage, known
as the resting membrane potential, is usually negative. This means the cell is more negative on the
inside. At this resting state, there are concentration
gradients of several ions across the cell membrane: more sodium and calcium outside
the cell, and more potassium inside the cell. These gradients are maintained by several
pumps that bring sodium and calcium OUT, and potassium IN. An action potential is essentially a brief
REVERSAL of electric polarity of the cell membrane and is produced by voltage-gated
ion channels. These channels are passageways for ions in
and out of the cell, and as their names suggest, are regulated by membrane voltage. They open at some values of membrane potential
and close at others. When membrane voltage INCREASES and becomes
LESS negative, the cell is LESS polarized, and is said to be depolarized. Reversely, when membrane potential becomes
MORE negative, the cell is repolarized. For an action potential to be generated, the
membrane voltage must depolarize to a critical value called the THRESHOLD. The pacemaker cells of the SA node SPONTANEOUSLY
fire about 80 action potentials per minute, each of which sets off a heartbeat, resulting
in an average heart rate of 80 beats per minute. Pacemaker cells do NOT have a TRUE RESTING
potential. The voltage starts at about -60mV and SPONTANEOUSLY
moves upward until it reaches the threshold of -40mV. This is due to action of so-called “FUNNY”
currents present ONLY in pacemaker cells. Funny channels open when membrane voltage
becomes lower than -40mV and allow slow influx of sodium. The resulting depolarization is known as
“pacemaker potential”. At threshold, calcium channels open, calcium
ions flow into the cell further depolarizing the membrane. This results in the rising phase of the action
potential. At the peak of depolarization, potassium channels
open, calcium channels inactivate, potassium ions leave the cell and the voltage returns
to -60mV. This corresponds to the falling phase of the
action potential. The original ionic gradients are restored
thanks to several ionic pumps, and the cycle starts over. Electrical impulses from the SA node spread
through the conduction system and to the contractile myocytes. These myocytes have a different set of ion
channels. In addition, their sarcoplasmic reticulum,
the SR, stores a large amount of calcium. They also contain myofibrils. The contractile cells have a stable resting
potential of -90mV and depolarize ONLY when stimulated, usually by a neighboring myocyte. When a cell is depolarized, it has more sodium
and calcium inside the cell. These positive ions leak through the gap junctions
to the adjacent cell and bring the membrane voltage of this cell up to the threshold of
-70mV. At threshold, fast sodium channels open creating
a rapid sodium influx and a sharp rise in voltage. This is the depolarizing phase. L-type, or slow, calcium channels also open
at -40mV, causing a slow but steady influx. As the action potential nears its peak, sodium
channels close quickly, voltage-gated potassium channels open and these result in a small
decrease in membrane potential, known as early repolarization phase. The calcium channels, however, remain open
and the potassium efflux is eventually balanced by the calcium influx. This keeps the membrane potential relatively
stable for about 200 msec resulting in the PLATEAU phase, characteristic of cardiac action
potentials. Calcium is crucial in coupling electrical
excitation to physical muscle contraction. The influx of calcium from the extracellular
fluid, however, is NOT enough to induce contraction. Instead, it triggers a MUCH greater calcium
release from the SR, in a process known as “calcium-induced calcium release". Calcium THEN sets off muscle contraction by
the same “sliding filament mechanism” described for skeletal muscle. The contraction starts about half way through
the plateau phase and lasts till the end of this phase. As calcium channels slowly close, potassium
efflux predominates and membrane voltage returns to its resting value. Calcium is actively transported out of the
cell and also back to the SR. The sodium/potassium pump then restores the
ionic balance across the membrane. Because of the plateau phase, cardiac muscle
stays contracted longer than skeletal muscle. This is necessary for expulsion of blood from
the heart chambers. The absolute refractory period is also much
longer - 250 msec compared to 1 msec in skeletal muscle. This long refractory period is to make sure
the muscle has relaxed before it can respond to a new stimulus and is essential in preventing
summation and tetanus, which would stop the heart from beating.
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