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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 DE-polarized. Reversely, when membrane potential becomes MORE negative, the cell is RE-polarized. For an action potential to be generated, the membrane voltage must DE-polarize 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 DE-polarization is known as “pacemaker potential”. At threshold, calcium channels open, calcium ions flow into the cell further DE-polarizing 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 DE-polarized, 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 RE-polarization 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.
