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Action Potential of Ventricular Cells vs. SA node:
There are different types of heart cells, each with unique membrane permeabilities and AP properties. These
differences specialize them for the important roles each contributes to the overall spread of excitation throughout the
heart muscle.

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The cardiac nodal cells have unique ion channel mechanisms that contribute to its pacemaker
potential and unsteady resting potential. Compared to other cardiac muscle cells, there is not a resting state, but
rather a slower depolarization phase. In fact, before the membrane potential repolarizes to more negative values,
outward K+ channels (that were open at start of repolarization phase) will start to close. Another unique feature of
these cells is that voltage gated channels are open when the membrane potential is still at a negative value. These

 Na+ channels allow an inward flow of Na+. Contributing further to the depolarization of the membrane are
the

 Ca++ channels, allowing for a brief inward flow and extra boost of ions to reach the pacemaker potential.
Once threshold is met, the AP fires and the depolarizing phase is continue by the  Ca++ channels.
Repolarization occurs when the K+ channels open, which is where I started my explanation of the cycle.




The AP propagated through the atria causes the cells in the ventricle to depolarize.
An AP fires when threshold is reached. 
a key point in these cells is the fact that propagation is much slower so
that the atria will be done contracting before ventricular excitation occurs. These cells are really very similar to those
found in skeletal and neuronal cells. Since the membrane is more permeable to K+ than Na+, the equilibrium is
closer to that of K+. Once threshold is obtained, the opening of voltage gated sodium channels occurs, which leads
to Na+ inward flow and depolarization of the membrane. Don't forget that the closure of the K+ channels also
contributes to this depolarization. These Na+ channels are then inactivated, but the opening of K+ channels is
delayed. These conditions in combination with an inward flow of Ca++ keeps the membrane potential suspended in
a plateau phase. (Membrane remains depolarized at a plateau phase near 0 mV) The end of the plateau phase
occurs when the K+ channels open and the Ca++ channels close, which leads to a rapid repolarization.

Automaticity: the pacemaker potential is due to the three unique ion channels that the SA node cell possess. It
allows the cell to slowly depolarize instead of having a resting state, thus exhibiting
. The SA node can
depolarize 100 times/ minute, if there is not any neural or hormonal input.
 èxcitation contraction coupling in cardiac muscle:
NOTè: èxcitation contraction coupling is simply referring to the mechanism by which the AP in cardiac muscle cells
causes the myofibrils to contract. When an AP passes over the cell's membrane, the AP spreads to the interior of the
cardiac muscle fiber (via the T tubules). L type Ca++ channels cause the release of Ca++ ions from the SR. In other
words, these voltage gated Ca++ channels lead to the initial depolarization of the cell and a small rise in intracellular
Ca++. This rise in Ca++ then leads to a much larger release of Ca++ from the SR. This promotes the sliding of actin
and myosin filaments, producing the muscle contraction.

















. At the end of the plateau of the AP,
Ca++ is returned to the SR (by Ca++/ATPase pumps and Na/Ca++ counter transporters) and the contraction
ceases. Another key point in cardiac muscle cells is that during a resting heartbeat, the amount of calcium released
is not enough to saturate all of the troponin sites. Thus, the strength of the contraction can be increased by an
increase in Ca++.

Absolute Refractory Period:

The cardiac muscle has a long absolute refractory period. In other words, a period of time where normal cardiac
impulses can't re-excite an area of cardiac muscle. This is a result of the long, extended plateau phase. This is
extremely important for proper functioning of the heart.