Cardiovascular Physiology: Action Potential, Excitation-Contraction Coupling, and Inotropic Effects

Running head: CARDIOVASCULAR PHYSIOLOGY
Cardiovascular Physiology
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1CARDIOVASCULAR PHYSIOLOGY
Cardiac action potential is defined as the temporary phenomenon in which the difference
between the internal and external membrane potential generates an electrical impulse (1). The
variation in the electrical potential difference is evident in the different compartments of the
heart. The excitory and contractile muscle systems detect these differences and constantly react
to the potential maintaining the proper functionality of the heart intact (2). Autorhythmicity of
the heart is maintained by the pacemaker potential, which is the ability of the heart’s excitory
muscles, which detects spontaneous depolarization and maintains the flow of potential
generation slowly, without any external influence (3).
Fig 1: action potential of cardiac muscles
Source: (4)

2CARDIOVASCULAR PHYSIOLOGY
Phase 4 is known as the resting phase, which is constant at -90mV since the K+ ions keep
leaking from the membranes through inward rectifier channels. The Na+ and Ca2+ remain closed
during this time (4).
Phase 0 is the depolarization phase where, triggering of action potential makes the pacemaker
cells raise the membrane potential from -90mV onwards. Na+ channels starts opening which
allows the ions to enter the cellular compartment so that the membrane potential is now at -70mv
creating an inward electronic pulse. Rapid Na+ influx causes membrane depolarization at 0mV
temporarily called overshooting. During this time Ca2+ ions starts leaking inside the cell
membrane slowly down the gradient making the membrane potential -40mV (4). (4)
Phase 1 is the early repolarization phase makes the membrane very positive and opens some of
the K+ channels to facilitate movement of the ions outside of the cell making it 0mV (4).
Phase 2 is known as the plateau phase where the Ca2+ ions come inside through the long
opening (L-type) receptors and K+ moves out of the cell and this process isss coupled by the
excitation-contraction process (4).
Phase 3 is the repolarization Ca2+ channels close and the current electric potential returns to
resting phase and the Na+ transmemebrane balance normalizes (4).
The excitation-contraction coupled phenomena are the cascade in which generation of
electric pulse leads to contraction of heart sarcolemma by conversion of electrical energy to
mechanical energy. The primary component for driving the phenomena is Ca2+ (5). The
generation of action potential opens the very slowly after the phase 0 and greater influx of
calcium is seen in the plateau phase. This causes calcium induction of calcium releases via
Sarcoplasmic Reiculum (SR). The calcium binds to calmodulin complex protein, which in turn