Biomedical Engineering 403

Electrical Conduction in the Heart

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4
Electrical Conduction in the Heart

Differences between myocardial action potentials and pacemaker potentials:
        Resting Potential of myocardial cells is more negative
        Very rapid rise in myocardial cell caused by fast Na+ channels
        Plateau (particularly in ventricular cell)
        Resting Potential of Pacemaker cell is unstable




Resting Potential
        approx -90 mV
        Concentration Gradients
        Sodium/Potassium Pump
        Calcium Currents

Resting cell membrane relatively permeable to K+, but not to Na+ and Ca++,
so 

        K+ tends to leave the cells following its concentration gradient
        and meanwhile electrostatic gradient brings K+ in
        but electrostatic force is slightly weaker than the diffusional
force, so K+ tends to leave cells

        Na+ tends to enter cells down its concentration gradient, so both
chemical and electrostatic forces pull Na+    into cells; Na+ leakage is
slow because of low permeability, but would gradually depolarize cell, if
not for

Sodium-Potassium Pump
        Uses enzyme Na+ K+-ATPase, which is located in the cell membrane
        Increased [Na+]i or [K+]o accelerate pump activity
        Na+ extrusion exceeds K+ introduction by 3 to 2 ratio, so it
creates a potential difference
        Digitalis partially inhibits this pump, making the resting
membrane potential less negative than normal





Action Potential
        Rapid Upstroke of Action Potential--caused by influx of Na+
                Peak amplitude of action potential is correlated with
[Na+]o
        Partial Repolarization
        Plateau
        Repolarization

Peak muscle force occurs with repolarization

Rapid Upstroke:
        When threshold  voltage (approx -65 mV) is reached, Na+ channels
in cell membrane open, allowing influx                 of Na+
        Any process that reduces the membrane potential activates the Na+
channels
        The influx of Na+ further depolarizes the membrane opening more
Na+ channels
        The influx of Na also initiates closing of channel, however
inactivation takes some time
        When membrane voltage reaches zero, the electrostatic pull on Na+
is neutralized, but Na+ keeps leaking in              down its
concentration gradient (the quantity of Na+ entering cell is not enough to
cause a             measurable change in [Na+]i, so chemical force remains
virtually constant
                at +20 mV Na+ keeps leaking in but slowly, as Na+ channels
are beginning to close
        When membrane potential reaches +30 mV, the gates are all closed
and Na+ influx ceases
        The channels remain closed during first half of depolarization,
therefore this is an absolute refractory period                 (protects
the heart from tetanus)

Early limited repolarization between upstroke and plateau phases:
        Represents an efflux of K+ from the cell because of concentration
gradient and positive charge of cell

Plateau
        The influx of positively charged Ca++ is balanced by the efflux of
an equal amount of K+
        The Ca++ channels open as a result of the positive charge of the
cell interior
        These Ca++ channels are blocked by calcium channel blockers, such
as Verapamil

Final Repolarization
        The efflux of K+ from the cell begins to exceed the influx of
Ca++.

Restoration of Ionic Concentrations
        Excess Na+ in the cell  is removed by Na+/K+ pump
        Excess Ca++ that entered the cell is eliminated by an Na+/Ca++
exchanger, which exchanges 3 Na+ for 1           Ca++.

Peak muscle contraction coincides with repolarization

Refractoriness

Effect of change in HR on action potential duration

Effect of calcium channel blockers

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