Biomedical Engineering Reference
In-Depth Information
6.5
Action Potential
The ionic composition, in particular sodium, potassium, and calcium contents, of
cardiomyocyte sarcoplasma is controlled by ion channels, pumps, and exchangers
that maintain steep ion concentrations and electrical gradients across the thin
sarcolemma (
6 nm) that surrounds myofibrils (Table
1.4
). The sarcolemma has
a high and low conductance for K
+
and Na
+
, respectively. The resting membrane
potential is about equal to
∼
88 mV (inside negative).
Strong, acute changes in intracellular calcium concentration that are related to
release from and reuptake into Ca
2
+
stores determine action potential features such
as channel conductance possibly via Ca
2
+
-binding proteins such as calmodulin,
therefore adapting ion channel functioning to the body's need. Calcium ions actually
modulate various ion channels in ventriculomyocytes. For example, Ca
2
+
regulates
the magnitude of ion flux (
i
Na
) through voltage-gated sodium channels without
affecting kinetic properties such as gating [
620
]. Voltage-gated Na
+
channels
control action potential upstroke. Cardiac action potentials result from time course
of depolarizing inward and repolarizing outward ionic currents through a set of ion
carriers (channels, exchangers, and pumps; Table
6.15
).
Action potential shape changes between neonatal and adult cardiomyocytes.
Neonatal cardiomyocytes indeed have action potentials with brief plateau and longer
duration than that of adults due to [
621
]: (1) decreased density and modified
inactivation of transient outward K
+
currents; (2) increased delayed rectifier K
+
currents; (3) Ca
2
+
influx through T-type (Ca
V
3) and L-type (Ca
V
1) Ca
2
+
channels;
(4) increased Ca
2
+
influx through Na
+
-Ca
2
+
exchangers; and (5) Ca
2
+
transients
from Ca
2
+
entry rather than release from the sarcoplasmic reticulum.
The heterogeneity of action potential shapes according to nodal cell type is
illustrated in Fig.
6.6
. Purkinje and ventricular action potentials exhibit a plateau
(phase 2). Atrial action potentials have a blunt triangular shape (absence of phases 1
and 2). The upstroke is slow because the fluxes elicited by Ca
2
+
channels are smaller
and these channels are activated more slowly than Na
+
channels (triangle-shaped
action potential). Activated non-selective cation channels induce a slow increase in
transmembrane voltage after the end of the action potential, up to the triggering
threshold for action potential.
The features of the action potential (initial depolarization rate, duration, etc.)
depend on the activities of involved ion channels of the nodal cells in the
different compartments of the conduction network and cardiomyocytes in walls of
atria and ventricles, and within the ventricle, according to the myocardium layer
(subendocardial, midmyocardial, and subepicardial; Table
6.16
). The duration of the
action potential depends on the nodal tissue territory with the following sequence
of increasing order: (1) distal Purkinje fibers (
−
400 ms, with upstroke of 500-
600 V/s), (2) proximal Purkinje fibers and His bundle, (3) midmyocardial layer,
(4) subendocardial layer, (5) subepicardial layer, and (6) atria, SAN, and AVN
(
∼
∼
150 ms, with upstroke of 2-10 V/s) [
468
].
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