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Membrane excitability (dV /dt ) and conduction velocity both decrease, until conduction
m max
failure occurs at [K ] >14.4mM (hyperkalemia alone) or [K ] >13.1mM (with additional presence of
+
+
0 0
acidosis). These values of extracellular potassium concentration are within the range measured
during acute ischemia. Importantly, the slowest velocity attainable just before propagation
210
fails is ~ 17cm/sec (hyperkalemia alone) or 27cm/sec (with acidosis), consistent with experimental
observations. 202,205 These are relatively fast velocities, consistent with macro-reentry circuits (rather
than micro-reentry circuits) as the mechanism of arrhythmias during acute ischemia. Clearly,
this finding is consistent with the principle established in the previous section, that reduced
membrane excitability cannot support very slow conduction and favors failure of propagation.

Conduction is I – dependent even at greatly elevated [K ] , with only very minor contribution
+
Na 0
from I .
Ca,L
Figure 3.7. Effects of ischemia on
AP propagation. “Comma shaped”
relationship between dV /dt max and
m
conduction velocity is shown for
hyperkalemia alone (non-acidotic,
solid trace) and hyperkalemia in
presence of acidosis (acidotic, dashed
trace). A. Theoretical simulations;
numbers indicate [K ] (in mM).
+
0
Propagation fails at [K ] =14.4mM
+
0
in the non-acidotic fiber and at
[K ] =13.1mM in the acidotic fiber.
+
0
B. Experimental data obtained
under similar conditions from guinea
pig papillary muscle. From Shaw and
Rudy [209], (experimental data from
Kagiyama et. al. [205]), with
permission from Wolters Kluwer
Health, Inc.