ASIDOSIS

Thus, both [Ca2+]i decline and shortening cause a progressive decline

in the
contractile state as systole gives way to diastole. Both the Ca2+
transient properties and the myofilament
Ca2+ sensitivity and cross-bridge cycling rate are altered under
physiologic conditions, such as
sympathetic stimulation and local acidosis or ischemia, as discussed
later.

Gap junctions can also change their electrical resistance. When the
intracellular calcium level rises, as in
myocardial infarction (MI), the gap junction may close to help seal off
injured from noninjured cells.
Acidosis increases and alkalosis decreases gap junctional resistance.
Increased gap junctional resistance
tends to slow the rate of action potential propagation, a condition
that could lead to conduction delay or
block. Cardiac-restricted inactivation of gap junctions decreases
transverse conduction velocity to a
greater degree than longitudinal conduction, thereby resulting in an
increased anisotropic ratio, which
may play a role in premature sudden death from ventricular
arrhythmias.

\
Conditions present during ischemia—acidosis, aster rates o
cell stimulation, and increased
extracellular potassium concentration (and consequently a
less negative diastolic membrane

Uremia, hyperkalemia, acidosis, and disorders of calcium-phosphorous

balance are all linked to higher
rates of atrial and ventricular arrhythmias

prognosis

In general, the specific

type, prognosis, and management of VT depend on the presence of
underlying structural heart disease.
With the exception of patients with inherited VT–sudden cardiac death
syndromes (see Chapter 33), if
structural heart disease is absent, the prognosis in patients with VT
and PVCs is generally very good,4
whereas in those with structural heart disease, the subsequent risk for
sudden cardiac death (SCD) is
increased.