inactivation also would decrease the maximal
degree of depolarization. These changes in
phase 0 would reduce the conduction velocity
within the ventricle. Blockade of fast sodium
channels is the primary mechanism of action
of Class I antiarrhythmic drugs such as quini-
dine and lidocaine.
CASE 2-1
Reentry requires that cells can be prematurely
reexcited by action potentials emerging from
adjacent conducting pathways. By increas-
ing the ERP of these cells, the action poten-
tial emerging from adjacent pathways may
encounter tissue that is still refractory and
therefore unexcitable, thereby preventing or
abolishing reentry.
CASE 2-2
Sympathetic nerve activity increases conduc-
tion velocity within the AV node (positive
dromotropic effect). This effect on the AV
node is mediated by norepinephrine binding
to P-adrenoceptors within the nodal tissue.
A P-blocker would remove this sympathetic
influence and slow conduction within the AV
node, which might prolong the PR interval.
Therefore, taking the patient off the P-blocker
might improve AV nodal conduction and
thereby decrease the PR interval to within the
normal range (0.12 to 0.20 seconds).
CASE 2-3
The QRS complex has no net voltage in lead
I (i.e., equally positive and negative voltages),
which indicates that the mean electrical axis
is perpendicular (90°) to lead I (see Rule 3);
therefore, it is either at -90° or +90° because the
axis for lead I is 0° by definition. Because the
QRS is positive in leads II and III, the mean
electrical axis must be oriented toward the
positive electrode on the left leg, which is used
for leads II and III. Therefore, the mean elec-
trical axis cannot be -90°, but is instead +90°.
Both aVL
and aVR
leads would have net negative
QRS voltages because the direction of the mean
electrical axis is away from these two leads,
which are oriented at -30° and -150°, respec-
tively (see Fig. 2.19). Furthermore, the net neg-
ative deflections in these two augmented leads
would be of equal magnitude because each lead
axis differs from the mean electrical axis by the
same number of degrees.
Dubin D. Rapid Interpretation of EKGs. 6th Ed. Tampa:
Cover Publishing, 2000.
Katz AM. Physiology of the Heart. 4th Ed. Philadelphia:
Lippincott Williams & Wilkins, 2006.
Lilly LS. Pathophysiology of Heart Disease. 5th Ed.
Philadelphia: Lippincott Williams & Wilkins, 2011.
Opie LH. The Heart: Physiology from Cell to Circula
tion. 4th Ed. Philadelphia: Lippincott Williams &
Wilkins, 2004.
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