CHAPTER 2 • ELECTRICAL ACTIVITY OF THE HEART
35
Left
Lateral
V1
V2 i
A
V3
V4
V5
v
J
a
■ FIGURE 2.20 Placement of the six precordial
chest leads and the normal appearance of the
ECG recording for leads V1
- V6. These electrodes
record electrical activity in the horizontal plane,
which is perpendicular to the frontal plane of the
limb leads.
and V overlies the left ventricular lateral wall.
6
The rules of interpretation are the same as for the
limb leads. For example, a wave of depolarization
traveling toward a particular electrode on the
chest surface elicits a positive deflection. Normal
electrical activation of the ventricles results in a
net negative deflection in V and a net positive
deflection in V6 as shown in Figure 2.20.
ELECTROPHYSIOLOGICAL
CHANGES DURING CARDIAC
ISCHEMIA
The ECG is a key tool for diagnosing myocar-
dial ischemia and infarction. A 12-lead ECG
can identify the extent, location, and progress
of damage to the heart following ischemic
injury For example, altered conduction can
result in exaggerated Q waves in specific leads
following some types of myocardial infarction.
Ischemia can also damage conduction path-
ways, leading to arrhythmias or changes in
the shape of the QRS complex. Furthermore,
ischemia can produce injury currents flow-
ing from the depolarized ischemic regions to
normal regions that can shift the isoelectric
portions of the ECG, resulting in upward or
downward shifts in the ST segment recorded
by overlying electrodes.
The mechanisms by which ischemia and
infarction alter the ECG are complex and not
fully understood. We do know, however, that
tissue hypoxia caused by ischemia results
in membrane depolarization. As ATP levels
decline during hypoxia, there is a net loss of
K+ as it leaks out of cells through KATP
channels
(normally inhibited by ATP) and as a result
of decreased activity of the Na+/K+-ATPase
pump. Increased extracellular K+, coupled
with decreased intracellular K+, causes mem-
brane
depolarization.
This
depolarization
inactivates fast sodium channels as previously
described, thereby decreasing action poten-
tial upstroke velocity. One result is decreased
conduction velocity. Changes in refractory
period and conduction velocity can lead to
reentry currents and tachycardia. Membrane
depolarization also alters pacemaker activity
and can cause latent pacemakers to become
active, leading to changes in rhythm and
ectopic beats. Finally, cellular hypoxia results
in the accumulation of intracellular calcium,
which can lead to afterdepolarizations and
tachycardia.
previous page 48 Cardiovascular Physiology Concepts  2nd Edition read online next page 50 Cardiovascular Physiology Concepts  2nd Edition read online Home Toggle text on/off