Page 357 - Cardiac Nursing

6
6
/30
xd
xd
6
/30
1
2:1
2:1
/09
/09
1
33
c.
3-3
p
p
33
3-3
q
q
q
In
87.
87.
A
A
A
33
33
a
ara
ara
t
t
p
p
p
M
Pa
Pa
6 A
6 A
M
g
e 3
In
a
g
g
e 3
c.
0-c
K34
0-c
16_
16_
K34
LWBK340-c16_ pp333-387.qxd 6/30/09 12:16 AM Page 333 Aptara Inc.
c.
LWB
LWB
CHAPTER
r
u
b
b
n
n
D
D
a
e
e
s
y
n
n
c
c
o
C
C
d
n
o
C
h
a
i
m
d
d
n
t
c
u
i
i
t
u
d
d
d
u
u
d
r
r
A A A A Arrhythmias and Conduction Disturbances
h
h
r
Carol Jacobson
id
o
au automatic rate off a subsidiiary pacemaker rises above that of thhe SA
v
b
te
bo
i
A
S
ry
t
MECHANISMS OF no de I ea ga to ne dr e le ma li ti , o
node. Increased vagall tone, druugs, electrolyte abnormalitieess, or dis-
a
ca
se
ut
of
ic
at
n
o
ARRHYTHMIAS ea ease off thhe SA node can ddecrease its ratee of automaticiity or can
b
it
us
ex
it
m
o
pu
ck
ca causee exit bllock off its impulse, thus allowing subsidiary pacemakers
ls
mi
a
to assume control of thhe heart. EExamples off clinical arrhhythmias due
am
pl
th
es
f
in
o
d
cl
al
ic
t
Ca rd ia ar rh yt h p ul se i ni ti at io n, a b
Cardiacc arrhythmias result from abnormal impulse initiation, ab-
normal impulse conduction, or both mechanisms together. Abnor- to shifting of the pacemaker from the SA node include atrial, junc-
mal impulse initiation includes enhanced normal automaticity, tional, or ventricular escape rhythms that occur due to sinus brady-
abnormal automaticity, and triggered activity resulting from after- cardia or AV block. Such “escape” pacemaker activity cannot be con-
depolarizations; abnormal impulse conduction includes conduc- sidered abnormal because it is a manifestation of the normal
tion block and reentry. 1–5 Although all of these mechanisms have automaticity of these cells. Sinus tachycardia is due to enhanced
been shown to cause arrhythmias in the laboratory, it is not pos- normal automaticity, and accelerated ventricular rhythm following
1,3
sible to prove which mechanism is responsible for a particular ar- myocardial infarction (MI) may be due to enhanced automaticity.
rhythmia using currently available diagnostic tools in the clinical Subsidiary pacemaker activity can be enhanced by factors that
setting. However, it is possible to postulate the mechanism of decrease the transmembrane resting potential (TRP), decrease the
many clinical arrhythmias based on their characteristics and be- threshold potential, or increase the rate of diastolic phase 4 depo-
havior and to list rhythms most consistent with known electro- larization of the subsidiary pacemaker cells. Figure 16-1 illustrates
physiologic mechanisms. 3–6 Some arrhythmias, such as atrioven- how these mechanisms can change the rate of firing of pacemaker
7
tricular nodal reentry tachycardia (AVNRT), atrial flutter, some cells.
ventricular tachycardias (VTs), and reentry tachycardias involving Enhanced normal automaticity can occur with enhanced sympa-
accessory pathways, have been proven to be caused by reentry. thetic activity; drugs such as digitalis and sympathomimetic agents;
This section describes the major mechanisms of arrhythmias and ischemia; stretch that occurs in heart failure (HF), cardiomyopathy,
lists arrhythmias suggested or proven to be caused by each mech- and ventricular aneurysms; and with genetic mutations that alter the
3–5,8,9
anism whenever possible. Knowledge of the cardiac action poten- function of ion channels in the cardiac membrane. Clinical ar-
tial is essential in understanding concepts presented here (see rhythmias that may be due to enhanced normal automaticity include
Chapter 1). sinus tachycardia, some atrial tachycardias (ATs), junctional tachy-
cardia, accelerated ventricular rhythm, and ventricular parasystole.
Automaticity is not the mechanism of most rapid tachycardias but it
Abnormal Impulse Initiation
can precipitate or trigger reentrant tachycardias that can occur at
Abnormal impulse initiation can be due to enhanced normal au- very rapid rates. 4
tomaticity, abnormal automaticity, or afterdepolarizations. It is Abnormal Automaticity. Atrial and ventricular myocardial
important to understand the property of normal automaticity be- cells that do not normally have automaticity can develop abnormal
fore considering these other mechanisms.
automaticity when their TRP is reduced and is referred to as de-
polarization-induced automaticity. 1,4 Subsidiary pacemakers like
Automaticity
those in the Purkinje system that are normally overdrive suppressed
Automaticity is the ability of certain cardiac cells to spontaneously
by the faster SA node can also develop abnormal automaticity
depolarize and initiate an electrical impulse without external stim-
when their TRP is reduced. This abnormal automaticity is thought
ulation. The sinus node (or sinoatrial [SA] node) is the normal
to be mediated by the slow inward current carried mainly by cal-
pacemaker of the heart because it has the fastest rate of auto-
cium (slow channels) because the normal fast sodium channels are
maticity. Other cells in the heart also have the property of auto- 1,3,4
inactivated at reduced membrane potentials. However, both
maticity, including cells in several areas of the atria, coronary si-
sodium and calcium channels may play a role in the development
nus, pulmonary veins, atrioventricular (AV) junction, AV valves,
of abnormal automaticity. Abnormal automaticity that develops at
and Purkinje system. The rates of these other pacemakers are
more negative diastolic potentials, between 70 and 50 mV, can
slower than the rate of the SA node; therefore, they are suppressed
be suppressed by sodium channel blockers, indicating that a
by the SA node under normal conditions, a phenomenon known
sodium current is involved, whereas automaticity that develops at
as overdrive suppression. The site of fastest impulse initiation is re-
less negative diastolic potentials, from 50 to 30 mV, can be
ferred to as the dominant pacemaker, whereas sites of impulse for- 2,4
suppressed by calcium channel blockers.
mation that are suppressed by the dominant site are called sub-
The resting potential of a cell can be reduced (e.g., from 90 to
sidiary or latent pacemakers.
70 mV) and the cell partially depolarized by anything that in-
Enhanced Normal Automaticity. Impulse initiation can be creases the extracellular potassium concentration, decreases the in-
shifted from the SA node to other parts of the heart if the rate of tracellular potassium concentration, increases the permeability of
the SA node drops below that of a subsidiary pacemaker or if the the membrane to sodium, or decreases the membrane permeability
333