Acs0802 Acute Cardiac Dysrhythmia

© 2003 WebMD Inc. All rights reserved. ACS Surgery: Principles and Practice
8 CRITICAL CARE 2 ACUTE CARDIAC DYSRHYTHMIA — 1

2 ACUTE CARDIAC DYSRHYTHMIA
Caesar Ursic, M.D., and Alden H. Harken, M.D.

Management of Acute Dysrhythmias

After successful cardiopulmonary resuscitation (CPR) or any mal heart, the so-called atrial kick adds almost nothing to cardiac
myocardial ischemic event, the most common source of hemody- output.2 If normal sinus rhythm is abolished and atrial fibrillation
namic instability is an abnormal heart rhythm. This chapter out- is electrically induced in a young healthy patient, the ventricles
lines the approach to a patient with an apparent acute cardiac and the rest of the cardiovascular system compensate almost
dysrhythmia. immediately to prevent a fall in cardiac output.3 On the other
The purpose of the heart’s electrical activity is to induce hand, loss of synchronous atrial activity in patients with end-stage
mechanical activity. Abnormal electrical activity that occurs in cardiac decompensation may decrease cardiac output by as much
the absence of hemodynamic compromise should be examined as 40%4; fortunately, such a degree of end-stage cardiac compro-
but treated with forbearance because therapy itself poses some mise is rare.
hazards: all antidysrhythmic agents, except oxygen, are nega-
tively inotropic. In the evaluation of a patient who appears to CARDIOVERSION
exhibit an acute cardiac dysrhythmia, four questions should be Cardioversion delivers sufficient electrical energy to the pre-
asked: cordium (or directly to the heart) to depolarize cells, even those
1. Does the patient actually have a cardiac dysrhythmia? in a relatively refractory state. Cardioversion imposes electrical
2. Does the patient require any therapy (i.e., is the patient suffi- reorganization on the heart. In theory, after this massive depolar-
ciently stable that treatment is NOT indicated)? ization, all the myocardial cells will repolarize simultaneously and
3. How soon should therapy be started (i.e., how unstable is the then reinstitute a synchronous beat [see Sidebar The Intracardiac
patient)? Cardioverter Defibrillator].
4. Which therapy is the safest and most effective? Certain precautions are necessary with cardioversion.The pro-
cedure is of no use in patients who are in asystole or who have
fine ventricular fibrillation (VF), because these patients have no
Patient Is Hemodynamically cardiac activity to organize—though, again, cardioversion does no
Unstable harm in such cases (as it is said, “you cannot fall off the floor”).
The choice of therapy is determined Supraventricular dysrhythmias such as atrial flutter can be con-
by the stability of the patient and the verted with extremely low energy levels (e.g., ≤ 5 joules), but
origin of the dysrhythmia. An electro- such low levels should not be employed in emergency situations.
cardiogram is helpful but not required. For a hemodynamically unstable patient, the initial cardioversion
Patients with asystole require CPR [see should be with 100 joules; if the dysrhythmia is not abolished, the
8:1 Cardiac Resuscitation]. All hemody- voltage should be increased rapidly (to a maximum of 360
namically unstable patients who have a joules).
dysrhythmia other than asystole should be treated immediately
by cardioversion. Actually, cardioversion of asystole will do no
Patient Is Hemodynamically
harm; it just will not help, because there is no underlying rhythm
Stable
to reorganize. If in doubt, therefore, one should proceed with
cardioversion.
VENTRICULAR RATE IS SLOW
The two primary goals in the management of an acute dys-
rhythmia are to control the ventricular rate and to maintain a nor- If the patient is bradycardic before
mal sinus rhythm. It is important to note that hemodynamic or after cardioversion, atropine should
instability in a patient who has a ventricular rate between 60 and be administered in a 0.5 mg I.V. push.
100 beats/min is almost certainly not the result of a cardiac This dose may be repeated at 2-
rhythm disturbance. Furthermore, heart rates in excess of 100 minute intervals. Because the effects of
beats/min do not necessarily require therapy. Most patients can atropine are transient, a temporary internal or external pacemak-
remain hemodynamically stable—and, in fact, increase their car- er should be used to maintain the heart rate. Insertion of an inter-
diac output—while raising their heart rate to 220 beats/min nal pacemaker consistently takes longer than predicted; an exter-
minus their age. In addition, it is not critical to reestablish normal nal pacemaker is a very effective temporizing maneuver [see
sinus rhythm in all cases.1 In a young, healthy patient with a nor- Sidebar Troubleshooting a Pacemaker].


Management of Acute Dysrhythmias

Patient has a cardiac dysrhythmia

Patient is hemodynamically stable Patient is hemodynamically unstable

Determine whether ventricular rate is slow or fast. Cardiovert (100–400 joules) all
(If at any time the patient becomes hemodynamically dysrhythmias except asystole.
unstable, proceed with cardioversion, 100–400 joules,
for all dysrhythmias except asystole.)

Ventricular rate is slow (< 60 beats/min) Ventricular rate is fast (> 100 beats/min)

Give 0.5 mg atropine I.V.; repeat at 2-min Obtain a full 12-lead ECG plus a long rhythm
intervals if necessary. Proceed to insertion of strip (any lead with good voltage).
temporary transvenous pacemaker. Determine whether QRS complex is narrow
Remember: External pacing can reverse or wide.
bradycardia rapidly and can be extremely
effective in an emergency.

QRS complex is wide (> 0.08 sec, QRS complex is narrow If QRS width is confusing Patient becomes
or 2 small boxes on ECG paper) (< 0.08 sec) and you cannot tell whether hemodynamically unstable
it is < or > 0.08 sec
Cardiovert (starting with an energy Give verapamil. Cardiovert (100–400 joules)
level of 100 joules), and give Mix 10 mg verapamil in 10 ml Give 6 mg adenosine I.V. all dysrhythmias except
lidocaine, 100 mg I.V. saline; give 1 mg/min until bolus × 2. asystole.
ventricular rate slows and begin
digitalization.

Ventricular rate slows Ventricular rate does
not slow
Treat as narrow-complex Treat with cardioversion as
Ventricular rate Ventricular rate slows (< 0.08 sec) tachycardia. a wide-complex (> 0.08 sec)
breaks suddenly tachycardia.
The patient has sinus tachycardia;
Begin digitalization. treat the underlying causes (e.g.,
fever, infection, hemorrhage,
stress, and pain).


The Intracardiac Cardioverter Defibrillator
Over 30 years ago, Michel Mirowski developed the first automatic intracar- heavy (though newer batteries are becoming lighter), and circuitry, which is
diac cardioverter defibrillator (ICD), a device that detects dangerous tachy- light, with a total weight of less than 100 g. Most implanted defibrillators are
arrhythmias and delivers a cardioverting shock.55 In the intervening time, it currently placed without a thoracotomy. A sensing and defibrillating lead
has become abundantly clear that some of the 400,000 Americans who die system (14 French) is inserted percutaneously via the subclavian vein into
“suddenly” of tachyarrhythmias each year could have been identified as high right ventricular–right atrial position. The distal electrode tip senses ventric-
risk, although they could not have been saved by pharmacologic or surgical ular fibrillation and tachycardia. The cardioverting energy is then discharged
treatment. For these patients, an ICD can be lifesaving.56 between a coil electrode on the diaphragmatic surface of the right ventricle
The ICD identifies dangerous rhythm patterns by means of two algo- and another coil electrode positioned in the superior vena cava.
rithms. The first of these algorithms analyzes the patient’s heart rate. The It is now clear that ICDs really do work and are capable of extending life.
patient’s maximum attainable sinus rate must be determined by exercise The most effective predictor of outcome in patients with ICDs is the severi-
testing before the device is implanted; the ICD is then programmed to de- ty of heart failure.60 The ICD does not prevent malignant arrhythmias: it is, in
tect heart rates above this value. (The ICD can be externally programmed essence, a safety net that cardioverts ventricular tachycardia or VF when it
to detect rates between 155 and 200 beats/min.57) occurs. Therefore, it must still be used in conjunction with antidysrhythmic
Using rate criteria alone, however, the ICD cannot discriminate between drugs.61,62
sinus tachycardia and ventricular or supraventricular tachycardia. Inappro- It is easy for a surgeon to become spooked by an ICD. The most effec-
priate shocks are the Achilles heel of the ICD: almost one third of patients tive strategy for managing a patient with an ICD is simply to ignore the ICD.
experience at least one inappropriate shock annually, when the device de- If such a patient is being transported to the OR, however, the device should
tects an episode of sinus tachycardia in which the rate exceeds the thresh- be inactivated before the electrocautery is used: the ICD will misinterpret
old programmed earlier. The ICD misinterprets the event as ventricular the cautery current as VF and respond by delivering a shock to the patient.
tachycardia and delivers a shock to the hemodynamically stable patient.58 The aura of mystery surrounding the ICD may be instantly eliminated by
Patients liken this to being punched hard in the chest. Although rarely of turning off the device (see below). Once the ICD is inactivated, the patient
electrophysiologic significance, an inappropriate shock can be psychologi- can be treated as any other patient would be. If external cardioversion is in-
cally crippling.59 dicated, the ICD can be disregarded; external cardioversion will not harm or
Although computer circuitry is facile and rapid, an ICD recognizes patterns activate it.
poorly. Fine (or even coarse) VF may not exhibit enough positive spikes to be
recognized as a tachyarrhythmia by the ICD. A second algorithm (the prob- How to Turn the ICD Off
ability density function algorithm) was developed to analyze electrophysio- 1. If you can find the industry representative to program the device to re-
logic data and improve the specificity of the ICD’s sensing circuitry. A unique main off, do so. Then treat the patient exactly as you would if the ICD
feature of ventricular fibrillation is the virtual absence of isoelectric time. were not present.
Conversely, during sinus tachycardia and supraventricular tachycardia, the 2. If you cannot find the representative or the situation is urgent:
ECG is at the isoelectric baseline much of the time. The probability density a. Palpate the ICD generator, which is typically implanted in the left
function algorithm enables the ICD to determine the proportion of time that subcostal region.
the ECG is spending at the isoelectric baseline and thereby to detect ven- b. Place a heavy pacemaker (or, better yet, an ICD magnet) over the
tricular fibrillation. upper corner of the device, toward the patient’s left shoulder. Older
The ICD typically requires more than 5 seconds to appreciate ventricular devices used to emit a soft beep (synchronous with the heartbeat) in
tachycardia or fibrillation. It then charges its energy storage capacitors for 15 response to a magnet when they were active. Unfortunately, that
seconds and delivers a 30-joule cardioverting shock. If necessary, the device feature has since been engineered out, and newer ICDs are silent.
will deliver a second, third, fourth, and fifth countershock. If the rhythm disor- c. Tape the magnet in place over the upper border of the device. As
der persists after the fifth countershock, the device will not recycle. long as the magnet is in place, the ICD is off and the electrocautery
ICD systems are not complex. The device consists of a battery, which is can be used safely.

VENTRICULAR RATE IS FAST
access the high-velocity Purkinje fibers as rapidly as a normal
If a patient is hemodynamically sta- impulse, and ventricular activation is delayed. The QRS complex
ble, a full 12-lead electrocardiogram is arising from an ectopic ventricular locus is therefore wider, signi-
helpful; a long rhythm strip should be fying aberrant ventricular conduction [see Figure 1].
obtained as well. The best ECG lead to Because dysrhythmias of supraventricular origin typically dis-
use for evaluating acute dysrhythmias is play a narrow QRS complex, the width of the QRS can generally
one that has good-voltage QRS com- be used to distinguish dysrhythmias of ventricular origin from
plexes and maximal P waves, if the lat- those of supraventricular origin [see Figure 2]. A wide QRS, how-
ter are present at all. ever, may also be produced by an impulse that originates in the
atrium and is aberrantly conducted to or through the ventricles
Electrocardiography (supraventricular rhythm with aberrancy). Such rhythms are rel-
A cardiac impulse produces a positive, or upward, deflection on atively uncommon, constituting approximately 10% of all wide-
the monitor or oscilloscope as it approaches an ECG electrode complex tachycardias; more important, these patients will not
and a negative, or downward, deflection as it moves away from the suffer if their dysrhythmias are treated as though they were of ven-
electrode. The important factor in dysrhythmia recognition, how- tricular origin.
ever, is not the direction of the impulse but its duration and loca- When the ventricular rate is fast and the QRS is narrow, the
tion. Normal conduction velocity is fast: an impulse is transmitted 12-lead ECG should be searched for P waves, which indicate the
by healthy Purkinje fibers at a rate of 2 to 3 m/sec.3 Hence, when presence of atrial activity. If P waves are absent and the QRS
an impulse that arises in the atrium (supraventricular) is transmit- complexes occur at irregular intervals [see Figure 3], the patient
ted via the atrioventricular (AV) node to the high-velocity Purkinje probably has atrial fibrillation. It is not crucial to know this, how-
system, the entire ventricle is electrically activated in 0.08 second ever; the focus should be on the width of the QRS complex. A cal-
(80 milliseconds; or two small boxes on ECG paper). An impulse cium channel blocker (verapamil or diltiazem) should be admin-
that is generated at an ectopic ventricular site, however, cannot istered to control the ventricular rate. For verapamil, 10 mg is


Patient with pacemaker experiences palpitations or presyncope

Obtain 30-second rhythm strip to assess pacing and sensing functions.

All wide (paced) QRS complexes Heart rate is adequate, and Some or all pacemaker artifacts
are preceded by pacemaker no pacemaker artifacts are visible are not followed by wide (paced)
artifacts QRS complexes
Place magnet over pacemaker
Pacing function is normal. to inactivate sensing circuit and Ventricular pacing threshold is
convert to fixed-rate mode. higher than pacemaker output.

No pacemaker artifacts Pacemaker artifacts that appear Pacemaker artifacts that appear
are visible with magnet at appropriate distances from at appropriate distances from
prior QRS complexes (i.e., outside prior QRS complexes (i.e.,
Pacemaker battery is dead. refractory period) provoke paced outside refractory period) do not
QRS provoke paced QRS

Sensing and pacing functions Consider two possibilities:
are normal. • Adequate pacemaker output may
not be reaching an excitable
portion of the ventricle, or
• Ventricular pacing threshold is
higher than pacemaker output.

Troubleshooting a Pacemaker
Few industries have benefited more from the United States space pro- Obtain drug history to rule out an increase in ventricular
gram than has the cardiac pacemaker industry. Much of the microcircuit- threshold caused by antidysrhythmic agents.
ry developed for the space shuttle is directly applicable to pacemakers. Obtain chest x-ray to determine whether endocardial
Yet the array of programmable parameters that has become standard in lead has been fractured or dislodged.
most implanted pacemakers, while providing therapeutic flexibility to
electrophysiologists, can be intimidating to the mere mortal surgeon. The
purpose of this discussion is to delineate simple methods for identifying
problems with the two dominant pacemaker functions: pacing and sens- Endocardial lead is intact and in good anatomic position
ing (see above and right).
Any of the following situations might prompt evaluation of pacemaker Reprogram pacemaker to higher output.
function: (1) the patient informs you that he or she has a pacemaker, (2)
you note a pacemaker bulge in the pectoral area, (3) a chest x-ray re-
veals a pacemaker with a wire descending onto the diaphragmatic sur-
face of the right ventricle, or (4) a patient with an implanted pacemaker All pacemaker artifacts are Intermittent capture
notes symptoms of palpitations or presyncope. At this point, you need followed by a paced beat persists
to obtain a 30-second rhythm strip to determine whether the pacemak-
er can capture the patient’s ventricle—that is, whether the pacemaker Relocate endocardial lead
emits an impulse that stimulates the ventricle to depolarize. to lower threshold site.
(continued)

mixed into 10 ml of saline, and 1 mg/min is given until the ven- Verapamil and diltiazem act by producing profound AV nodal
tricular rate slows. For diltiazem, 0.25 mg/kg—15 to 20 mg is a blockade (see below); however, they are also peripheral vasodila-
reasonable dose for the average patient—is given over 2 minutes; tors.6 Moderate to profound systemic hypotension can be antici-
the dose can be repeated in 15 minutes at 20 to 25 mg (0.35 pated until the patient converts to sinus rhythm.
mg/kg) over 2 minutes. A patient with a wide-complex tachycar- Much has been written about the risks of using calcium chan-
dia—or any patient who is hemodynamically unstable—is treated nel blockers in patients who are already receiving beta blockers.
by cardioversion (see above), commonly followed by administra- Abrupt and complete AV block rarely occurs, however, and in the
tion of lidocaine, 100 mg I.V., whereas a patient with a narrow- vast majority of patients, persistent supraventricular tachycardia
complex tachycardia should be treated with verapamil3,5 or dilti- poses a greater risk than the possibility of third-degree heart
azem to retard impulse conduction through the AV node. block. Therefore, previous beta blockade should not be consid-
Therefore, it is not necessary to identify the speciﬁc type of dys- ered a contraindication to the use of a calcium channel blocker.
rhythmia in order to treat it effectively. Some clinicians may prefer to use adenosine.


Troubleshooting a Pacemaker (continued)
Ventricular Capture heart rate has recovered, and the rhythm strip will look like rhythm strip b. In
a a patient in whom heart rate is adequate and no pacemaker artifacts are
visible, it is necessary to override the pacemaker’s sensing circuit to deter-
mine whether the pacemaker is capable of emitting a pacing impulse that
will capture the ventricle. The pacemaker’s sensing circuit may be inactivat-
ed by placing a magnet over the pacemaker. Alternatively, the pacemaker
may be reprogrammed to a paced rate that is faster than the patient’s in-
trinsic heart rate. In this fashion, capture may easily be assessed. (Unfortu-
nately, the programmers are expensive and are therefore often locked in
some inaccessible closet. Programmers have great theoretical value but
very little practical value to the surgeon.)
c

Note the pacemaker artifact (↑) that precedes each wide QRS complex in
rhythm strip a, above. The QRS complex is wide because ventricular acti-
vation does not originate from the AV node, and ventricular conduction is
therefore aberrant. At this point, you know that your patient is pacing, and
you can determine the pacing rate. You do not, however, know the pacing
threshold (i.e., the minimum voltage required for ventricular capture) or the
safety margin between pacemaker output and pacing threshold. At this
moment (and presumably yesterday and tomorrow), this pacemaker is ap-
propriately discharging its most important function—pacing the heart and Magnet
maintaining an adequate rate.
In rhythm strip c, above, a magnet has converted the patient’s pacemaker
Ventricular Sensing from the demand mode to the fixed-rate mode. The pacemaker artifacts
b that precede the wide (paced) QRS complexes in this rhythm strip (black
arrows) show that the pacing function of this pacemaker is intact. Occa-
sionally, a pacemaker artifact occurs during the electrical refractory period
that immediately follows the QRS complex (red arrows). Pacing during the
refractory period will not result in ventricular capture. Pacing during the re-
fractory period should not result in ventricular capture and must not be in-
terpreted as intermittent capture. In a patient whose pacemaker seems to
be sensing appropriately (as in rhythm strip b), the magnet permits assess-
ment of ventricular capture. Rhythm strip c demonstrates normal ventricu-
lar capture in the presence of a magnet.
Some or All Pacemaker Artifacts Are Not Followed by Wide QRS
In rhythm strip b, above, normal P waves are followed by regular QRS com- Complexes
plexes, and no pacemaker artifacts are evident. It is most likely that this pa- If a pacemaker impulse that occurs outside the refractory period is not fol-
tient’s pacemaker has been programmed to fire at a paced rate that is lowed by a wide QRS complex, two possibilities should be considered.
slower than this patient’s intrinsic heart rate, and the pacemaker is thus ap- First, an adequate pacemaker impulse may not be reaching an excitable
propriately sensing each QRS complex. It is unlikely but possible, however, portion of the ventricle because of fracture or dislodgment of the endocar-
that the pacemaker is not sensing appropriately. Instead, one of the follow- dial lead. This problem can usually be identified by a chest x-ray. Second, if
ing problems may be occurring: (1) the pacemaker battery is dead, which the chest x-ray shows that the lead is intact and in good anatomic position,
is unlikely unless the battery was implanted more than 5 years ago, (2) the the pacemaker output is not sufficient to reach the pacing threshold. Occa-
intracardiac electrode has been fractured, which is also unlikely, because sionally, this problem is caused by fibrosis at the endocardial electrode tip. If
current leads are remarkably durable, (3) the intracardiac electrode has the pacemaker can be reprogrammed to a higher output, the capture prob-
been dislodged (this is an uncommon late problem that typically results in lem should resolve. Otherwise, the lead must be repositioned to a site at
pacemaker artifacts unrelated to each QRS complex), or (4) the patient is which the pacing threshold is lower.
taking an antidysrhythmic drug that has profoundly depressed ventricular
excitability below threshold level for capture (this problem is very rare and Occasional Pacemaker Artifacts Closely Follow a Spontaneous QRS
can be excluded by taking a drug history). It is overwhelmingly likely, there- Complex
fore, that rhythm strip b simply demonstrates that the pacemaker is sensing If the patient’s rhythm strip looks like rhythm strip c, in the absence of a
appropriately. magnet, the pacemaker is not sensing properly. In the demand mode, most
pacemakers require at least a 2.5 mV signal to suppress output. Thus, if
Assessing Ventricular Capture When the Spontaneous Heart Rate Is the pacemaker emits stimuli in spite of a normal spontaneous heart rate, an
High adequate QRS signal either is not being sensed (the lead tip may be lodged
Typically, by the time you see the syncopal patient in the emergency de- at the site of a prior myocardial infarction or scar) or is not being transmitted
partment or recovery room, the patient is sufficiently excited that his or her to the pacemaker (because of lead fracture or dislodgment).

Adenosine (see below) produces conduction delay in the AV utes, by a ﬁnal 12 mg I.V. push over 2 seconds.2,7
node and deserves recognition as a second very good option Patients receiving adenosine complain of a frightening feeling
(albeit only a transiently effective one) for treatment of paroxys- of breathlessness and pressure that is not angina or dyspnea.This
mal narrow-complex tachycardia or for diagnosis of supraventric- feeling typically resolves within 30 seconds. Facial ﬂushing is also
ular tachycardia with aberrancy (including Wolff-Parkinson-White common. Unlike verapamil, adenosine is associated with
syndrome). Adenosine is given in a 6 mg I.V. push, followed 2 hypotension in fewer than 1% of patients.Transient atrial or ven-
minutes later by a 12 mg I.V. push and then, after another 2 min- tricular ectopy, with varying degrees of AV block, occurs in more


ventricular rate between 60 and 100 beats/min is the ultimate
goal of antidysrhythmia therapy).
Adenosine
Adenosine is an endogenous nucleoside that has differential
antidysrhythmic effects in both supraventricular and ventricular
tissue. The appeal of adenosine as a therapeutic and diagnostic
tool is that it depresses automaticity and conduction within the
SA and AV nodes.9 Two clinically relevant types of adenosine
Figure 1 This tracing depicts frequent ventricular ectopic depo- receptors are present in cardiac tissue: (1) A1 receptors, which are
larizations interspersed among depolarizations from a supraven- present on AV nodal tissue and cardiomyocytes and which thus
tricular source. Note that the QRS depolarizations of supraven- mediate AV block and even bradycardia; and (2) A2 receptors,
tricular origin are narrow, whereas the QRS complexes of ectopic which reside on vascular endothelial and smooth muscle cells and
ventricular origin are wide. mediate coronary vasodilatation.10 A3 receptors are present in the
myocardium, and selective activation of these has a cardioprotec-
tive (cardiac preconditioning) effect; however, these receptors are
not relevant in antidysrhythmic therapy.11
Adenosine and acetylcholine exhibit identical cardiac effects
and share similar receptor-effector coupling systems. Adenosine
and acetylcholine provide an opposing balance to the sympathet-
ic neurotransmitters norepinephrine and epinephrine. Thus, pre-
dictably, the adenosine antagonists caffeine, theophylline, and
aminophylline provoke tachycardia and ectopy.
Because of the rapid intravascular metabolism of adenosine
Figure 2 In a wide-complex tachycardia, each impulse is con- (half-life, 6 seconds), an intravenous bolus of adenosine (6 mg or
ducted aberrantly through the ventricles. The QRS complex is 100 µg/kg) produces a negligible effect on systemic blood pres-
therefore prolonged to more than 0.08 second and occupies more sure, as confirmed by multiple clinical studies.Thus, adenosine is
than two small boxes on the ECG tracing.
safe, but its effects are transient.
Adenosine is useful in blocking AV nodal conduction. Intra-
than half of patients. None of the side effects of adenosine neces- cardiac recordings exhibit prolongation of the A-H interval with no
sitate therapy. alteration in conduction distal to the His bundle and on into the
Compared with calcium channel blockers, adenosine has cer- ventricular myocardium (the His-Purkinje system is unaffected).
tain advantages. Because of its rapid onset and short duration of In more than 90% of cases, adenosine is effective in terminat-
action, and because its side effects are trivial and self-limited, ing supraventricular tachycardia. Interestingly, adenosine has
adenosine can be used diagnostically. If, as is often the case, the proved as effective at terminating atrioventricular reentry (85%) as
QRS width is confusing and it is therefore uncertain whether the at terminating atrioventricular node reentry (86%).9 Because of
rhythm disorder is supraventricular (QRS < 0.08 second) or ven- adenosine’s short half-life, however, the supraventricular dysrhyth-
tricular (QRS > 0.08 second), a 6 mg I.V. bolus of adenosine may mia is likely to recur within minutes in up to one third of patients.
be infused, and repeated if necessary. If the dysrhythmia slows or For that reason, adenosine is often used diagnostically, to discrim-
breaks, it was supraventricular. If it does not break, proceed to inate supraventricular from ventricular dysrhythmias (see above).
cardioversion (see above). On the other hand, even if a dysrhyth- Several clinical studies have compared adenosine with vera-
mia responds to adenosine, the profound neuroendocrine and pamil for therapeutic AV nodal blockade, with predictable results.
electrolyte perturbations that provoked the dysrhythmias in the Both agents block the AV node and control the ventricular rate:
first place—perturbations that are very common in the surgical cumulative efficacy with either agent is more than 90%.
intensive care unit—are likely to persist, and the dysrhythmia dis- Postconversion dysrhythmias in the two groups were similar.
order typically recurs. Continuous (therapeutic) infusion of Spontaneous reinitiation of supraventricular dysrhythmias occurs
adenosine (150 to 300 µg/kg/min) is rational from a physiologic more frequently with adenosine, whereas systemic hypotension is
standpoint but is frighteningly expensive. Therefore, if adenosine more commonly associated with verapamil (at least until the dys-
works transiently, it is appropriate to follow with one of the rhythmia breaks). Thus, for help in seconds (approximately 20
longer-acting calcium channel blockers. seconds), use adenosine (6 mg I.V. bolus, may be repeated); for
help in minutes (3 to 5 minutes), use verapamil (1 mg/min I.V. up
Calcium Channel Blockers
Both the sinoatrial (SA) node and the AV node are activated by
the movement of calcium through the so-called slow calcium
channels.8 Calcium channel blockers are the most powerful
agents currently available for blocking the transmission of im-
pulses across the AV node. A supraventricular dysrhythmia pro-
duces an acceleration in the ventricular rate because impulses
generated by an ectopic source above the AV node are transmit-
ted too rapidly to the ventricle [see Figure 4]. Calcium channel
blockers produce a pharmacologic blockade of the AV node, Figure 3 P waves are absent and the QRS complexes are narrow
reducing the number of impulses reaching the ventricles and and irregular in this ECG tracing from a patient with atrial
thereby controlling the ventricular rate (Remember, keeping the fibrillation.


arrest.16 Amiodarone also proved superior to lidocaine (78% ver-
sus 27%) for termination of ventricular tachycardia in a random-
ized, prospective study of 29 patients with ventricular tachycardia
refractory to external shock therapy.17
Another prospective, double-blind study comparing amio-
darone with ibutilide (another class III antiarrhythmic agent)
showed the drugs to be equally efficacious in the conversion of
Figure 4 In a narrow-complex tachycardia, the entire ventricle is atrial fibrillation to sinus rhythm and in the subsequent mainte-
activated in less than 0.08 second. Presumably, the impulse origi- nance of sinus rhythm.18 Although two patients (10%) in the
nated at a supraventricular source and accessed the ventricle via amiodarone group experienced hypotension during treatment,
the high-velocity Purkinje system. long-term maintenance therapy using the oral form of amiodarone
may make it the drug of choice for this purpose, given ibutilide’s
to 10 mg); and for help in hours, infuse digoxin, 0.5 mg I.V. lack of oral bioavailablity. Amiodarone was also found superior to
Although digitalis effectively blocks the AV node, it should be both sotalol and propafenone in preventing the recurrence of atri-
remembered that digitalis actually increases automaticity and al fibrillation in a randomized, prospective multicenter study of
excitability in both the atrium and the ventricle. The calcium 403 patients with a mean follow-up period of 16 months.19
channel blockers are superior to digoxin in controlling the ven- Although gratifyingly effective, amiodarone has significant side
tricular rate.8 effects.20 In trials of low-dose amiodarone (200 mg/day), thyroid,
The adverse effects of adenosine, like the beneficial effects, are neurologic, cutaneous, ocular, bradycardic, and hypotensive
transient.9 Facial flushing, chest pressure (adenosine has been problems were statistically more frequent; interestingly, pul-
implicated in the sensation of angina), and transient third-degree monary fibrosis was not.21
heart block are very common. Significant side effects are rare. For the first 24 hours, the recommended dosages for adults are
Nebulized adenosine can cause bronchoconstriction, especially in a loading dose of 150 mg I.V. over the first 10 minutes (15
asthmatic patients. Bronchoconstriction has not been reported mg/min) followed by 360 mg I.V. over the next 6 hours (1
after intravenous administration of adenosine. mg/min); a maintenance infusion of 540 mg (0.5 mg/min) is
given over the remaining 18 hours. The maintenance infusion
Magnesium may be continued for up to 3 weeks, at the rate of 0.5 mg/min, or
Magnesium is the second most abundant cation in humans. It the patient may be converted to oral dosing at 400 to 1,600 mg
is involved in many enzymatic reactions that influence the produc- daily, depending on the duration of the preceding I.V. infusion.
tion and utilization of cellular energy. Abnormalities in electrolyte
homeostasis (potassium and calcium in particular) are associated
Cardiac Dysrhythmias during Pregnancy
with a robust increase in cardiac myocellular excitability and auto-
maticity, especially when these abnormalities are concurrent with Fortunately, cardiac dysrhythmias are not frequent in young
myocardial ischemia.12 Multiple clinical studies confirm the effica- women of childbearing age. When rhythm problems do occur,
cy of intravenous magnesium infusion even when the measured they tend not to be hemodynamically destabilizing. The most
serum values are normal.The mechanism is unknown.When con- commonly used obstetric drug with electrophysiologic side
fronted with a patient exhibiting either supraventricular or ventric- effects is magnesium sulfate.22 When magnesium is infused intra-
ular ectopy, it is safe (and often effective) to administer magnesium venously into the mother, the fetus may exhibit a dose-dependent
chloride at a dosage of 7 g or 100 mg/kg I.V. over 1 to 3 hours. It bradycardia and a progressive decrease in healthy heart rate vari-
is not necessary to measure the serum magnesium concentration ability.23,24 Antidysrhythmic (indeed, any) drugs should be avoid-
first; the serum value will not influence therapy. ed during the first trimester of pregnancy, although most anti-
dysrhythmic agents carry relatively little risk.22 Quinidine, pro-
Amiodarone cainamide, lidocaine, digoxin, adenosine, and beta blockers all
Amiodarone is a class III antiarrhythmic drug that exerts its pri- have a long record of safety during pregnancy. Flecainide has
mary effect by prolongation of the myocardial action potential and proved to be effective in treating fetal supraventricular tachycar-
refractory period and by delay of both SA node function and AV dia complicated by hydrops. Phenytoin and amiodarone have
conduction.Amiodarone is also unique among these compounds by been associated with congenital abnormalities.22
virtue of exhibiting, to varying degrees, the pharmacologic traits of The important point is that if the mother is hemodynamically
all four classes of antiarrhythmic drugs [see Discussion, Anti- unstable and exhibits a dysrhythmia, direct current cardioversion
dysrhythmic Agents, below].13 Among these is its ability to inhibit is safe and effective.
alpha- and beta-adrenergic stimulation without the classic side
effects associated with beta receptor blockade. It also reduces trans-
Proarrhythmia with Antidysrhythmic Drugs
mural proarrhythmic heterogeneity (which predisposes to arrhyth-
mias) in the human heart [see Discussion, Pathophysiology of Proarrhythmic manifestations of ostensibly antiarrhythmic
Cardiac Dysrhythmias, Reentrant Dysrhythmias, below].14 drugs have been linked primarily to agents that prolong repolar-
Intravenous amiodarone was approved in the United States for ization. Early afterdepolarizations associated with agents that
use against malignant ventricular tachyarrhythmias in 1995. retard repolarization or an increase in spatial and temporal dis-
Rates of effective suppression for ventricular arrhythmias have persion of repolarization are the putative mechanisms of drug-
been reported to be as high as 91% in uncontrolled trials.15 induced or drug-enhanced arrhythmias.25,26
Intravenous amiodarone has also proved effective against refrac- The class III antidysrhythmic agents have traditionally been
tory ventricular tachycardia and VF. In one double-blind, ran- the agents most likely to cause dysrhythmias.26 The best way of
domized, placebo-controlled trial, amiodarone significantly preventing dysrhythmias, however, is to follow the general policy
improved survival in patients suffering out-of-hospital cardiac of not using drugs at all if they are not needed.27


Discussion
Antidysrhythmic Agents
or ventricular muscle. At therapeutic levels, digitalis has an anti-
Verapamil (or another calcium channel blocker), lidocaine, and dysrhythmic action that is mediated almost exclusively via the
adenosine are the only drugs essential for the acute treatment of vagus nerve. Toxic doses of digitalis, however, may produce an
cardiac dysrhythmias. Because patients may already be taking oral increased automaticity characterized by multifocal premature
agents for chronic dysrhythmias, however, it is important to be ventricular depolarizations [see Pathophysiology of Cardiac Dys-
aware of the actions and side effects of these drugs when treating rhythmias, below]. Caution must be observed in digitalizing a
an individual with an acute dysrhythmia. Antidysrhythmic drugs patient who is prone to atrial dysrhythmias, because digitalis
have been classified on the basis of their dominant electrophysio- increases atrial excitability and hence increases the risk of atrial
logic effect28; this classification has been reviewed and placed in a ectopy. Because digitalis also induces AV nodal blockade mediat-
clinical context.5 Adenosine has a unique receptor that modulates ed by the vagus nerve, however, any atrial dysrhythmias produced
cyclic adenosine monophosphate (cAMP), resulting in choliner- by digitalization will be less clinically significant.31,32
gic activity. It is not similar to other antidysrhythmic agents and is
therefore unclassified.
Cellular Electrophysiology
CLASS I AGENTS (MEMBRANE ACTIVE)
Electromechanical activity of all muscle, including the heart, is
Class I agents are fast sodium channel blockers. All class I determined by the concentration and flow of ions, particularly
agents—which include lidocaine, procainamide, quinidine, and calcium, potassium, and sodium. Knowledge of cardiac electro-
disopyramide—are local anesthetics. These agents block the fast physiology can serve as a conceptual framework on which to build
inward sodium current and thereby decrease both the amplitude a rational therapeutic program. Direct observation of cellular elec-
of the action potential, or phase 0 depolarization (see below), and trical activity using a glass microelectrode reveals that the cell
conduction velocity. These agents also depress the rate of sponta- membrane is semipermeable: it permits easy passage of cations
neous phase 4 depolarization, or automaticity, and thus are useful such as sodium, potassium, and calcium but provides a barrier to
for abolishing premature ventricular contractions (PVCs); class I anions and proteins. Negatively charged intracellular proteins that
agents are sometimes termed PVC killers. Because these agents cannot cross the cell membrane create a transmembrane potential
slow the conduction velocity, they can actually increase the likeli- in which the interior of the cell is negatively charged relative to the
hood of reentrant cardiac dysrhythmias in some patients.25,27 exterior. The membrane potential of a cell, EK, is proportional to
the difference between the logarithms of the intracellular potassi-
CLASS II AGENTS (BETA BLOCKERS)
um concentration, [K]i, and the extracellular potassium concen-
Class II agents are beta blockers and include such drugs as pro- tration, [K]o:
pranolol. Sympathetic hyperactivity, marked by increased release
EK = c(log [K]i – log [K]o)
of catecholamines, is one of the major causes of cardiac dysrhyth-
mias that result from increased automaticity (hyperexcitabili- The proportionality constant, c, varies with temperature, but at
ty).25,27,29 Beta-adrenergic blockade has produced a decrease in 37° C it is –60 mV. Thus, under physiologic conditions,
such automatic dysrhythmias under both clinical and experimen-
EK = –60 mV × log [K]i / [K]o
tal conditions.29
This relation, termed the Nernst equation, can be used to cal-
CLASS III AGENTS (TO PROLONG REPOLARIZATION)
culate the myocardial cell membrane potential if the potassium
Class III agents, such as bretylium, act directly on the myocar- concentrations are known. For example, if the potassium concen-
dial cell membrane to delay phases 2 and 3 of repolarization and tration is normal—that is, 150 mEq/L intracellularly and 3.8
thereby prolong refractoriness. Bretylium is effective in terminat- mEq/L extracellularly—then the membrane potential is
ing reentrant dysrhythmias because it prolongs the refractory peri-
EK = –60 mV × log 150 / 3.8
od of the ectopic focus to beyond the point at which an impulse
EK = –90 mV
reenters the circuit.1,2 Bretylium apparently has no effect on either
automaticity or conduction velocity.30 If, however, the serum potassium concentration rises to 6.0
mEq/L, then the membrane potential also changes:
CLASS IV AGENTS (CALCIUM CHANNEL BLOCKERS)
EK = –60 mV × log 150 / 6.0
Class IV agents, of which verapamil and diltiazem are the most
EK = –80 mV
effective, block the movement of calcium across the slow calcium
channels but have virtually no effect on the so-called fast sodium Thus, the resting membrane potential is determined primarily
channels.28 Because both the SA node and the AV node are com- by the concentration gradient for potassium across the cell mem-
posed of slow-response fibers that are activated by the movement brane. The transmembrane potential can be calculated if the
of calcium ions across the slow channels, the class IV agents are transmembrane potassium concentrations are measured with a
particularly effective in preventing unwanted supraventricular glass microelectrode. Under clinical conditions, however, only the
impulses from reaching the ventricles. These agents decrease the serum potassium level can be measured.This value does not pro-
conduction velocity through the AV node and increase the refrac- vide an adequate guide to the transmembrane electrical voltage,
tory period of the AV node. because many physiologic factors are capable of altering the intra-
cellular potassium concentration.13 Such factors include elec-
CLASS V AGENTS (UNCLASSIFIED)
trolyte and acid-base balance, the level of osmotic and metabolic
The vagus nerve innervates the SA node, the atria, and the AV activity, and the serum levels of glucose and insulin.
node, but it has almost no influence over the His-Purkinje system Any factor that causes osmotic movement of water into the cell


+50 ents. An energy-dependent (ATP-dependent) sodium-potassium
pump counteracts a significant influx of sodium and efflux of
potassium in the resting cell to maintain this resting membrane
potential. As noted, when the extracellular potassium concentra-
tion rises from a typical value of 3.8 mEq/L to 6.0 mEq/L, the
Phase 1 resting membrane potential increases from –90 mV to –80 mV.
This effect would tend to increase automaticity, but it is super-
Membrane Potential (mV )

0 seded by the effect of hyperkalemia on the sodium current. A rise
Phase 2 in the extracellular potassium level progressively impairs the flux
of sodium through sodium-specific channels, leading to an over-
all decrease in myocardial excitability.34
Phase 0
Phase 0
Phase 3 During phase 0, an electrical stimulus causes the sodium-spe-
– 50 cific fast channels and the calcium-specific slow channels to open,
Threshold usually for no longer than 1 msec. As positive ions rush in, depo-
larization occurs as the membrane potential rises to threshold, or
–60 mV, and an action potential is generated [see Figure 5]. Under
normal physiologic conditions, the stimulus that produces an
action potential is electrical, but any stimulus—electrical, physical
Phase 4 (such as a precordial thump), or chemical—that depolarizes a
–100 membrane up to threshold (again, –60mV) can generate an
0 500 1,000 action potential. There are various abnormalities that can cause
Time (msec) the resting membrane potential to move toward threshold. For
example, conditions that produce a decrease in energy supply (or,
Figure 5 The standard Purkinje (or ventricular muscle) action alternatively, an increase in energy demand) will have this effect
potential has five distinct phases: phase 0, rapid depolarization; because energy is required to maintain the potassium and sodium
phase 1, early repolarization; phase 2, plateau; phase 3, rapid
gradients across the resting membrane. Under such conditions,
repolarization; and phase 4, diastole.
automaticity is enhanced because lesser stimuli can achieve the
threshold potential, and the cardiac muscle is said to be hyperex-
will dilute and thus decrease the intracellular potassium concen- citable, or irritable.
tration.The transmembrane gradients of sodium and calcium are
Phases 1 and 2
maintained by energy-requiring pumps in the cell membrane.
When these pumps are inactivated, as during myocardial Phase 1 is characterized by repolarization to the plateau phase,
ischemia,12 sodium and calcium can leak into the cell. If, as often or phase 2. During phase 2, the slow calcium channels as well as
occurs, sodium leaks into the cell faster than potassium leaks out, the fast sodium channels are activated, and the membrane poten-
water will be drawn in, producing myocardial edema. Tissue aci- tial remains relatively constant for as long as 100 msec.35 The long
dosis can also alter the transmembrane potassium gradient. In duration of this plateau phase is the most dramatic difference
acidosis, hydrogen ions can leak into the cell in exchange for between an action potential in cardiac muscle and one in skeletal
potassium, thereby decreasing the intracellular potassium con- muscle. During this interval, termed the effective refractory peri-
centration and increasing the membrane potential. Variations in od, the myocardium is relatively resistant to further excitation.
glucose transport can also affect the potassium gradient. Under
the influence of insulin and epinephrine, glucose may move across Phase 3
the membrane into the myocardial cell, drawing in water by During phase 3, potassium channels reopen to promote efflux
osmosis. The decline in intracellular potassium concentration of potassium from the cell. Rapid repolarization ensues, and the
stimulates the sodium pump to exchange extracellular potassium resting membrane potential is reestablished at –90 mV.
for intracellular sodium. Concurrent administration of glucose
and insulin is the standard method for treating hyperkalemia Spontaneous Phase 4 Depolarization
because it shifts potassium from the extracellular fluid back into Unlike ordinary atrial and ventricular muscle, the Purkinje
the cells. fibers do not have a stable phase 4 diastolic potential [see Figure
6]. Instead, these fibers undergo continuous depolarization dur-
ACTION POTENTIAL GENERATION
ing diastole as a result of deactivation of the potassium efflux cur-
Stimulation of either cardiac muscle or skeletal muscle pro- rent.35,36 If the Purkinje fibers reach the threshold voltage, they
duces an action potential. Unlike a skeletal muscle action poten- will fire an action potential. Under normal conditions, however,
tial, which lasts only several milliseconds, a cardiac action poten- the SA and AV nodes exhibit faster diastolic depolarization and
tial may persist for as long as several hundred milliseconds.33 The reach threshold sooner than the Purkinje fibers. Because the cells
standard Purkinje, or ventricular muscle, action potential has five in the SA node normally reach threshold first—winning the race,
discernible phases [see Figure 5]. so to speak—the SA node typically assumes the pacemaker func-
tion of the heart. Premature ventricular contractions develop
Phase 4 when a hyperexcitable cell or fiber in ventricular myocardium
In phase 4, the resting membrane potential, or diastolic poten- undergoes rapid diastolic depolarization and reaches threshold
tial, of the cell is generated by active metabolic processes that pro- before the cells in the SA node.This cell or fiber then assumes the
duce substantial transmembrane potassium and sodium gradi- pacemaker function of the heart for that beat. The PVCs (or,


+ 50
or automaticity.37,38 Hypokalemia also increases the size of the
sodium channels, however, thereby promoting more rapid influx

of sodium during phase 0. Because the net result of hypokalemia
0 is increased automaticity, the effect of hypokalemia on sodium
influx appears to override its effect on membrane hyperpolariza-
tion. Hypokalemia is one of the most easily treated (and overtreat-
Threshold ed) forms of hyperexcitability.
– 50

Hypercalcemia
Phase 4 Calcium is a potent inotropic agent, mediating the interaction
–100
between actin and myosin that produces muscle contraction.35
Figure 6 In normal cardiac Purkinje fibers, the membrane High extracellular calcium levels may cause myocardial work to
potential does not remain flat during phase 4 but instead rises exceed the energy supply and thus impair the function of the
gradually. This spontaneous phase 4 depolarization is the result of membrane pump. As a result, the resting membrane potential
a resting potassium current. drifts up toward threshold, enhancing automaticity. Excess calci-
um also appears to promote spontaneous oscillations in mem-
brane potential [see Slow Afterdepolarizations, below].39 Because
more accurately, premature ventricular depolarizations) that of calcium’s inotropic effect, such oscillations are accompanied by
result from such ventricular ectopy can be abolished by overdrive muscle activity.
pacing. In this situation, a mechanical pacemaker is used to pace
the heart at a rate faster than that of the PVC (i.e., the R–R inter- Elevated Catecholamine Levels
val is shorter). The artificial device thereby wins the race; it Increased catecholamine levels also appear to predispose to
assumes the pacemaker function and regularizes the heart rate, automaticity, as evidenced by an increase in the incidence of mul-
producing a beneficial cosmetic effect on the ECG without alter- tiple PVCs reported in patients who have been infused with high
ing the hyperexcitability of the diseased cell. doses of catecholamines, such as epinephrine or dopamine.
Catecholamines increase both heart rate and contractility. As with
Pathophysiology of Cardiac Dysrhythmias hypercalcemia, elevated catecholamine levels may increase car-
diac work beyond the limits of energy supply and cause the mem-
All dysrhythmias are caused by enhanced automaticity, reentry, brane potential to move closer to threshold. This effect on the
or a combination of these two mechanisms. energy-dependent membrane pumps has been observed in isolat-
AUTOMATIC DYSRHYTHMIAS ed preparations of Purkinje muscle fibers. The addition of cate-
cholamines to preparations of Purkinje muscle fibers has
Any area of myocardial tissue that independently depolarizes, decreased the outward potassium current to the point that the
reaches threshold, and fires is termed automatic, and the electri- resting membrane potential was shifted as much as 25 mV toward
cal impulse that activates the adjacent myocardium generates an depolarization, enhancing automaticity.36,37 In addition to affect-
automatic rhythm. Acute dysrhythmias tend to be automatic; such ing the operation of the membrane pumps, catecholamines can
automatic dysrhythmias are frequently seen in patients in emer- produce large spontaneous oscillations in membrane voltage.36,40
gency departments and coronary care units and in patients under- Catecholamines are elaborated endogenously; a patient who is in
going surgery. Five common clinical phenomena that tend to pain, for example, may be releasing large amounts of epinephrine
increase automaticity have been identified: local myocardial into the circulation. In such cases, morphine can be used effec-
hypoxia, hypokalemia, hypercalcemia, increased catecholamine tively as an antidysrhythmic agent.40
levels, and drugs (most commonly digitalis).
Drugs
Local Myocardial Hypoxia
Digitalis is the prototypical cardiac stimulant. Typically, any
Energy-dependent cell membrane pumps maintain the resting
membrane potential, and when oxygen supply to myocardial tis-
sue is inadequate because of ischemia, the pumps fail to function
properly. Consequently, the potassium gradient declines, and the
membrane potential drifts closer toward threshold. Small mem-
brane potential fluctuations or stimuli of less than normal magni-
tude are then sufficient to bump the membrane potential up to
threshold and initiate an action potential.Ventricular muscle cells,
not only those cells in specialized conduction tissue, can sponta-
neously generate electrical fluctuations, or oscillations, in mem-
brane potential [see Slow Afterdepolarizations, below]. If the rest-
ing membrane potential is initially closer to normal because of
local myocardial hypoxia, then these spontaneous oscillations are
more likely to achieve threshold and fire an action potential.37
Hypokalemia
Figure 7 ECG demonstrates multifocal PVCs, indicating a dif-
Extracellular hypokalemia increases the resting membrane fuse hyperexcitability of the ventricles. Such hyperexcitability
potential, drawing it further away from threshold and producing may arise from a metabolic abnormality such as hypokalemia or
hyperpolarization. This effect tends to decrease tissue excitability, a pharmacologic cause such as digitalis toxicity.


Origin

a b c

Figure 8 Schematic diagram portrays a conceptual framework for understanding the generation of reentrant dysrhythmias. In
normal conduction (a), as in sinus rhythm or ventricular pacing, an impulse is propagated along two different anatomic pathways
and is extinguished at the bottom. In (b), one pathway has a region of slow conduction (red area), which results in a rate-depen-
dent block. In (c), the impulse is also blocked in the right limb (red area), but it travels over the alternative pathway sufﬁciently
slowly (zigzag line) for the origin to be able to repolarize before the initial impulse returns; the conducted impulse then depolar-
izes the origin and reenters the circuit.

agent other than oxygen that causes the heart to pump harder fronts and because all cardiac tissue has a long refractory period,
and faster also increases cardiac excitability. Digitalis toxicity can it is highly unlikely that any cells will remain excitable at the com-
produce diffuse myocardial hyperexcitability, manifested by so- pletion of each beat. However, disorders such as myocardial
called automatic ventricular ectopy. In this condition, the cardiac ischemia, ﬁbrosis, and necrosis slow electrical conduction and also
impulse originates from multiple sites in the ventricle. In patients produce nonconductive areas that interrupt the normal electrical
with ventricular ectopy caused by digitalis intoxication, the whole wavefront.44 These conditions set up one of the requirements for
myocardium becomes hyperexcitable and spontaneous depolar- reentry: areas of differential myocardial repolarization.45
izations derive from multiple different sites.When the QRS com- A circuit whose length exceeds the duration of the reentrant
plex originates at multiple loci, the ECG will exhibit multiple impulse circuit is required for the initiation of reentry (i.e., in
morphologies, and multifocal PVCs are apparent on the ECG— order to sustain continuous conduction); such a circuit may
the classic multifocal ectopy of digitalis toxicity [see Figure 7].41-43 develop because of anatomic or physiologic heterogeneity in
myocardial tissue.44,45 Slow conduction, a shortened refractory
REENTRANT DYSRHYTHMIAS
period, and anatomic heterogeneity all favor reentry [see Figure
In the normally functioning heart, the rich cell-cell conduction 8]. The circuit wavelength of an impulse is the product of the
pathways promote uniform activation of the atria or ventricles in conduction velocity and the duration of the longest refractory
waves. Because activation occurs by means of large electrical wave period in the circuit.46 For example, for normal myocardium, the

Figure 9 In electrophysiologic testing, the electrical com-
plexes are spread out to facilitate the recognition of ventricu-
lar electrical morphology. In (a), critically timed paced stim-
uli capture one ventricle, but when pacing is stopped, the
rhythm reverts to sinus rhythm. In (b), critically timed paced
stimuli achieve rate-dependent block in one arm of a reen-
trant circuit. When the activation wave front returns to the
origin, this tissue is no longer refractory and undergoes depo-
larization. With reexcitation, the conditions for reentry are
met, and the impulse continues after pacing stops.


a +50 patient with a history of cardiac dysrhythmias can reveal whether
latent substrates of reentry are present. Because organized ven-
Early Afterdepolarization tricular reentry does not occur in normal myocardium, all reen-
Membrane Potential (mV)

trant dysrhythmias, whether they are induced or spontaneous, are
0 pathologic. Rapidly paced stimuli may provoke a decrease in
action potential duration and shorten refractoriness in myocardi-
um in which the conduction velocity has already been reduced.
Critically timed premature paced stimuli may then penetrate
– 50 selective zones of myocardium, leading to a reentrant dysrhyth-
mia [see Figure 9].48 A ventricular tachydysrhythmia that can be
induced by programmed stimulation carries an ominous progno-
sis unless it can be abolished by pharmacotherapy or surgery.48
–100
SLOW AFTERDEPOLARIZATIONS
b +50
Damaged atrial and ventricular muscle exhibits resting mem-
Late Afterdepolarization brane potential instability.49 The oscillations in membrane poten-
Membrane Potential (mV)

tial may at times be large enough to raise the membrane voltage
0 to threshold level and cause the cell to fire. The phenomenon of
oscillatory instability, which was first recognized in the 1940s,50 is
now thought to play an important role in the genesis of cardiac
dysrhythmias. Injury,49 elevated calcium levels,33 digitalis,41,42 and
catecholamines all promote membrane oscillatory instability,
– 50 which may be manifested as either early or late afterdepolariza-
tions. Both phenomena occur after an action potential; however,
an early afterdepolarization occurs before repolarization of the
–100 cell, whereas a late afterdepolarization occurs after repolarization
[see Figure 10]. Both early and late afterdepolarizations may be
Figure 10 Membrane oscillatory instability may be manifested followed by extreme membrane oscillatory instability that leads to
by either (a) early afterdepolarizations or (b) late afterdepolar- slow-response action potentials [see Figure 11]. If any of these
izations. If the late afterdepolarizations achieve the threshold slow potentials reach threshold, they may result in either orga-
voltage, they can fire an action potential (dotted lines). nized electrical activity (premature ventricular depolarization) or
disorganized electrical activity (fibrillation).
The recognition of slow potentials, depressed fast responses,
conduction velocity is 200 cm/sec and the refractory period is 0.4 and very slow conduction was originally based on in vitro studies
second; therefore, the circuit length for a normally conducted of cardiac tissue.51 For example, bathing superfused Purkinje
myocardial impulse would have to be 80 cm. Because the reen- fibers in a solution with a high potassium concentration inacti-
trant circuit would have to be extraordinarily tortuous to encom- vates the fast sodium channels and markedly alters normal phase
pass 80 cm, it would appear that concomitant slow conduction is 0 depolarization. Under such circumstances, slow potentials that
essentially mandatory to shorten the circuit wavelength and per- are less than 80 mV in amplitude, that depolarize at a rate of 1 to
mit initiation of a reentrant dysrhythmia. Regions such as the AV
and SA nodes normally exhibit slow conduction, and therefore,
any disturbance that produces minor additional slowing in these
+50
areas predisposes to reentry. It has also been suggested that Slow-Response Action Potentials
extreme anatomic heterogeneity might permit microreentry.45
For example, a tortuous path over stunned, slowly conducting
ventricular muscle in an individual with heterogeneous myocar-

dial infarction might achieve the prerequisites for reentry.
In vitro studies have investigated physiologic factors that might 0
produce changes in conduction and excitability that predispose to
reentrant dysrhythmias. For example, abnormal conduction has
been observed in a Purkinje network subjected to local changes
in potassium concentration.33,40 The decrease in conduction
velocity can vary in different areas of the Purkinje network, lead-
– 50
ing to functional conduction block.37,38 In T- or X-shaped
Purkinje preparations, the impulses either summate electrically
or, conversely, inhibit each other when they arrive at the same
junction simultaneously. It is difficult to study the cardiac
microenvironment in living animals or humans, but in these stud-
ies,47 electrical instability results when the Purkinje network is –100
subjected to potassium fluctuations (which certainly occur with Figure 11 Early afterdepolarizations may lead to slow-response
induced cardioplegia during cardiac surgery, and probably occur action potentials. If any of these potentials reach threshold, they
in myocardial ischemia). may lead to either organized electrical activity (premature ventricu-
Electrophysiologic testing with programmed stimulation in a lar depolarization) or disorganized electrical activity (fibrillation).

Acs0802 Acute Cardiac Dysrhythmia

Acs0802 Acute Cardiac Dysrhythmia

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Similar to Acs0802 Acute Cardiac Dysrhythmia

Similar to Acs0802 Acute Cardiac Dysrhythmia (20)

More from medbookonline

More from medbookonline (20)

Acs0802 Acute Cardiac Dysrhythmia