Cardiac Arrhythmias and Their Electrocardiographic Interpretation pdf - The Heart

volume output per beat even during periods of rest. When the athlete is at rest,

that of a normal person, which allows the athlete’s heart to pump a large stroke

The athlete’s heart is larger and considerably stronger than

beats per minute. Bradycardia is shown by the electrocardiogram in Figure 13–2.

The term “bradycardia” means a slow heart rate, usually defined as fewer than 60

and this elicits sympathetic reflexes to increase the heart rate.

often increases the heart rate to 150 to 180 beats per minute.

passes into a state of shock or semishock, sympathetic reflex stimulation of the heart

discuss at multiple points in this text. For instance, when a patient loses blood and

Many factors can cause the sympathetic nervous system to excite the heart, as we

node, which in turn directly increases its excitability and rate of rhythm.

progressive debility of the heart muscle as a result of the fever. Fever causes tachy-

ture of about 105°F (40.5°C); beyond this, the heart rate may decrease because of

(18 beats per degree Celsius) increase in body temperature, up to a body tempera-

The heart rate increases about 10 beats per minute for each degree Fahrenheit

of the heart by the sympathetic nerves, or toxic conditions of the heart

increased body temperature, stimulation

The general causes of tachycardia include

is about 150 per minute instead of the normal 72 per minute.

that the heart rate, as determined from the time intervals between QRS complexes,

with tachycardia is shown in Figure 13–1. This electrocardiogram is normal except

faster than 100 beats per minute. An electrocardiogram recorded from a patient

fast heart rate,

The term “tachycardia” means

Tachycardia

Abnormal Sinus Rhythms

5. Spontaneous generation of spurious impulses in almost any part of the heart

4. Abnormal pathways of impulse transmission through the heart

3. Blocks at different points in the spread of the impulse through the heart

2. Shift of the pacemaker from the sinus node to another place in the heart

1. Abnormal rhythmicity of the pacemaker

electrocardiography. The causes of the cardiac arrhythmias are usually one or a com-

effects on heart pumping, as well as their diagnosis by

The purpose of this chapter is to discuss the

function as primer pumps for the ventricles.

the beat of the ventricles, so that the atria no longer

because of abnormal rhythm of the heart. For instance,

Their Electrocardiographic

Cardiac Arrhythmias and

147

Interpretation

Some of the most distressing types of heart malfunction
occur not as a result of abnormal heart muscle but

sometimes the beat of the atria is not coordinated with

physiology of common cardiac arrhythmias and their

bination of the following abnormalities in the rhythmicity-conduction system of the
heart:

usually defined in an adult person as

cardia because increased temperature increases the rate of metabolism of the sinus

Simple weakening of the myocardium usually increases the heart rate because

the weakened heart does not pump blood into the arterial tree to a normal extent,

Bradycardia

Bradycardia in Athletes.

excessive quantities of blood pumped into the arterial tree with each beat initiate
feedback circulatory reflexes or other effects to cause bradycardia.

ventricles. Inflammation results frequently from

Inflammation of the A-V node or A-V bundle

conduction from the atria to the ventricles.

Compression of the A-V bundle

ischemia of the A-V node and bundle in the same

the ventricles. Coronary insufficiency can cause

Ischemia of the A-V node or A-V bundle fibers

bundle of His.

bundle,

The only means by which impulses ordinarily can pass

atrioventricular (A-V) node, so that the rate of the ven-

the atria. However, the ventricles pick up a new rhythm,

sudden cessation of P waves, with resultant standstill of

nomenon is demonstrated in Figure 13–4, which shows

blocked before it enters the atrial muscle. This phe-

In rare instances, the impulse from the sinus node is

Intracardiac Conduction

Result from Block of Heart

Abnormal Rhythms That

ratory and expiratory cycles of respiration. The spillover

“spillover” of signals from the medullary respiratory

mia, as shown in Figure 13–3, this results mainly from

sinus node. In the “respiratory” type of sinus arrhyth-

with each respiratory cycle by as much as 30 per cent.

, the heart rate increased and decreased

quiet respiration (left half of the record). Then,

diogram. Note from this record that the heart rate

by the height of

half of the record) during deep respiration. A cardiota-

heart rate, at first during normal and then (in the second

cardiotachometer

Figure 13–3 shows a

ally stops the heart for 5 to 10 seconds.

Indeed, sometimes this reflex is so powerful that it actu-

effects on the heart, including extreme bradycardia.

baroreceptor reflex, causing intense vagal-acetylcholine

artery walls are excessively sensitive. Therefore, even

In these patients, the pressure receptors

syndrome.

giving a parasympathetic effect. Perhaps the most strik-

acetylcholine at the vagal endings in the heart, thus

Vagal Stimulation as a Cause of Bradycardia.

148

Unit III

The Heart

Any circulatory

reflex that stimulates the vagus nerves causes release of

ing example of this occurs in patients with carotid sinus

(baroreceptors) in the carotid sinus region of the carotid

mild external pressure on the neck elicits a strong

Sinus Arrhythmia

recording of the

chometer is an instrument that records
successive spikes the duration of the interval between
the successive QRS complexes in the electrocar-

increased and decreased no more than 5 per cent during

during

deep respiration

Sinus arrhythmia can result from any one of many cir-

culatory conditions that alter the strengths of the sym-
pathetic and parasympathetic nerve signals to the heart

center into the adjacent vasomotor center during inspi-

signals cause alternate increase and decrease in the
number of impulses transmitted through the sympa-
thetic and vagus nerves to the heart.

Signals Within the

Pathways

Sinoatrial Block

the impulse usually originating spontaneously in the

tricular QRS-T complex is slowed but not otherwise
altered.

Atrioventricular Block

from the atria into the ventricles is through the A-V

also known as the

Conditions that

can either decrease the rate of impulse conduction in
this bundle or block the impulse entirely are as follows:
1.

often delays or blocks conduction from the atria to

way that it can cause ischemia of the myocardium.

by scar tissue or by

calcified portions of the heart can depress or block

can depress conductivity from the atria to the

Sinus tachycardia (lead I).

Figure 13–1

Sinus bradycardia (lead III).

Figure 13–2

100

120

Heart rate

when breathing deeply.

the record when the subject was breathing normally; to the right,

Sinus arrhythmia as recorded by a cardiotachometer. To the left is

Figure 13–3

SA block

Figure 13–4

Sinoatrial nodal block, with A-V nodal rhythm during the block
period (lead III).

ventricular escape.

ventricles. This is called

the blocked point in the node, or in the A-V bundle,

block, usually in the distal part of the A-V node beyond

seconds, some part of the Purkinje system beyond the

than their natural rate of rhythm. However, after a few

This means that ventricular

overdrive suppression.

30 seconds. This results from the phenomenon called

Each time A-V conduction ceases, the ventricles often

weeks or longer before conduction returns. This condi-

be a few seconds, a few minutes, a few hours, or even

impulses are not conducted. The duration of block may

that is, impulses are conducted from the atria into the

patients with A-V block, the total block comes and goes;

Stokes-Adams Syndrome—Ventricular Escape.

or A-V bundle.

often by rhythmical signals generated in the A-V node

are beating at their own natural rate, controlled most

cles have “escaped” from control by the atria, and they

is less than 40 per minute. Furthermore,

is about 100 beats per minute, whereas the

QRS-T complexes, as shown in Figure 13–7. Note that

Therefore, the P waves become dissociated from the

usually originating in the A-V node or A-V bundle.

from the atria into the ventricles occurs. In this instance,

bundle becomes severe, complete block of the impulse

tion causing poor conduction in the A-V node or A-V

When the condi-

other times, rhythms of 3:2 or 3:1 also develop.

beating twice for every single beat of the ventricles. At

dropped, so that a “2:1 rhythm” develops, with the atria

At times, every other beat of the ventricles is

failure of conduction from the atria to the ventricles.

Figure 13–6 shows P-R intervals of 0.30 second, as

block.

ventricles. This condition is called

wave, and it is said that there are “dropped beats” of the

instance, there will be an atrial P wave but no QRS-T

tricles and sometimes is not strong enough. In this

0.25 to 0.45 second, the action potential sometimes is

When conduction through the A-V

stops entirely. One means for determining the severity

the A-V bundle is depressed so much that conduction

to 0.45 second because, by that time, conduction through

duction. The P-R interval seldom increases above 0.35

delay

0.30 second instead of the normal 0.20 or less. Thus, first

longed P-R interval; the interval in this instance is about

Figure 13–5 shows an electrocardiogram with pro-

block.

0.20 second, the P-R interval is said to be prolonged, and

general, when the P-R interval increases to greater than

faster heartbeat and increases with slower heartbeat. In

when the heart is beating at a normal rate. This so-

The usual

Prolonged P-R (or P-Q) Interval—First Degree Block.

syndrome,

through the A-V node. Such vagal excitation

Extreme stimulation of the heart by the vagus nerves

by diphtheria or rheumatic fever.

different types of myocarditis, caused, for example,

Cardiac Arrhythmias and Their Electrocardiographic Interpretation

Chapter 13

149

in rare instances blocks impulse conduction

occasionally results from strong stimulation of the
baroreceptors in people with carotid sinus

discussed earlier in relation to

bradycardia.

Incomplete Atrioventricular
Heart Block

lapse of time between beginning of the P wave and
beginning of the QRS complex is about 0.16 second

called P-R interval usually decreases in length with

the patient is said to have first degree incomplete heart

degree block is defined as a

of conduction from

the atria to the ventricles but not actual blockage of con-

of some heart diseases—acute rheumatic heart disease,
for instance—is to measure the P-R interval.

Second Degree Block.

bundle is slowed enough to increase the P-R interval to

strong enough to pass through the bundle into the ven-

second degree heart

well as one dropped ventricular beat as a result of

Complete A-V Block (Third Degree Block).

the ventricles spontaneously establish their own signal,

the rate of rhythm of the atria in this electrocardiogram

rate of ven-

tricular beat
there is no relation between the rhythm of the P waves
and that of the QRS-T complexes because the ventri-

In some

ventricles for a period of time and then suddenly

tion occurs in hearts with borderline ischemia of the
conductive system.

do not start their own beating until after a delay of 5 to

excitability is at first in a suppressed state because the
ventricles have been driven by the atria at a rate greater

begins discharging rhythmically at a rate of 15 to 40
times per minute and acting as the pacemaker of the

Prolonged P-R interval caused by first degree A-V heart block

Figure 13–5

(lead II).

Dropped beat

tricles to receive the excitatory signals (lead V

Second degree A-V block, showing occasional failure of the ven-

Figure 13–6

Figure 13–7

Complete A-V block (lead II).

originated in the A-V node or in the A-V bundle. The

Figure 13–10 shows a premature contraction that

A-V Nodal or A-V Bundle Premature

felt in the radial artery. Thus, a deficit in the number of

contraction is depressed or almost absent. Therefore,

mally, and the stroke volume output during that

ule, the ventricles will not have filled with blood nor-

When the heart contracts ahead of sched-

such contractions.

alcoholism, and use of various drugs can also initiate

smoking, lack of sleep, ingestion of too much coffee,

otherwise healthy people. Indeed, they often occur in

sinus node discharge also late in appearing.

in the premature cycle, and this made the succeeding

sinus node. Consequently, the sinus node discharged late

node, and the impulse had to travel through a consid-

compensatory pause.

prolonged, which is called a

node. Also, the interval between the premature con-

ectopic origin of the beat is in the atria near the A-V

cycle; the P-R interval is shortened, indicating that the

The P wave of this beat occurred too soon in the heart

Figure 13–9 shows a single premature atrial contraction.

Premature Atrial Contractions

is also frequent during cardiac catheterization; large

feine. Mechanical initiation of premature contractions

system, or myocardium caused by drugs, nicotine, or caf-

and (3) toxic irritation of the A-V node, Purkinje

ent points in the heart, which press against the adjacent

areas of ischemia; (2) small calcified plaques at differ-

rhythm. Possible causes of ectopic foci are (1) local

in the heart, which emit

extrasystole,

been expected. This condition is also called

Premature Contractions

electrical alternans.

cause incomplete intraventricular block, resulting in

such as ischemia, myocarditis, or digitalis toxicity, can

heartbeat. Also, many conditions that depress the heart,

occurred, because when the rate of the heart is rapid, it

heart rate), which is probably the reason the block has

tachycardia

This electrocardiogram also shows

electrical alternans,

tricular Purkinje system. Figure 13–8 shows the condi-

Most of the same factors that can cause A-V block can

that take control of the ventricles.

electrodes usually connected to the right ventricle. The

electrical stimulator planted beneath the skin, with

artificial pacemaker,

Consequently, most of these patients are provided

detrimental to the patient’s health or even causes death.

Stokes-Adams syndrome.

the person. These periodic fainting spells are known as

until the ventricles “escape.” After escape, however, the

heart does not pump any blood for 5 to 30 seconds,

4 to 7 seconds without blood supply, most patients faint

150

Unit III

The Heart

Because the brain cannot remain active for more than

a few seconds after complete block occurs because the

slowly beating ventricles usually pump enough blood to
allow rapid recovery from the faint and then to sustain

the

Occasionally the interval of ventricular standstill at

the onset of complete block is so long that it becomes

with an

a small battery-operated

pacemaker provides continued rhythmical impulses

Incomplete Intraventricular Block—
Electrical Alternans

also block impulse conduction in the peripheral ven-

tion known as

which results from

partial intraventricular block every other heartbeat.

(rapid

may be impossible for some portions of the Purkinje
system to recover from the previous refractory period
quickly enough to respond during every succeeding

A premature contraction is a contraction of the heart
before the time that normal contraction would have

premature beat, or ectopic beat.

Causes of Premature Contractions.

Most premature con-

tractions result from ectopic foci
abnormal impulses at odd times during the cardiac

cardiac muscle so that some of the fibers are irritated;

numbers of premature contractions often occur when
the catheter enters the right ventricle and presses
against the endocardium.

traction and the next succeeding contraction is slightly

One

of the reasons for this is that the premature contraction
originated in the atrium some distance from the sinus

erable amount of atrial muscle before it discharged the

Premature atrial contractions occur frequently in

athletes whose hearts are in very healthy condition.
Mild toxic conditions resulting from such factors as

Pulse Deficit.

the pulse wave passing to the peripheral arteries after a
premature contraction may be so weak that it cannot be

radial pulses occurs when compared with the actual
number of contractions of the heart.

Contractions

P wave is missing from the electrocardiographic record

Partial intraventricular block—“electrical alternans” (lead III).

Figure 13–8

Premature beat

Atrial premature beat (lead I).

Figure 13–9

heart. This is believed to be caused most frequently by

cles, can occasionally cause rapid rhythmical discharge

including the atria, the Purkinje system, or the ventri-

Paroxysmal Tachycardia

therefore is the locus of the ectopic focus.

ture contraction is near the base of the ventricles, which

its positive end toward the apex. Thus, the first portion

leads II and III are both strongly positive. Plotting these

13–11 the point of origin of the PVC as follows: Note

can determine from the electrocardiogram in Figure

analysis are explained. Applying these principles, one

In Chapter 12, the principles of vectorial

Vector Analysis of the Origin of an Ectopic Premature Ventricular

explained later in the chapter.

the ventricles are coming out of refractoriness, as

causing fibrillation, just at the end of the T wave when

ated by one of the PVCs. This is especially true when

neous lethal ventricular fibrillation, presumably initi-

of such PVCs is not to be taken lightly. Statistics show

infarcted or ischemic areas of the heart. The presence

toxic states, and even emotional irritability. Conversely,

factors as cigarettes, coffee, lack of sleep, various mild

overall pumping by the heart; they can result from such

slow conduction of the

QRS complex, because the

3. After almost all PVCs, the T wave has an electrical

Figure 13–11.

electrical potentials, as shown for the PVCs in

depolarized ahead of the other; this causes large

electrocardiogram. When a PVC occurs, the

heart, the depolarization waves of the two sides

nearly simultaneously; consequently, in the normal

through the heart, it passes through both ventricles

following reasons: when the normal impulse passes

2. The QRS complex has a high voltage for the

prolonged. The reason is that the impulse is

1. The QRS complex is usually considerably

effects in the electrocardiogram, as follows:

ing with normal contractions. PVCs cause specific

The electrocardiogram of Figure 13–11 shows a series

Premature Ventricular Contractions

contractions.

general, A-V nodal premature contractions have

but the P wave itself cannot be discerned as such. In

cles; this P wave slightly distorts the QRS-T complex,

of the premature contraction. Instead, the P wave is

Cardiac Arrhythmias and Their Electrocardiographic Interpretation

Chapter 13

151

superimposed onto the QRS-T complex because the
cardiac impulse traveled backward into the atria at
the same time that it traveled forward into the ventri-

the same significance and causes as atrial premature

of premature ventricular contractions (PVCs) alternat-

conducted mainly through slowly conducting
muscle of the ventricles rather than through the
Purkinje system.

of the heart—mainly of opposite polarity to each
other—partially neutralize each other in the

impulse almost always travels in only one direction,
so that there is no such neutralization effect,
and one entire side or end of the ventricles is

potential polarity exactly opposite to that of the

impulse through the cardiac muscle causes the
muscle fibers that depolarize first also to repolarize
first.

Some PVCs are relatively benign in their effects on

many other PVCs result from stray impulses or re-
entrant signals that originate around the borders of

that people with significant numbers of PVCs have a
much higher than normal chance of developing sponta-

the PVCs occur during the vulnerable period for

Contraction.

that the potentials of the premature contractions in

potentials on the axes of leads II and III and solving by
vectorial analysis for the mean QRS vector in the heart,
one finds that the vector of this premature contraction
has its negative end (origin) at the base of the heart and

of the heart to become depolarized during this prema-

Some abnormalities in different portions of the heart,

of impulses that spread in all directions throughout the

Premature beat

A-V nodal premature contraction (lead III).

Figure 13–10

III

–

III

premature contractions is plotted in accordance with the princi-

large abnormal QRS-T complexes (leads II and III). Axis of the

Premature ventricular contractions (PVCs) demonstrated by the

Figure 13–11

ples of vectorial analysis explained in Chapter 12; this shows the
origin of the PVC to be near the base of the ventricles.

the heart muscle, of its specialized conducting system,

sudden electrical shock of the heart, or (2) ischemia of

rillation. Especially likely to initiate fibrillation are (1)

one moment, but 1 second later, the ventricles are in fib-

minutes.

flow to the brain, and irretrievable death of tissues

ble amounts. Therefore, after fibrillation begins, uncon-

partial contraction, pumping either no blood or negligi-

the ventricles, the ventricular chambers neither enlarge

required for a pumping cycle of the heart. Despite

tion of all the ventricular muscle at once, which is

be relaxing. Thus, there is never a coordinate contrac-

the same time, while equally as many other portions will

over—never stopping. When this happens, many small

portion, then another, and eventually feeding back onto

first one portion of the ventricular muscle, then another

berserk within the ventricular muscle mass, stimulating

minutes, is almost invariably fatal. Ventricular fibrilla-

which, if not stopped within 1 to 3

The most serious of all cardiac arrhythmias is

Ventricular Fibrillation

cardiac muscle, may be used to block irritable foci

, which increases

lar tachycardia. Conversely,

repeated stimulation of the ventricular muscle, as we

ischemic damage is present in the ventricles. Second,

serious condition for two reasons. First, this type of

Ventricular paroxysmal tachycardia is usually a

tricular tachycardia. The electrocardiogram of ventricu-

Figure 13–13 shows a typical short paroxysm of ven-

Ventricular Paroxysmal Tachycardia

weakness during the paroxysm, but only seldom does

after adolescence. In general, supraventricular tachy-

occurs in young, otherwise healthy people, and they gen-

supraventricular tachycardias,

Atrial or A-V nodal paroxysmal tachycardia, both of

complexes but totally missing or obscured P waves.

A-V node. This usually causes almost normal QRS-T

A-V Nodal Paroxysmal Tachycardia.

not near the sinus node.

because the P wave is abnormal in shape, the origin is

of this paroxysmal tachycardia is in the atrium, but

of the preceding beat. This indicates that the origin

wave is partially superimposed onto the normal T wave

wave is seen before each QRS-T complex, and this P

trocardiogram during the rapid heartbeat, an inverted P

about 150 beats per minute. On close study of the elec-

Figure 13–12 demonstrates in the middle of the record

Atrial Paroxysmal Tachycardia

dine and lidocaine, either of which depresses the normal

may also be used. Two drugs frequently used are quini-

of a vagal reflex to stop the paroxysm. Various drugs

regions of the carotid sinuses, which may cause enough

iting a vagal reflex. A type of vagal reflex sometimes

the sinus node.

paroxysm usually ends as suddenly as it began, with

few minutes, a few hours, or much longer. Then the

beginning suddenly and lasting for a few seconds, a

becomes rapid in paroxysms, with the paroxysm

The term “paroxysmal” means that the heart rate

rapid rhythm in the irritable focus, this focus becomes

up local repeated self–re-excitation. Because of the

152

Unit III

The Heart

re-entrant circus movement feedback pathways that set

the pacemaker of the heart.

the pacemaker of the heart instantly shifting back to

Paroxysmal tachycardia often can be stopped by elic-

elicited for this purpose is to press on the neck in the

increase in sodium permeability of the cardiac muscle
membrane during generation of the action potential,
thereby often blocking the rhythmical discharge of the
focal point that is causing the paroxysmal attack.

a sudden increase in the heart rate from about 95 to

Paroxysmal tachycardia

often results from an aberrant rhythm that involves the

which are called

usually

erally grow out of the predisposition to tachycardia

cardia frightens a person tremendously and may cause

permanent harm come from the attack.

lar paroxysmal tachycardia has the appearance of a
series of ventricular premature beats occurring one
after another without any normal beats interspersed.

tachycardia usually does not occur unless considerable

ventricular tachycardia frequently initiates the lethal
condition of ventricular fibrillation because of rapid

discuss in the next section.

Sometimes intoxication from the heart treatment

drug digitalis causes irritable foci that lead to ventricu-

quinidine

the refractory period and threshold for excitation of

causing ventricular tachycardia.

ventricu-

lar fibrillation,

tion results from cardiac impulses that have gone

itself to re-excite the same ventricular muscle over and

portions of the ventricular muscle will be contracting at

massive movement of stimulatory signals throughout

nor contract but remain in an indeterminate stage of

sciousness occurs within 4 to 5 seconds for lack of blood

begins to occur throughout the body within a few

Multiple factors can spark the beginning of ventricu-

lar fibrillation—a person may have a normal heartbeat

or both.

Atrial paroxysmal tachycardia—onset in middle of record (lead I).

Figure 13–12

Ventricular paroxysmal tachycardia (lead III).

Figure 13–13

muscle begins to come out of the refractory state. Some

in a refractory state. After about 0.25 second, part of this

directions, leaving all the muscle beneath the electrode

stimulating electrode. The first cycle of the electrical

a 60-cycle electrical stimulus is applied through a

central point in the ventricles of heart A in Figure 13–15,

electric shock caused by 60-cycle alternating electric

tion.” One of the best ways to explain this process in

wave fronts that have the appearance of a “chain reac-

Instead, they have degenerated into a series of multiple

impulse moving in a circle, as shown in Figure 13–14.

different directions over the cardiac muscle. The re-

In ventricular fibrillation, one sees many separate and

ignore the pace-setting effects of the sinus node.

disturbances, re-entry can cause abnormal patterns of

repetitive electrical stimulation. Thus, in many cardiac

response to various drugs, such as epinephrine, or after

blood potassium levels, or (d) many other factors. (3)

Purkinje system, (b) ischemia of the muscle, (c) high

typically occurs in dilated hearts. (2) Decreased rate of

states of the human heart, as follows: (1) A long pathway

also continue around and around the circle.

In this case, the impulse could

Third,

the refractory state, and the impulse can continue

time, the originally stimulated muscle might be out of

the impulse returns to the 12 o’clock position. By this

enough, an increased interval of time will elapse before

Second, if the length of the pathway remains constant

pathway around the circle is too long,

First, if the

movement.”

has already been excited. This is called a “circus

to cause “re-entry” of the impulse into muscle that

impulse to continue to travel around the circle, that is,

refractory muscle cannot transmit a second impulse. But

a refractory state, the impulse then dies out because

tion. If the originally stimulated muscle fibers are still in

strips cut in the form of circles. If such a strip is stimu-

Figure 13–14 shows several small cardiac muscle

initiate re-entry and lead to “circus movements,” which

sequence of events does not occur. Therefore, let us

Under some circumstances, however, this normal

action potential to begin in the atrial sinus node.

Therefore, that impulse dies, and the heart awaits a new

refractory and cannot conduct the impulse farther.

has traveled through the extent of the ventricles, it has

When the

Ventricular Fibrillation

Cardiac Arrhythmias and Their Electrocardiographic Interpretation

Chapter 13

153

Phenomenon of Re-entry—“Circus
Movements” as the Basis for

normal cardiac impulse in the normal heart

no place to go because all the ventricular muscle is

explain more fully the background conditions that can

in turn cause ventricular fibrillation.

lated at the 12 o’clock position so that the impulse travels
in only one direction, the impulse spreads progressively
around the circle until it returns to the 12 o’clock posi-

there are three different conditions that can cause this

the time the impulse returns to the 12 o’clock position,
the originally stimulated muscle will no longer be
refractory and the impulse will continue around the
circle again and again.

but the velocity of conduction becomes decreased

around the circle again and again.

the refractory period of the muscle might

become greatly shortened.

All these conditions occur in different pathological

conduction frequently results from (a) blockage of the

A shortened refractory period commonly occurs in

cardiac contraction or abnormal cardiac rhythms that

Chain Reaction Mechanism
of Fibrillation

small contractile waves spreading at the same time in

entrant impulses in fibrillation are not simply a single

fibrillation is to describe the initiation of fibrillation by

current.

Fibrillation Caused by 60-Cycle Alternating Current.

At a

stimulus causes a depolarization wave to spread in all

portions come out of refractoriness before other

Absolutely

refractory

Absolutely

refractory

Relatively

refractory

LONG PATHWAY

NORMAL PATHWAY

pathway.

pathway and continued propagation of the impulse in the long

Circus movement, showing annihilation of the impulse in the short

Figure 13–14

Stimulus

point

Dividing

impulses

Blocked

impulse

fibrillatory

Continued propagation of

culature are present.

Initiation of fibrillation in a heart when patches of refractory mus-

Figure 13–15

impulses in the fibrillating ventricle.

volts of 60-cycle alternating current applied for 0.1

of the heart, fibrillation can usually be stopped using 110

When electrodes are applied directly to the two sides

may begin again immediately.

rillation often is still present, in which case fibrillation

becoming the pacemaker. However, the same re-entrant

5 seconds, after which it begins to beat again, usually

potentials stop, and the heart remains quiescent for 3 to

and causing them all to become refractory. All action

fibers of the ventricles at the same time, thus stimulat-

sides of the heart. The current penetrates most of the

ness simultaneously. This is accomplished by passing

throws the ventricles into fibrillation, a strong high-

of the Ventricles

electroshock through the heart, as explained in the next

stopped by some heroic therapy, such as immediate

during ventricular fibrillation, this state is lethal unless

pointed out, because no pumping of blood occurs

longer after ventricular fibrillation begins. As already

are usually only 0.2 to 0.3 millivolt. Minute voltages of

decay rapidly so that after 20 to 30 seconds, they

when ventricular fibrillation first begins, but they

The voltages of the waves in the electrocardiogram

any specific cycle.

small patches of muscle at a time, and electrocardio-

tern can be ascribed to ventricular fibrillation. Instead,

lar waves. Thus, no repetitive electrocardiographic pat-

changes into a new pattern of low-voltage, very irregu-

the ventricles disappear, and the electrocardiogram

After another few seconds, the coarse contractions of

causes coarse, irregular waves in the electrocardiogram.

large masses of muscle contract simultaneously, and this

first few seconds of ventricular fibrillation, relatively

dency toward a regular rhythm of any type. During the

bizarre (Figure 13–16) and ordinarily shows no ten-

In ventricular fibrillation, the electrocardiogram is

Electrocardiogram in Ventricular

ally around refractory areas of muscle, which will lead

blocked by refractory areas. In fact, a single electric

increasing the number of impulses, whereas others are

impulses traveling in all directions, some dividing and

that develops in fibrillation. Here one can see many

Heart B in Figure 13–15 demonstrates the final state

muscle comes out of refractoriness, an impulse is close

the impulses. Therefore, any time a single area of cardiac

cause more and more patches of refractory muscle, and

initiated: More and more impulses are formed; these

travel, greatly lengthening the conductive pathway, which

time. Furthermore, this irregular pattern of impulse

until, finally, there are many small depolariza-

chain

impulses. In this way, many new wave fronts are contin-

refractory area, it, too, divides to form two more

impulses. Then, when each of these reaches another

refractory area. Thus, a single impulse becomes two

area in the heart, it travels to both sides around the

A. When a depolarization wave reaches a refractory

division of impulses,

Third, one of the most important features of fibrilla-

than normally.

the heart. (2) The

tion through the heart muscle decreases,

dispose to circus movement: (1) The

changes in the cardiac muscle itself, both of which pre-

Second, the rapid stimulation of the heart causes two

but not other directions.

develop—that is,

First, block of the impulses in some directions but suc-

areas. Then, several events transpire in rapid succession,

then are blocked. But other impulses pass between the

tances, until they reach refractory areas of the heart, and

Thus, in heart A, certain impulses travel for short dis-

directions through the heart but not in all directions.

tory muscle. Now, continuing 60-cycle stimuli from the

muscle, and dark patches, which represent still refrac-

many lighter patches, which represent excitable cardiac

portions. This state of events is depicted in heart A by

154

Unit III

The Heart

electrode can cause impulses to travel only in certain

refractory areas and continue to travel in the excitable

all occurring simultaneously and eventuating in a state
of fibrillation.

cessful transmission in other directions creates one of
the necessary conditions for a re-entrant signal to

transmission of some of the depolar-

ization waves around the heart in only some directions

velocity of conduc-

which allows a

longer time interval for the impulses to travel around

refractory period of the muscle is

shortened, allowing re-entry of the impulse into previ-
ously excited heart muscle within a much shorter time

tion is the

as demonstrated in heart

ually being formed in the heart by progressive
reactions
tion waves traveling in many directions at the same

travel causes many circuitous routes for the impulses to

is one of the conditions that sustains the fibrillation. It
also results in a continual irregular pattern of patchy
refractory areas in the heart.

One can readily see when a vicious circle has been

the refractory patches cause more and more division of

at hand to re-enter the area.

shock during this vulnerable period frequently can lead
to an odd pattern of impulses spreading multidirection-

to fibrillation.

Fibrillation

the ventricular muscle contracts at as many as 30 to 50

graphic potentials change constantly and spasmodically
because the electrical currents in the heart flow first in
one direction and then in another and seldom repeat

in ventricular fibrillation are usually about 0.5 millivolt

0.1 millivolt or less may be recorded for 10 minutes or

section.

Electroshock Defibrillation

Although a moderate alternating-current voltage
applied directly to the ventricles almost invariably

voltage alternating electrical current passed through the
ventricles for a fraction of a second can stop fibrillation
by throwing all the ventricular muscle into refractori-

intense current through large electrodes placed on two

ing essentially all parts of the ventricles simultaneously

with the sinus node or some other part of the heart

focus that had originally thrown the ventricles into fib-

Ventricular fibrillation (lead II).

Figure 13–16

contraction and the next. Then an additional but

impulse for about 0.35 second after a previous one, at

larly. Because the A-V node will not pass a second

atrial muscle at the A-V node rapidly but also irregu-

When the atria are fibrillating, impulses arrive from the

Irregularity of Ventricular Rhythm During Atrial Fibrillation.

tricles, but their timing is irregular, as explained next.

voltage wavy record. Conversely, the QRS-T complexes

from the atria or only a fine, high-frequency, very low

the electrocardiogram, one can see either no P waves

pletely electrically neutralize one another. Therefore, in

polarity at any given time, they usually almost com-

through the atria during atrial fibrillation. Because the

the electrocardiogram during atrial fibrillation. Numer-

Figure 13–18 shows

although at reduced efficiency of overall heart pumping.

to the lethality of ventricular fibrillation, a person can

decreased only 20 to 30 per cent. Therefore, in contrast

ventricles, and the efficiency of ventricular pumping is

so, blood flows passively through the atria into the

become useless as primer pumps for the ventricles. Even

pump blood in atrial fibrillation. Therefore, the atria

blood during ventricular fibrillation, neither do the atria

For the same reasons that the ventricles will not pump

as well as slow conduction, both of which predispose to

damming of blood in the atria. The dilated atrial walls

ventricles, or from ventricular failure with excess

mass. A frequent cause of atrial fibrillation is atrial

of ventricular fibrillation, except that the process occurs

The mechanism of atrial fibrillation is identical to that

(shown to the right in Figure 13–19).

without atrial fibrillation. Likewise, fibrillation often

tissue. Therefore, ventricular fibrillation often occurs

through the A-V bundle, the atrial muscle mass is

heart is revived, the person may die from the effects of

ment or even destruction of brain tissue. Even if the

8 minutes usually causes permanent mental impair-

cardiopulmonary resuscitation,

defibrillation, is called

the chest wall along with artificial respiration. This, plus

ble. Indeed, fibrillating hearts have been pumped by

pumping, electrical defibrillation often becomes possi-

supply develops. Then, after a few minutes of hand

the heart later. In this way, small quantities of blood are

nary blood flow. However, it is still possible to revive the

begins, the heart is usually too weak to be revived by

an Aid to Defibrillation

Hand Pumping of the Heart

dog was defibrillated 130 times through the chest wall,

In our laboratory, the heart of a single anesthetized

electrodes on the chest wall, as shown in Figure 13–17,

thousandths of a second. When applied through two

Cardiac Arrhythmias and Their Electrocardiographic Interpretation

Chapter 13

155

second or 1000 volts of direct current applied for a few

the usual procedure is to charge a large electrical
capacitor up to several thousand volts and then to cause
the capacitor to discharge for a few thousandths of a
second through the electrodes and through the heart.

and the animal lived thereafter in perfectly normal
condition.

(Cardiopulmonary Resuscitation) as

Unless defibrillated within 1 minute after fibrillation

defibrillation because of the lack of nutrition from coro-

heart by preliminarily pumping the heart by hand
(intermittent hand squeezing) and then defibrillating

delivered into the aorta and a renewed coronary blood

hand for as long as 90 minutes followed by successful
defibrillation.

A technique for pumping the heart without opening

the chest consists of intermittent thrusts of pressure on

or CPR.

Lack of blood flow to the brain for more than 5 to

brain damage or may live with permanent mental
impairment.

Atrial Fibrillation

Remember that except for the conducting pathway

separated from the ventricular muscle mass by fibrous

occurs in the atria without ventricular fibrillation

only in the atrial muscle mass instead of the ventricular

enlargement resulting from heart valve lesions that
prevent the atria from emptying adequately into the

provide ideal conditions of a long conductive pathway

atrial fibrillation.

Pumping Characteristics of the Atria During Atrial Fibrillation.

live for months or even years with atrial fibrillation,

Electrocardiogram in Atrial Fibrillation.

ous small depolarization waves spread in all directions

waves are weak and many of them are of opposite

are normal unless there is some pathology of the ven-

least 0.35 second must elapse between one ventricular

Several thousand volts

for a few milliseconds

Handle for

application

of pressure

Electrode

Application of electrical current to the chest to stop ventricular

Figure 13–17

fibrillation.

Atrial fibrillation (lead I). The waves that can be seen are ventric-

Figure 13–18

ular QRS and T waves.

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Greenland P, Gaziano JM: Clinical practice: selecting asymp-

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Heart Association Task Force on Practice Guidelines

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to years.

implanted electronic cardiac pacemaker

To treat the condition, rhythmical electrical impulses

semipermanent cardiac arrest, which can cause death.

establishing a normal heart rhythm. In some patients,

affected that the automatic rhythmicity disappears.

across their membranes, and their excitability may be so

because of inadequate respiration. The hypoxia pre-

That is, no spontaneous rhythm remains.

This results from

cardiac arrest.

Cardiac Arrest

the atria, giving a 2:1 or 3:1 rhythm.

traction of semicoordinate masses of muscle. However,

atrial flutter. The P waves are strong because of con-

Figure 13–20 shows a typical electrocardiogram in

every single beat of the ventricles.

fore, there are usually two to three beats of the atria for

to pass more than a fraction of the atrial signals. There-

periods of the A-V node and A-V bundle are too long

passed into the ventricles, because the refractory

reach the A-V node too rapidly for all of them to be

pumped by the atria is slight. Furthermore, the signals

while the other side is relaxing, the amount of blood

However, because one side of the atria is contracting

the atria, usually between 200 and 350 beats per minute.

13–19. Atrial flutter causes a rapid rate of contraction of

the atrial muscle mass, as shown to the left in Figure

lation, in that the electrical signal travels as a single

movement in the atria. It is different from atrial fibril-

if the heart is capable of this.

into refractoriness for a few seconds; a normal rhythm

shock through the heart, which throws the entire heart

atrial fibrillation be converted by electroshock. The pro-

back to a normal rhythm by electroshock, so too can

Electroshock Treatment of Atrial Fibrillation.

minute.

heart rate, usually between 125 and 150 beats per

impulses in the atria, the ventricle is driven at a fast

tion. Also, because of the rapid rate of the fibrillatory

heartbeats in the electrocardiogram of Figure 13–18, is

irregularity, demonstrated by the variable spacing of the

second, causing a very irregular heartbeat. In fact, this

arrive at the A-V node. Thus, the interval between suc-

156

Unit III

The Heart

variable interval of 0 to 0.6 second occurs before one of
the irregular atrial fibrillatory impulses happens to

cessive ventricular contractions varies from a minimum
of about 0.35 second to a maximum of about 0.95

one of the clinical findings used to diagnose the condi-

In the same

manner that ventricular fibrillation can be converted

cedure is essentially the same as for ventricular fibrilla-
tion conversion—passage of a single strong electric

often follows

Atrial Flutter

Atrial flutter is another condition caused by a circus

large wave always in one direction around and around

note in the record that a QRS-T complex follows an
atrial P wave only once for every two to three beats of

A final serious abnormality of the cardiac rhythmicity-
conduction system is
cessation of all electrical control signals in the heart.

Cardiac arrest is especially likely to occur during deep

anesthesia, when many patients develop severe hypoxia

vents the muscle fibers and conductive fibers from main-
taining normal electrolyte concentration differentials

In most instances of cardiac arrest from anesthesia,

prolonged cardiopulmonary resuscitation (many
minutes or even hours) is quite successful in re-

severe myocardial disease can cause permanent or

from an

have

been used successfully to keep patients alive for months

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Figure 13–19

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