Arrhythmias and Sudden Cardiac Death
Nathan D. Wong, PhD
What are arrhythmias?
Normal cardiac rhythm results from electrical impulses
that start in the sinoatrial (or sinus) node. They spread in a
timely way through the atha to the atrioventricular (AV)
node. From there each impulse travels over the many
specialized fibers of the His-Purkinje system, distributing the
electrical ignition signal to the ventricular muscle cells.
The transmission of impulses is delayed a fraction within
the AV node. This allows time for the atrial contraction that
helps fill the ventricles with blood.
The term arrhythmia refers to any change from this normal
sequence of beginning and conducting impulses. Some
arrhythmias are so brief (for example, a temporary pause or
premature beat) that the overall heart rate isnít significantly
affected. However, if arrhythmias last for some time, they
may cause the heart rate to be too slow or too fast.
The term bradycardia is used to describe a rate of less
than 60 beats per minute. Tachycardia usually refers to a
heart rate of more than 100 beats per minute. Tachycardia
may be nonsustained (lasting only seconds) or sustained
(lasting for minutes or hours).
How do arrhythmias occur?
Cells in the heartís conduction system, from the sinus
node down to the outer branches of the His-Purkinje
system, can fire automatically and begin electrical activity.
Normally, the sinus node contains the heartís most rapidly
firing cells. (This allows this area to be a natural pace-
maker.) Subsidiary pacemakers elsewhere in the heart
provide a back-up rhythm when the sinus node doesnít
work properly or when the transmission of impulses is
blocked somewhere in the conduction system.
Under certain conditions the automatic
firing rate of secondary pacemaker tissue
may become too fast. If such an abnormal
locus fires faster than the sinus node, it
may take over control of the heart rhythm and
Arrhythmias also may develop because of
abnormalities in how impulses are
conducted. Delays in the spreading of
impulses can occur anywhere in the conduc-
tion system. When the transmission of
impulses is intermittently or completely
blocked (heart block), bradycardia may
result. In such cases, subsidiary pacemaker
cells (located beyond the conduction block)
may maintain cardiac rhythm.
In another type of abnormal conduction,
impulses get caught in a merry-go-round-like
sequence. This process, called reentry, is a
common cause of tachycardias. Regardless of
what causes them, tachycardias may be
subclassified according to where they arise. Thus, ventricular
tachycardias originate in the heartís lower chambers.
Supraventricular tachycardias arise higher in the heart
either in the upper chambers (atria) or the middle region (AV
node or the very beginning portion of the His-Purkinje
What are the symptoms of arrhythmias?
Arrhythmias can produce a broad range of symptoms,
from barely perceptible to cardiovascular collapse and death.
When theyíre very brief, arrhythmias are most likely to be
almost symptomless. For example, a single premature beat
may be perceived as a palpitation or skipped beat.
Premature beats that are frequent or occur in rapid succes-
sion during a nonsustained or sustained tachycardia may
cause a greater awareness of heart palpitations or a fluttering
sensation in the chest or neck.
When arrhythmias last long enough to affect how well the
heart works, more serious symptoms may develop. At slower
rates, the heart may not be able to pump enough blood to
the body. This can cause fatigue, lightheadedness, loss of
consciousness or even death. Death occurs if the heart rate
is zero or so slow that the heart and brain stop working.
Tachycardias can reduce the heartís ability to pump by
interfering with the ventricular chambersí ability to properly fill
with blood. They do this by reducing the time for such filling
or by interfering with the booster effect normally provided by
timely contraction of the atria (or both).
Loss of this atrial kick during tachycardia may be caused
by a change from the usual sequence of atrial and ventricular
activation. It also can be caused by rapid chaotic
electrical activity in the upper chambers (cailled atrial fibrillation).
The reduced pumping efficiency that can develop
during tachycardia may be made worse by underlying heart
muscle abnormalities or atherosclerotic blocks in the coronary
arteries. Itís not surprising, then, that tachycardias can
produce shortness of breath, chest pain, lightheadedness or
loss of consciousness.
When the heartís ability to work is significantly reduced for
a prolonged time, cardiac arrest and death are likely. This may
result from very fast ventricular tachycardias and ventricular
fibrillation (an extremely rapid, chaotic rhythm during which
the heart merely quivers). If the heart can continue to pump
normally, though, some ventricular tachycardias (even those
that last for minutes or hours) may be well tolerated without a
loss of consciousness or cardiac arrest.
Tachycardias sometimes can cause serious injury to other
organ systems. For example, the brain, kidneys, lungs or
liver may be damaged during prolonged cardiac arrest. Also,
blood clots can form in the upper heart chambers as a result
of atrial fibrillation. They may break free and cause a stroke
or damage other organs.
Who is prone to arrhythias?
Although thereís great variation in their severity, arrhythmias
occur throughout the population. On an everyday level,
heart rate speeds up (sinus tachycardia) during physical
activity, stress or excitement, and slows down (sinus bradycardia)
during sleep. Even beyond these daily changes,
probably everyone at one time or another develops premature
atrial or ventricular beats. In fact, during a 24-hour
period about one-fifth of healthy adults are likely to have
frequent or multiple types of ventricular premature beats.
(This includes short episodes of ventricular tachycardia in a
small percentage of monitored people.)
The prevalence of atrial and ventricular arrhythmias tends
to increase with age, even when thereís no overt sign of
heart disease. Certain congenital conditions may predispose
a person to arrhythmias. For example, an incompletely
developed conduction system can cause chronic heart block
and bradycardia. On the other hand, people born with extra
conduction pathways, either near the AV node or bridging
the atria and ventricles, are prone to reentrant supraventricular
Still, acquired heart disease is the most important factor
predisposing a person to arrhythmias. The main causes are
atherosclerosis, hypertension and inflammatory or degenerative
conditions. The scarring or abnormal tissue deposits
found with these diseases can cause bradycardias; they do
this by interfering with the work of the sinus node or overall
AV conduction. Likewise, they can cause tachycardias (originating
in either the atria or ventricles) by causing cells to fire
abnormally or by creating islands of electrically inert tissue.
(impulses circulate in a reentrant fashion around these areas.)
A variety of other factors may predispose a person to
develop arrhythmias. Prominent among them is the part of
the autonomic nervous system thatís involved in cardiovascular
regulation. One element of this control system slows
the sinus rate and depresses AV nodal conduction. (These
effects may prevail during sleep or in athletically well-trained
people.) The opposing element of the autonomic nervous
system tends to speed up the firing rate of the sinus node
and other pacemaker tissue in the heart. Further, it may also
make it easier for reentrant tachycardias to occur.
Many chemical agents may provoke arrhythmias, sometimes
with serious consequences. Known factors include
high or low blood and tissue concentrations of a variety of
minerals, such as potassium, magnesium and calcium.
These play a vital role in starting and conducting normal
impulses in the heart. Addictive substances, especially
alcohol, cigarettes and recreational drugs, can provoke
arrhymias, as can various cardiac medications. Even drugs
used to treat an arrhythmia may provoke another arrhythmia.
How are arrythmias diagnosed?
An electrocardiogram is the standard clinical tool for diagnosing
arrhythmias. Such a recording shows the relative
timing of atrial and ventricular electrical events. It can be
used to measure how long it takes for impulses to be transmitted
through the atria, AV conduction system and ventricles.
An arrhythmia is considered documented if it can be
recorded on an electrocardiogram. Often, though, the electrocardiogram
of a person who complains of symptoms that
suggest arrhythmia doesnít show anything (because of the
fleeting nature of arrhythmias).
Suspected arrhythmias sometimes may be documented
by using a small, portable recording module, called a Holter
monitor. This can record 24 hours of continuous electrocardiographic
signals. For suspected arrhythmias that occur
less than daily, a patient can wear an event monitor. It
provides for a continuously updated memory loop and can
allow the heart to be monitored by telephone.
These electrocardiographic techniques are passive; they
require an arrhythmia to spontaneously occur. Other options
that provoke arrhythmias and make their diagnosis (and
thus their proper treatment) easier also are used. For
example, treadmill testing may be considered for people
whose suspected arrhythmias are clearly exercise related.
In patients prone to passing out, tilt table studies may repro-
duce the faint when itís due to abnormal nervous system
reflexes that cause the heart rate to slow down and the
blood pressure to drop.
Electrophysiologic testing has become extremely valuable
for provoking known, but infrequently occurring, arrhythmias
and for unmasking suspected arrhythmias. This procedure
is performed under local anesthesia. It involves placing
temporary electrode catheters through peripheral veins (and
sometimes through arteries) into the heart using fluoroscopic
guidance. Then these catheters are positioned in the
atria, ventricles or both, and at strategic locations along the
conduction system. Their purpose is to record cardiac elec-
trical signals and map the spread of electrical impulses
during each beat.
This technique shows where the heart block is (AV node
vs. His-Purkinje system). It also shows the origin of tachycardia
(supraventricular vs. ventricular) far better than is
usually possible using an electrocardiogram. The ability to
electrically stimulate the heart at programmed rates and
induce precisely timed premature beats lets a doctor assess
electrical properties of the heartís conduction system. Most
significantly, it also triggers latent tachycardia or bradycardia.
Induced tachycardias can usually be stopped by
rapid pacing via the electrode catheters. Sometimes an
externally applied shock may be required if the patient loses
consciousness during the tachycardia.
Being able to turn on and turn off tachycardias during
electrophysiologic studies allows antiarrhythmic drugs to be
quickly tested for effectiveness. This can be done during a
single study using intravenous therapy or during short
follow-up studies with oral medication. Worldwide experience
with electrophysiologic testing has shown it to be
relatively safe; the rate of complications is very low.
When should arrythmias be treated?
Once an arrhythmia has been documented,
itís important to try to find out where
it starts in the heart. Itís also necessary to
find out whether itís abnormal or merely
reflects the heartís normal physiologic
processes. The arrhythmia must be
abnormal and clinically significant before it
justifies an antiarrhythmic intervention. In
other words, it must either cause symptoms
or put a person at risk for more serious
arrhythmias or complications of arrhythmias
in the future.
In some patients whose symptoms
suggest arrhythmias, tachycardias or bradycardias
may be found during diagnostic
(particulady electrophysiologic) tests. In such
cases, a doctor must judge whether the
arrhythmia is a likely enough explanation for
the patientís original symptoms to justify
therapy. The risks and benefits of the intervention
also must be taken into account.
How are bradycardias treated?
Potentially life-threatening bradycardias may be treated
acutely with medication. Such medication increases the
automatic fidng rate of cardiac pacemaker tissue and
improves the transmission of impulses through the conduction
Another way to maintain the cardiac rhythm is to insert a
temporary pacemaker. This involves using a thin, flexible
electrode wire. One end is positioned inside the heart; the
other is connected to an external temporary pulse generator
that can electrically stimulate the heart via the wire. If symptomatic
bradycardia persists or is likely to recur, despite
eliminating reversible causes, then implanting a permanent
pacemaker is appropriate. This device consists of a pulse
generator, which can be as small as a silver dollar. The
pulse generator is hooked up to one or two pacemaker
leads that are permanently affixed to a ventricular or atrial
site, or to both.
Permanent pacemakers deliver electrical stimuli to the
heart when the heartís spontaneous rate falls below a set
value. Physiologic sensors are being incorporated into these
devices to let the pacemakerís rate vary according to the
The pacemaker generator is implanted under the skin
below the collarbone. Typically it works for 8-12 years before
it needs to be replaced.
How are tachycardias treated?
Symptomatic tachycardias and premature beats may be
treated with a variety of antiarrhythmic drugs. These may be
given intravenously on an acute basis, or in oral form for
long-term treatment. These drugs act by suppressing the
abnormal firing of pacemaker tissue or by depressing the
transmission of impulses in tissues that either conduct too
rapidly or that participate in reentry. In patients with atrial
fibrillation, a blood thinner (anticoagulant) is often added to
reduce the risk of blood clots and stroke.
When tachycardias or premature beats occur often, the
effectiveness of antiarrhythmic drug therapy may be gauged
by electrocardiographic monitoring in a hospital, by using a
24-hour Holter monitor or by serial drug evaluation with
The relative simplicity of antiarrhythmic drug therapy must
be balanced against two disadvantages. One is that the
drugs must be taken daily for an indefinite period. The
second is the risk of side effects. While side effects are
inherent in all medication, those associated with antiarrhythmic
drugs can be most difficult to manage. These side
effects include proarrhythmia, which is more frequent
occurrence of preexisting arrhythmias or the appearance of new
arrhythmias as bad or worse than those being treated.
A host of nondrug therapies are being used to treat
patients with symptomatic tachycardias. Ablative techniques
refer to therapeutic methods that physically
destroy the cardiac tissue that causes or
contributes to a tachycardia. Until recently,
such therapy was only feasible through
surgery (often involving an open heart
procedure). In such a surgical approach, the
culprit cardiac tissue is removed or
destroyed by local heating or cooling.
Newer advances now permit therapeutic
ablations to be done using a transcatheter
approach. In this technique, an electrode
catheter inserted through a vein during electrophysiologic
studies is used to perform
targeted electrocautery in the heart. A
patient may be cured of tachycardia through
ablative therapy, so that antiarrhythmic medication
is no longer needed. Transcatheter
ablation is rapidly becoming the treatment of
choice for many supraventricular tachycardias.
Electrical therapy is also available for
treating tachycardias. On an acute basis,
many pathological tachycardias can be
stopped by an electric shock delivered to the
heart or by rapid overdrive pacing with an
electrode catheter. Implantable devices can
provide automatic electrical therapy on a chronic basis for
patients with recurrent tachycardias.
The greatest advance in this area is the implantable
cardioverter defibrillator. Itís used in patients at risk for recurrent
sustained ventricular tachycardia or fibrillation. This
device consists of electrode patches, leads or both, which
may be used to deliver electric shocks. It also has at least
one other electrode lead to sense the cardiac rhythm and, if
necessary, pace the heart.
These various leads are tunnelled from the heart to a
pulse generator. (The generator is currently a little larger
than a cigarette pack). Itís usually implanted in a pouch
beneath the skin on the left side of the abdomen. Right now
at least one of the electrode patches must be put on the
heartís surface or on its surrounding sac. This is done in an
open-chest procedure. New generation devices, now being
evaluated, will require an electrode patch to be put only
beneath the skin in the chest wall area and electrode wires
inserted into the heart via veins. This will make implanting
them much simpler.
When the implantable cardioverter defibrillator detects
ventricular tachycardia or fibrillation, it shocks the heart to
restore the normal rhythm. New devices are becoming avail-
able that can provide for overdrive pacing to electrically
convert sustained ventricular tachycardia, backup pacing
in the event of bradycardia, and a host of other sophisticated
functions (such as storage of detected arrhythmic events
and capability to perform noninvasive electrophysiologic
Implantable cardioverter defibdilators have already been
very useful in preventing sudden death in patients with
known sustained ventricular tachycardia or fibrillation.
Studies are now being done to find out whether they may
have a role in preventing cardiac arrest in high-risk patients
who havenít yet had, but are at risk for, life-threatening
What is sudden cardiac death (SCD)?
Itís the sudden, abrupt loss of heart function (i.e., cardiac
arrest) in a person who may or may not have diagnosed
heart disease, but in whom the time and mode of death
occur unexpectedly. The unexpected nature of the event is
the key point in the definition.
How common is the sudden cardiac death syndrome?
About half of all deaths from heart disease are sudden
and unexpected, regardless of the underlying disease. Thus
50 percent of all deaths due to atherosclerosis of the coronary
arteries are sudden, as are 50 percent of deaths due to
degeneration of the heart muscle, or to cardiac enlargement
in patients with high blood pressure.
Sudden death is a major health problem; about 250,000
sudden cardiac deaths occur each year among U.S. adults.
Controlling SCD might significantly reduce death from heart
What is the impact of sudden cardiac death?
The shock of sudden cardiac death lies in its unexpectedness.
Although the direct medical costs are much less than
for lingering illnesses, its economic and social impacts are
huge. Sudden cardiac death occurs at an average age of
about 60 years, claims many people during their most
productive years and devastates unprepared families.
What causes sudden cardiac death?
SCD is the result of an unresuscitated cardiac arrest,
which may be caused by almost all known heart diseases.
Most cardiac arrests are due to rapid and/or chaotic activity
of the heart (ventricular tachycardia or fibrillation); some are
due to extreme slowing of the heart. These events are
called life-threatening arrhythmias and are responsible for
The term massive heart attack, commonly used in the
media to describe sudden death, only infrequently is responsible.
Heart attack more properly refers to death of heart
muscle tissue due to the loss of blood supply. While a heart
attack may cause cardiac arrest and sudden cardiac death,
the terms arenít synonymous.
Can the cardiac arrest that causes sudden cardiac death be reversed?
Cardiac arrest is reversible in most victims if itís treated
within a few minutes. This first became clear in the early
1960s with the development of coronary care units and electrical
devices that shocked the heart to turn an abnormally
rapid rhythm into a normal one. Before then, heart attack
victims had a 30 percent chance of dying if they got to the
hospital alive; 50 percent of these deaths were a consequence
of cardiac arrest.
In-hospital survival after cardiac arrest in heart attack
patients improved dramatically when the DC defibrillator and
bedside monitoring were developed. Later, it also became
clear that cardiac arrest could be reversed outside a hospital
by appropriately staffed emergency rescue teams trained to
perform CPR and to defibrillate. Thus, the problem isnít the
ability to reverse cardiac arrest, but reaching the victim in
time to do so. The American Heart Association supports the
concept of the need for a chain of survival to rescue the
person who suffers cardiac arrest in the community.
Whoís at risk for sudden cardiac death?
Underlying heart disease is nearly always found in victims
of sudden cardiac death. Typically in adults this takes the form
of atherosclerotic heart disease. Two or more major coronary
arteries are narrowed in 90 percent of cases; scarring from a
prior heart attack is found in two-thirds of victims. Itís not surprising,
then, that predisposing factors for sudden cardiac death
are similar to risk factors for atherosclerotic heart disease
and include cigarette smoke and high blood pressure.
A heart thatís scarred or enlarged from any cause is
prone to develop life-threatening ventricular arrhythmias.
The first six months after a heart attack is a particularly high-risk
period for sudden cardiac death in patients who have
atherosclerotic heart disease. A thickened heart muscle
from any cause (typically high blood pressure or valvular
heart disease) - especially when thereís congestive heart
failure, too - is an important predisposing factor for sudden
Under certain conditions, various heart medications can
set the stage for arrhythmias that cause sudden cardiac
death. In particular, so-called antiarrhythmic
drugs, even at normally prescribed
doses, sometimes may produce lethal
ventricular arrhythmias (proarrhythmic effect).
Regardless of whether thereís
organic heart disease, significant changes in
blood levels of potassium and magnesium
(from using diuretics, for example) also can
cause life-threatening arrhythmias and
When sudden cardiac death occurs in
young adults, atherosclerotic heart disease
usually isnít the cause. More often these
young victims have a thickened heart
muscle (hypertrophic cardiomyopathy)
without accompanying high blood pressure.
Certain electrical abnormalities within the
heart may be responsible for sudden cardiac death in the
young. These include a short circuit between the upper and
lower chambers (Wolff-Parkinson-White syndrome). This
sometimes can allow dangerously rapid rates to develop in
the lower chamber when thereís a rapid rhythm disturbance
in the upper chamber and a congenitally prolonged electrical
recovery after each heartbeat (long-QT syndrome) that may
set the stage for fatal ventricular arrhythmias.
Less often, inborn abnormalities of the blood vessels,
particularly the coronary arteries and aorta, may be present
in young sudden death victims.
Adrenalin released during intense physical or athletic
activity often acts as a trigger for sudden cardiac death
when these predisposing conditions are present.
In young people without organic heart disease, recreational
drug abuse is an important cause of sudden cardiac death.
How can survivors of unexpected cardiac arrest be protected from fatal recurrences?
Survivors of unexpected cardiac arrest (aborted sudden
cardiac death) due to ventricular tachycardia or fibrillation
are at risk for recurrent arrest. This is especially true if they
have underlying heart disease. Patients with atherosclerotic
heart disease are at risk of recurrent cardiac arrests when
the first, aborted sudden death episode occurs in the
absence of a new heart attack, because this implies a
persistent underlying tendency toward electrical instability.
To find the treatment program most likely to prevent recurrent
cardiac arrest in a patient, itís critical to identify any
predisposing anatomic or electrophysiologic abnormalities.
This often requires cardiac catheterization (to show the
heart and coronary blood vessels) and electrophysiologic
testing. Itís also necessary to determine the possible contribution
of reversible causes; if theyíre identified and removed
or corrected, the risk of recurrent cardiac arrest can be
markedly reduced or eliminated. Such factors may include
excessive doses of various cardiac drugs, the presence of
antiarrhythmic agents and abnormal blood levels of various
minerals, especially potassium.
The treatment program used to prevent fatal recurrences
in survivors of cardiac arrest due to ventricular tachycardia
or fibrillation must be chosen based upon several factors
that depend on the individual. These include the underlying
cardiac condition, how well the heart can pump and the
demonstration of ventricular tachycardia or fibrillation during
For example, cardiac arrest survivors with the Wolff-Parkinson-White
syndrome (who otherwise have normal
hearts) may be satisfactorily treated simply with a catheter
procedure that destroys the short circuit between the upper
and lower heart chambers. At the other extreme, a heart
transplant may be recommended for patients whoíve had a
cardiac arrest as a result of very severe heart failure.
In cardiac arrest survivors with atherosclerotic heart
disease but without a new heart attack, attention must be
paid to both the degree of narrowing in the coronary arteries
and the presence of ventricular tachycardia and fibrillation
that can occur during electrophysiologic testing. Therapy
limited to reversing or blunting the effects of reduced blood
supply to the heart (through bypass surgery, angioplasty or
medication) is likely to protect only a minority of these
aborted sudden death patients from recurrent cardiac arrest.
The reason is that such treatments alone donít stabilize the
electrical abnormalities in scarred heart muscle that can
lead to recurrent cardiac arrest.
A number of therapies exist for controlling potentially life-threatening
ventricular tachyarrhythmias that result from
diseased or scarred heart muscle. Antiarrhythmic medication
may protect against subsequent sudden death in certain
subsets of cardiac arrest survivors (for example, in persons
whose hearts pump well who are given a drug that
suppresses ventricular tachycardia induced during electrophysiologic
testing). However, antiarrhythmic medication is
limited by the need for life-long dosing and the potential for
intolerable or lethal side effects. Consequently, thereís been
increasing reliance on the use of implantable cardioverterdefibrillators.
They can automatically detect ventricular
tachycardia or fibrillation when it occurs and, within seconds,
deliver a lifesaving electrical shock to restore the normal
Rapid heart rhythms account for the great majority of
sudden cardiac deaths. Still, very slow rhythms due to
conduction system failure are sometimes responsible for
cardiac arrest. Persons resuscitated from this uncommon
type of cardiac arrest are treated with a permanent pacemaker
after acute reversible causes, such as drug toxicity,
have been ruled out.
What are the hopes for the future?
If the past is any indication, thereís great hope for the
future. The dramatic progress during the past 30 years,
focused largely on very high-risk groups (such as cardiac
arrest survivors), has shown what can be achieved. At the
same time, recent advances in treating heart attack victims
appear to be reducing the significant risk of sudden death
during the first year after a heart attack.
In the future, we need to develop ways to identify potential
victims. People whose risk may not be very high account
for the vast majority of sudden death victims in absolute
numbers - perhaps 80 percent of the deaths per year.
Once identified, it will be possible to devise broader strategies
to prevent sudden cardiac arrest.
Last Updated: August 9, 1995