Hi Everyone, I know this is lengthy, but maybe some of you in the group
would like to print this info I found surfing around today.. something
to read for reassurance when the pvc's start up cindy:
The Merck Manual of Medical Information--Home
Edition
Section 3. Heart and Blood Vessel Disorders
Chapter 16
Abnormal Heart Rhythms
The heart is a muscular organ with four chambers designed to
work efficiently,
reliably, and continuously over a lifetime. The muscular
walls of each chamber
contract in a precise sequence, pushing along the most blood
while expending the
least possible energy during every heartbeat.
The contraction of the muscle fibers in the heart is
controlled by an electrical
discharge that flows through the heart in a precise manner
along distinct pathways
and at a controlled speed. The rhythmic discharge that begins
each heartbeat
originates in the heart's pacemaker (sinoatrial node), which
lies in the wall of the
right atrium. The rate of discharge is influenced by nerve
impulses and by levels of
hormones circulating through the bloodstream.
The part of the nervous system that regulates the heart rate
automatically is the
autonomic nervous system, which consists of the sympathetic
and
parasympathetic nervous systems. The sympathetic system
speeds up the heart
rate; the parasympathetic system slows it down. The
sympathetic system supplies
the heart with a network of nerves, the sympathetic plexus.
The parasympathetic
system supplies the heart through a single nerve, the vagus
nerve.
Heart rate is also influenced by the sympathetic system's
circulating
hormones--epinephrine (adrenaline) and norepinephrine
(noradrenaline)--which
speed up the heart rate. Thyroid hormone influences heart
rate as well. With too
much thyroid hormone, the heart beats too fast; with too
little, it beats too slowly.
The normal heart rate at rest is usually between 60 and 100
beats per minute.
However, much lower rates may be normal in young adults,
particularly those who
are physically fit. Variations in heart rate are normal. The
heart rate responds not
only to exercise and inactivity but also to stimuli such as
pain and anger. Only
when the heart rate is inappropriately fast (tachycardia) or
slow (bradycardia) or
when the electrical impulses travel in abnormal pathways is
the heartbeat
considered to have an abnormal rhythm (arrhythmia). Abnormal
rhythms may be
regular or irregular.
Electrical Pathway
The electrical discharge from the pacemaker flows first
through the
left and right atria, causing muscle tissue to contract in
sequence
and blood to be ejected from the atria to the ventricles. The
electrical
discharge then reaches the atrioventricular node between the
atria
and the ventricles. This node delays transmission of the
electrical
discharge to allow the atria to contract completely and the
ventricles
to fill with as much blood as possible during ventricular
diastole, the period of
ventricular relaxation.
After passing through the atrioventricular node, the
electrical discharge travels
down the bundle of His, a group of fibers that divide into a
left bundle for the left
ventricle and a right bundle for the right ventricle. The
discharge then spreads in
an orderly manner over the surface of the ventricles,
initiating ventricular
contraction (systole), during which blood is ejected from the
heart.
Various problems can occur with this flow of electrical
current, resulting in
arrhythmias ranging from harmless to life threatening. Each
type of arrhythmia has
its own cause, but some causes can trigger a variety of
arrhythmias. Minor
arrhythmias may be triggered by excessive alcohol
consumption, smoking, stress,
or exercise. Overactive and underactive thyroid function and
some drugs, especially
those used to treat lung disease and some used to treat high
blood pressure, may
affect the rate and rhythm of the heart. The most common
cause of arrhythmias is
heart disease, particularly coronary artery disease, abnormal
heart valve function,
and heart failure. Sometimes arrhythmias occur without any
detectable underlying
heart disease or other cause.
Symptoms
The awareness of one's heartbeat (called palpitations) varies
widely among people.
Some people can feel even normal heartbeats. At times when
lying on the left side,
most people can feel the heart beating. Also, people may be
aware of abnormal
heartbeats. Often, the awareness of one's heartbeat is
disturbing, but usually it
doesn't result from an underlying disease. Rather, it results
from unusually strong
contractions that occur periodically for a variety of
reasons.
A person who has a certain type of arrhythmia tends to have
that same arrhythmia
repeatedly. Some types of arrhythmias cause few or no
symptoms but eventually
cause problems. Other arrhythmias never cause serious
problems but do cause
symptoms. Often, the nature and severity of the underlying
heart disease are more
important than the arrhythmia itself.
When arrhythmias affect the heart's ability to pump blood,
they can produce
light-headedness, dizziness, and fainting (syncope). (see
page 108 in Chapter 23,
Low Blood Pressure) Arrhythmias that produce these symptoms
require prompt
attention.
Diagnosis
A person's description of symptoms often can help a doctor
make a preliminary
diagnosis and determine the severity of the arrhythmia. The
most important
considerations are whether a person with palpitations
describes the heartbeats as
fast or slow, regular or irregular, brief or prolonged;
whether the person feels
dizzy, light-headed, or faint or even loses consciousness;
and whether chest pain,
shortness of breath, or other unusual sensations occur along
with the palpitations.
A doctor also needs to know whether the palpitations occur at
rest or only during
strenuous or unusual activity and whether they start and stop
suddenly or
gradually.
Usually, some additional testing is needed to determine the
exact nature of the
condition. Electrocardiography (see illustration, page 74) is
the main diagnostic
procedure for detecting arrhythmias. This test provides a
graphic representation of
the arrhythmia.
However, an electrocardiogram (ECG) shows the heart rhythm
over only a very
brief time, and often arrhythmias are intermittent. Thus, a
portable monitor (Holter
monitor), (see illustration, page 75) which is worn for 24
hours, can provide more
information. This monitor can record sporadic arrhythmias as
the person goes
about a normal daily routine. The person also keeps a diary
of symptoms during
the 24-hour period. People with suspected life-threatening
arrhythmias are
generally hospitalized for monitoring.
When a sustained, life-threatening arrhythmia is suspected,
electrophysiologic
studies may be helpful. A catheter containing wires is
threaded through a vein and
into the heart. Electrical stimulation and sophisticated
monitoring are combined to
determine the type of arrhythmia and the most likely response
to treatment. Most
serious arrhythmias can be detected by this technique.
Prognosis and Treatment
The prognosis depends in part on whether an arrhythmia begins
in the heart's
normal pacemaker, the atria, or the ventricles. In general,
those starting in the
ventricles are more serious, although many of them aren't
harmful.
Most arrhythmias neither cause symptoms nor interfere with
the pumping action of
the heart, so they pose little or no risk. Nevertheless,
arrhythmias can cause
considerable anxiety if a person becomes aware of them.
Understanding their
harmlessness may be reassurance enough. Sometimes, when a
doctor changes a
person's medications or adjusts the dosages, or when a person
avoids alcohol or
strenuous exercise, arrhythmias occur less often or even
stop.
Antiarrhythmic drugs are useful for suppressing arrhythmias
that cause intolerable
symptoms or pose a risk. No single drug cures all arrhythmias
in all people.
Sometimes several drugs must be tried until a satisfactory
one is found.
Antiarrhythmic drugs can produce side effects and can worsen
or even cause
arrhythmias.
Artificial pacemakers, electronic devices that act in place
of the heart's own
pacemaker, are programmed to imitate the normal conduction
sequence of the
heart. Usually, they're implanted surgically under the skin
of the chest and have
wires running to the heart. Because of low-energy circuitry
and new battery
designs, these units now last about 8 to 10 years. New
circuitry has almost
completely eliminated the risk of interference from
automobile distributors, radar,
microwaves, and airport security detectors. Some
equipment--such as machines
used in magnetic resonance imaging (MRI) and diathermy
(physical therapy used to
bring heat to muscles)--may, however, interfere with
pacemakers.
The most common use of pacemakers is to treat abnormally slow
heart rates.
When the heart slows below a set threshold, the pacemaker
begins to fire off
electrical impulses. Very rarely, a pacemaker is used to
deliver a series of impulses
to stop an abnormally fast rhythm and slow the heart rate.
Such pacemakers are
used only for fast rhythms that start in the atria.
Sometimes an electric shock to the heart can stop an abnormal
rhythm and restore
a normal one; using an electric shock for this purpose is
called cardioversion,
electroversion, or defibrillation. Cardioversion may be used
for arrhythmias starting
in the atria or the ventricles. Usually, a large machine that
delivers the shock (a
defibrillator) is used by a team of doctors and nurses to
stop a life-threatening
arrhythmia. However, a defibrillator about the size of a pack
of cards can be
implanted surgically. These small devices, which
automatically sense life-threatening
arrhythmias and deliver a shock, are used in people who would
otherwise die when
their heart suddenly stops. Because these defibrillators
don't prevent arrhythmias,
the person usually takes drugs as well.
Certain types of arrhythmias can be corrected by surgical and
other invasive
procedures. For example, arrhythmias caused by coronary
artery disease may be
controlled by angioplasty or coronary artery bypass surgery.
(see page 125 in
Chapter 27, Coronary Artery Disease) When an arrhythmia is
caused by an irritable
spot in the electrical system of the heart, the spot can be
destroyed or removed.
Most often, the spot is destroyed by catheter ablation
(delivery of radiofrequency
energy through a catheter inserted in the heart). After a
heart attack (myocardial
infarction), some people have life-threatening episodes of an
arrhythmia called
ventricular tachycardia. This arrhythmia may be triggered by
an injured area of
heart muscle that can be identified and removed during open
heart surgery.
Atrial Ectopic Beats
An atrial ectopic beat is an extra heartbeat caused by
electrical activation of the
atria before the normal heartbeat.
Atrial ectopic beats occur as additional heartbeats in
healthy people and rarely
cause symptoms. Sometimes they're caused by or worsened by
alcohol, cold
remedies containing drugs that stimulate the sympathetic
nervous system (such as
ephedrine or pseudoephedrine), or drugs used to treat asthma.
Diagnosis and Treatment
Atrial ectopic beats may be detected by physical examination
and are confirmed by
an electrocardiogram (ECG). If treatment is necessary because
ectopic beats occur
frequently and cause intolerable palpitations, a doctor may
prescribe a beta-blocker
to slow the heart rate.
Paroxysmal Atrial Tachycardia
Paroxysmal atrial tachycardia is a regular, fast (160 to 200
beats per minute)
heart rate that occurs suddenly and is triggered in the
atria.
Several mechanisms can produce paroxysmal atrial
tachycardias. The fast rate may
be triggered by a premature atrial beat that sends an impulse
on an abnormal path
to the ventricles.
The fast heart rate tends to start and stop suddenly and may
last anywhere from
a few minutes to many hours. It's almost always experienced
as an uncomfortable
palpitation and is often associated with other symptoms, such
as weakness.
Usually, the heart is otherwise normal, and the episodes are
more unpleasant than
dangerous.
Treatment
Episodes of the arrhythmia often can be stopped by one of
several maneuvers that
stimulate the vagus nerve and thus slow the heart rate. These
maneuvers, which
are usually conducted by a doctor, include having the person
strain as if having a
difficult bowel movement, rubbing the person's neck just
below the angle of the
jaw (which stimulates a sensitive area on the carotid artery
called the carotid
sinus), and plunging the person's face into a bowl of
ice-cold water. These
maneuvers work best when they're used shortly after the
arrhythmia starts.
If these maneuvers don't work, the episode will usually stop
if the person simply
goes to sleep. However, most people seek medical intervention
to end the episode.
A doctor can usually stop an episode promptly by giving an
intravenous dose of
the drug verapamil or adenosine. Rarely, the drugs don't
work, and cardioversion
(delivery of a shock to the heart) may be used.
Prevention is more difficult than treatment, but several
drugs may be effective
when used alone or in combination. In rare cases, an abnormal
pathway in the
heart may need to be destroyed by catheter ablation (delivery
of radiofrequency
energy through a catheter inserted in the heart).
Atrial Fibrillation and Flutter
Atrial fibrillation and atrial flutter are very fast
electrical discharge patterns that
make the atria contract extremely rapidly, thus causing the
ventricles to contract
faster and less efficiently than normal.
These abnormal rhythms may occur sporadically or may persist.
During fibrillation
or flutter, the contractions of the atria are so fast that
the atrial walls simply
quiver, so blood isn't pumped effectively to the ventricles.
In fibrillation, the atrial
rhythm is irregular, so the ventricular rhythm is also
irregular; in flutter, the atrial
and ventricular rhythms usually are regular. In both cases,
the ventricles beat more
slowly than the atria because the atrioventricular node and
the bundle of His can't
conduct electrical impulses at such a fast rate, and only
every second to fourth
impulse gets through. Still the ventricles beat too fast to
fill completely. Therefore,
inadequate amounts of blood are pumped out of the heart,
blood pressure falls,
and heart failure may occur.
The heart may go into atrial fibrillation or flutter with no
other sign of heart
disease, but more often the cause is an underlying problem,
such as rheumatic
heart disease, coronary artery disease, high blood pressure,
alcohol abuse, or too
much thyroid hormone (hyperthyroidism).
Symptoms and Diagnosis
Symptoms of atrial fibrillation or flutter depend largely on
how fast the ventricles
beat. A modest ventricular rate--less than about 120 beats
per minute--may
produce no symptoms. Higher rates cause unpleasant
palpitations or chest
discomfort. With atrial fibrillation, the person may be aware
of the rhythm
irregularities.
The diminished pumping ability of the heart may make the
person feel weak, faint,
and short of breath. Some people, especially the elderly,
develop heart failure,
chest pain, and shock.
In atrial fibrillation, the atria don't empty completely into
the ventricles with each
beat. Over time, some blood inside the atria may stagnate and
clot. Pieces of the
clot may break off, pass into the left ventricle, and
continue into the general
circulation, where they may block a smaller artery. (Pieces
of a clot that block an
artery are called emboli.) Most often, the pieces of a clot
break off shortly after
atrial fibrillation converts to a normal rhythm, either
spontaneously or with
treatment. Blockage of an artery in the brain may cause a
stroke. Rarely, a stroke
is the first sign of atrial fibrillation.
The diagnosis of atrial fibrillation or flutter is suspected
from the symptoms and
confirmed by an electrocardiogram (ECG). With atrial
fibrillation, the pulse is
irregular. With atrial flutter, the pulse is more likely to
be regular but rapid.
Treatment
Treatments for atrial fibrillation and flutter are designed
to control the rate at which
the ventricles contract, treat the disorder responsible for
the abnormal rhythm,
and restore the normal rhythm of the heart. With atrial
fibrillation, treatment is
also usually given to prevent clots and emboli.
The first step in treating atrial fibrillation or flutter is
usually to slow the ventricular
rate to improve the heart's efficiency in pumping blood.
Contractions of the
ventricles usually can be slowed and strengthened with
digoxin, a drug that slows
the conduction of impulses to the ventricles. When digoxin
alone doesn't help,
giving a second drug--a beta-blocker such as propranolol or
atenolol or a calcium
channel blocker such as diltiazem or verapamil--usually does.
Treatment of the underlying disease rarely alleviates atrial
arrhythmias unless the
disease is hyperthyroidism.
Though occasionally atrial fibrillation or flutter
spontaneously reverts to a normal
rhythm, more often it must be converted to normal. Sometimes
such a conversion
can be achieved with certain antiarrhythmic drugs. However,
electric shock
(cardioversion) is often the most effective approach. Success
by any means is less
likely the longer the atria have been in their abnormal
rhythm (especially after 6
months or more), the more the atria are enlarged, and the
more severe the
underlying heart disease has become. When conversion is
successful, the risk that
the arrhythmia will return is high, even if the person takes
preventive drugs such
as quinidine, procainamide, propafenone, or flecainide.
If all other treatments fail, the atrioventricular node can
be destroyed by catheter
ablation (delivery of radiofrequency energy through a
catheter inserted in the
heart). This procedure interrupts conduction from the
fibrillating atria to the
ventricles, but a permanent artificial pacemaker is required
for the ventricles
afterward.
The risk of developing blood clots is highest in people with
atrial fibrillation who
have an enlarged left atrium or who have mitral valve
disease. (see page 93 in
Chapter 19, Heart Valve Disorders) The risk that a clot will
be dislodged and cause
a stroke is particularly high in people who have intermittent
but persistent episodes
of atrial fibrillation or whose fibrillation is converted to
the normal rhythm. Because
anyone with atrial fibrillation is at risk of a stroke,
anticoagulant therapy generally is
recommended to prevent clots unless there's a specific reason
not to give it, such
as high blood pressure. However, anticoagulant therapy itself
carries a risk of
excessive bleeding that can lead to hemorrhagic stroke and
other bleeding
complications. Therefore, a doctor balances the potential
benefits and risks for
each person.
Wolff-Parkinson-White Syndrome
Wolff-Parkinson-White syndrome is an abnormal heart rhythm in
which electrical
impulses are conducted along an extra pathway from the atria
to the ventricles,
causing episodes of a rapid heart rate.
Wolff-Parkinson-White syndrome is the most common of several
disorders that
involve such extra (accessory) pathways. This extra pathway
is present at birth
but seems to conduct impulses through the heart only
occasionally. It may become
apparent as early as the first year of life or as late as age
60.
Symptoms and Diagnosis
Wolff-Parkinson-White syndrome can cause sudden episodes of a
very rapid heart
rate with palpitations.
In the first year of life, babies may develop heart failure
if the episode is prolonged.
They sometimes seem out of breath or lethargic, stop eating
well, or have rapid,
visible pulsations of the chest.
The first episodes may occur in the teens or early twenties.
Typical episodes begin
suddenly, often during exercise. They may last for only a few
seconds or may
persist for several hours, rarely more than 12 hours. In a
young and otherwise
physically fit person, the episodes usually cause few
symptoms, but very rapid
heart rates are uncomfortable and distressing and can cause
fainting or heart
failure. The rapid heart rate sometimes changes to atrial
fibrillation. Atrial fibrillation
is particularly dangerous in about 1 percent of people with
Wolff-Parkinson-White
syndrome because the extra pathway can conduct the rapid
impulses to the
ventricles much more successfully than the normal pathway
can. The result is an
extremely rapid ventricular rate that may be life
threatening. Not only is the heart
very inefficient when it beats so rapidly, but this extremely
rapid heart rate may
progress to ventricular fibrillation, which is immediately
fatal.
The diagnosis of Wolff-Parkinson-White syndrome with or
without atrial fibrillation
is made using an electrocardiogram (ECG).
Treatment
Episodes of the arrhythmia often can be stopped by one of
several maneuvers that
stimulate the vagus nerve and thus slow the heart rate. These
maneuvers, which
are usually conducted by a doctor, include having the person
strain as if having a
difficult bowel movement, rubbing the person's neck just
below the angle of the
jaw (which stimulates a sensitive area on the carotid artery
called the carotid
sinus), and plunging the person's face into a bowl of
ice-cold water. The
maneuvers work best when they're used shortly after the
arrhythmia starts. When
these maneuvers don't work, drugs such as verapamil or
adenosine usually are
given intravenously to stop the arrhythmia. Other
antiarrhythmic drugs are then
used for long-term prevention of episodes of rapid heart
rate.
In infants and children under age 10, digoxin may be given to
suppress episodes
of rapid heart rate. Adults must not take digoxin because it
can speed up
conduction in the extra pathway and increase the risk of
developing fatal
ventricular fibrillation. For this reason, the drug is
usually stopped before a person
reaches puberty.
Destruction of the extra conduction pathway by catheter
ablation (delivery of
radiofrequency energy through a catheter inserted in the
heart) is successful more
than 95 percent of the time. The risk of death during the
procedure is less than 1
in 1,000. Catheter ablation is particularly useful for young
people who might
otherwise face a lifetime of taking antiarrhythmic drugs.
Ventricular Ectopic Beats
A ventricular ectopic beat (premature ventricular
contraction) is an extra
heartbeat caused by electrical activation of the ventricles
before the normal
heartbeat.
Ventricular ectopic beats occur commonly and don't indicate
danger in people who
don't have heart disease. However, when they occur frequently
in a person who
has heart failure or aortic stenosis or who has had a heart
attack, they may be
followed by more dangerous arrhythmias such as ventricular
fibrillation, which can
cause sudden death.
Symptoms and Diagnosis
Isolated ventricular ectopic beats have little effect on the
pumping action of the
heart and usually don't cause symptoms, unless they're
extremely frequent. The
main symptom is the perception of a strong or skipped beat.
Ventricular ectopic beats are diagnosed using an
electrocardiogram (ECG).
Treatment
In an otherwise healthy person, no treatment is needed other
than decreasing
stress and avoiding alcohol and over-the-counter cold
remedies containing drugs
that stimulate the heart. Drug therapy is usually prescribed
only if symptoms are
intolerable or the pattern of ectopic beats suggests danger.
Beta-blockers are
usually tried first because they're relatively safe drugs.
However, many people
don't want to take them because of the sluggishness they can
cause.
After a heart attack, a person who is experiencing frequent
ventricular ectopic
beats may reduce the risk of sudden death by taking
beta-blockers and
undergoing angioplasty or coronary artery bypass surgery (see
page 125 in
Chapter 27, Coronary Artery Disease) to relieve the
underlying coronary artery
blockage. Antiarrhythmic drugs can suppress ventricular
ectopic beats, but they
also may increase the risk of a fatal arrhythmia. Therefore,
they're used very
carefully in selected patients after sophisticated cardiac
studies and risk evaluation.
Ventricular Tachycardia
Ventricular tachycardia is a ventricular rate of at least 120
beats per minute
triggered in the ventricles.
Sustained ventricular tachycardia (ventricular tachycardia
lasting at least 30
seconds) occurs in various heart diseases that damage the
ventricles. Most
commonly, it occurs weeks or months after a heart attack.
Symptoms and Diagnosis
A person with ventricular tachycardia almost always has
palpitations. Sustained
ventricular tachycardia can be dangerous and often requires
emergency treatment
because the ventricles can't fill adequately and pump blood
normally. Blood
pressure tends to fall, and heart failure follows. Sustained
ventricular tachycardia is
also dangerous because it can worsen until it becomes
ventricular fibrillation--a
form of cardiac arrest. Sometimes, ventricular tachycardia
causes few symptoms,
even at rates of up to 200 beats per minute, but it may still
be extremely
dangerous.
The diagnosis of ventricular tachycardia is made with an
electrocardiogram (ECG).
Treatment
Treatment is given for any episode of ventricular tachycardia
that causes
symptoms and for episodes that last more than 30 seconds even
without
symptoms. If episodes cause blood pressure to fall below
normal, cardioversion is
needed immediately. Lidocaine or similar drugs are given
intravenously to suppress
ventricular tachycardia. If episodes of ventricular
tachycardia persist, a doctor may
conduct an electrophysiologic study and try other drugs. The
one that works best
during electrophysiologic testing can be continued to help
prevent recurrences.
Sustained ventricular tachycardia is usually triggered by a
small abnormal area in
the ventricles, and this trigger area can sometimes be
removed surgically. In some
people with ventricular tachycardia that doesn't respond to
drug therapy, a device
called an automatic cardioverter-defibrillator may be
implanted.
Ventricular Fibrillation
Ventricular fibrillation is a potentially fatal,
uncoordinated series of very rapid
ineffective contractions throughout the ventricles caused by
multiple chaotic
electrical impulses.
Ventricular fibrillation is electrically similar to atrial
fibrillation, but it has a much
graver prognosis. In ventricular fibrillation, the ventricles
merely quiver and don't
carry out coordinated contractions. Because no blood is
pumped from the heart,
ventricular fibrillation is a form of cardiac arrest and is
fatal unless treated
immediately.
The causes of ventricular fibrillation are the same as those
of cardiac arrest. The
most common cause is inadequate blood flow to the heart
muscle because of
coronary artery disease or a heart attack. Other causes are
shock and very low
levels of potassium in the blood (hypokalemia).
Symptoms and Diagnosis
Ventricular fibrillation leads to unconsciousness in seconds.
If untreated, the
person usually has convulsions and develops irreversible
brain damage after about
5 minutes because oxygen is no longer reaching the brain.
Death soon follows.
A doctor considers a diagnosis of ventricular fibrillation
when a person suddenly
collapses. On examination, no pulse or heartbeat is detected,
and blood pressure
can't be measured. The diagnosis is confirmed by an
electrocardiogram (ECG).
Treatment
Ventricular fibrillation must be treated as an emergency.
Cardiopulmonary
resuscitation (CPR) must be started within a few minutes and
then followed as
soon as possible by cardioversion (an electric shock
delivered to the chest). Drugs
are then given to help maintain the normal heart rhythm.
When ventricular fibrillation occurs within a few hours of a
heart attack and the
person isn't in shock or doesn't have heart failure, prompt
cardioversion has a 95
percent success rate, and the prognosis is good. Shock and
heart failure are signs
of major damage to the ventricles; if they're present, even
prompt cardioversion
has only a 30 percent success rate, and 70 percent of
resuscitated survivors die.
Heart Block
Heart block is a delay in electrical conduction through the
atrioventricular node,
which lies between the atria and the ventricles.
Heart block is graded as first-degree, second-degree, or
third-degree, depending
on whether conduction to the ventricles is slightly delayed,
intermittently delayed,
or completely blocked.
In first-degree heart block, every impulse from the atria
reaches the ventricles,
but it's slowed for a fraction of a second as it moves
through the atrioventricular
node. This conduction problem produces no symptoms.
First-degree heart block is
common among well-trained athletes, teenagers, young adults,
and people with a
highly active vagus nerve. However, the condition also occurs
in rheumatic fever
and sarcoid heart disease and may be caused by drugs. The
diagnosis is made by
observing the conduction delay on an electrocardiogram (ECG).
In second-degree heart block, not every impulse from the
atria reaches the
ventricles. This block results in the heart beating slowly or
irregularly. Some forms
of second-degree block progress to third-degree heart block.
In third-degree heart block, impulses from the atria to the
ventricles are
completely blocked, and the heart rate and rhythm are paced
from either the
atrioventricular node or the ventricles themselves. Without
stimulation from the
heart's normal pacemaker (sinoatrial node), the ventricles
beat very slowly, less
than 50 beats per minute. Third-degree heart block is a
serious arrhythmia that
can affect the heart's pumping ability. Fainting (syncope),
dizziness, and sudden
heart failure are common. When the ventricles beat faster
than 40 beats per
minute, symptoms are less severe but include tiredness, low
blood pressure when
the person stands up, and shortness of breath. The
atrioventricular node and the
ventricles are not only slow as substitute pacemakers but
they're frequently
irregular and unreliable.
Treatment
First-degree block requires no treatment even when it's
caused by heart disease.
Some cases of second-degree block may require an artificial
pacemaker.
Third-degree block almost always requires an artificial
pacemaker. A temporary
pacemaker may be used in an emergency until a permanent one
can be implanted.
Most people need an artificial pacemaker for the rest of
their lives, although normal
rhythms sometimes return after recovery from an underlying
cause, such as a
heart attack.
Sick Sinus Syndrome
Sick sinus syndrome includes a wide variety of abnormalities
of natural pacemaker
function.
This syndrome may result in a persistently slow heartbeat
(sinus bradycardia) or a
complete blockage between the pacemaker and the atria (sinus
arrest) in which the
impulse from the pacemaker fails to make the atria contract.
When this happens,
an escape pacemaker lower in the atrium or even in the
ventricle usually takes over.
An important subtype of the sick sinus syndrome is the
bradycardia-tachycardia
syndrome, in which rapid atrial rhythms, including atrial
fibrillation or flutter,
alternate with prolonged periods of slow heart rhythms. All
types of sick sinus
syndrome are particularly common in the elderly.
Symptoms and Diagnosi