Arrhythmias (Palpitations)

ORIGIN OF THE HEARTBEAT
Arrhythmia is the term used for an irregularity or rapidity
of the heartbeat or an abnormal heart rhythm. The patient
experiences the sensation as stronger, more forceful, or
rapid heartbeats, or skipping of beats; this sensation is
commonly called palpitations. The sinus node, a very
small group of specialized cells, is located in the upper
right corner of the heart (see Fig. 1). The node is about
303 mm thick. Through its genetic code and the influx
and efflux of sodium and potassium into its cells, this
natural pacemaker spontaneously fires infinitesimal electrical
discharges that are conducted through electric cablelike
bundles to the atria and ventricles causing the heart
muscle to contract about 70 times a minute. The sinoatrial
(SA) node’s spontaneous depolarization and repolarization
provides a unique and miraculous automatic pacemaker
stimulus that activates the atria and atrioventricular (AV)
node, which conducts the activation current down the
bundle branches to activate the ventricular muscle mass.
Cardiac cells outside the SA node normally do not exhibit
spontaneous depolarization. The SA discharge rate, usually
50–100 beats per minute, is under autonomic, neural,
chemical, and hormonal influence. The rate slows or gets
faster depending on the needs of the body. The sinus node
is like a powerful generator and has complete control of
the heart rate.

Cells outside the sinus node pacemaker, for example,
ventricular muscle cells, possess pacemaker activity that
is so weak that the normal electrical discharge from the
sinus node suppresses them. Myocardial cells normally
lack the ability for either spontaneous formation or rapid
conduction of the electrical impulse. For these functions
most cardiac cells are dependent on cardiac pacemaker
cells and the conduction system that consists of nodes,
bundle branches, and a terminal branching network of
specialized conducting tissue — the Purkinje fibers that
ramify the myocardium. The sinus node undergoes spontaneous
depolarization and has no resting phase; myocardial
tissue must be depolarized and have a resting potential. Occasionally, pacemaker
cells outside the SA node may interrupt the normal heartbeat,
causing a premature beat, which is also called an extra
beat.
The electrical conducting system of the heart is vital to
life. Damage to the electrical system can occur when the
coronary arteries are blocked and fail to supply sufficient
blood to the electrical system as may happen after several
heart attacks. The electrical system can also be affected.

II. PALPITATIONS, PREMATURE BEATS, AND IRREGULAR BEATS
A. Definition
The word ‘‘palpitation’’ is used by doctors and by some
patients to describe the heartbeat when it is fast, pounding,
skipping, or irregular.

B. Causes
Premature beats may be due to either heart disease or
extracardiac conditions, but often, they have no definable
cause. Heart diseases that affect the heartbeat include
disturbance of the blood supply to the heart due to
coronary artery disease; diseases of the heart valves, usually
due to prior rheumatic fever; and a common condition
called mitral valve prolapse. Valve problems are easily
excluded by a physician, who can hear murmurs or clicks
when listening with the stethoscope. Echocardiography
(cardiac ultrasound) can clarify the cause. Heart muscle
diseases (cardiomyopathy) are fortunately rare. Alcohol
abuse can also cause cardiomyopathy. Viruses that cause
a flu-like illness can produce microscopic scars in the
heart muscle (myocarditis) that may trigger extra beats.
Myocarditis can be difficult to exclude if the patient is not
seen during the acute phase.

Investigations of extra beats should include blood
tests (to exclude anemia, a low serum potassium, or thyroid
overactivity), chest x-ray, echocardiography, Holter
monitor (24-h ECG recording), and a stress test.
Extracardiac precursors include alcohol, smoking,
stimulants such as caffeine, amphetamines (diet pills),
and nicotinic acid in megavitamins and several drugs.
In susceptible individuals, disturbances of the heartbeat
(arrhythmias) are more common 12–24 h after alcohol
consumption. Other causes include thyroid overactivity
and low oxygen in the blood due to lung diseases.
Premature or extra beats commonly occur in young
individuals with normal hearts and cause no harmful
effects. In the normal heart, they bear no relation to heart
attacks, sudden cardiac death, or heart failure, and they do
not harm the heart.

Drug treatment is not indicated for patients with a
normal heart because the side effects outweigh the benefits.
Some patients, who are terribly bothered by numerous
extra beats in the presence of a normal heart or mitral
valve prolapse, respond to beta-blockers (see the chapter
Beta-Blockers). Five to 15 pauses or premature beats per
minute in a normal heart is of no significance and requires
no drug treatment. Patients may have an extra beat that
occurs after each normal heartbeat and more commonly
after two normal beats. In the majority of individuals with
premature beats, there is no good reason why they should
occur at a particular time of the day or month. Several
studies have utilized the 24-h Holter monitor to show that
more than 66% of normal individuals studied have
ventricular premature beats (VPBs). Unless serious heart
disease is present, all the bumpings, flutterings, thumpings,
and irregular beats can be ignored.

C. Diagnosis
1. Atrial Premature Beats
Premature beats that arise from the atrium are called atrial
premature beats (APBs). An atrial premature P-wave has
a morphology different from that of the sinus P-wave
and is usually followed a QRS complex similar to that of
the normally conducted sinus beat (see Fig. 2). Atrial
premature beats may trigger atrial tachycardia or atrial
fibrillation.
2. Ventricular Premature Beats
Premature beats that arise in the ventricle are called ventricular
premature beats. These are bizarre looking beats
with a wide QRS complex and an ST segment sloping off
in a direction opposite to the abnormal QRS complex (see
Fig. 3). There is no preceding P-wave and the extra beat
is followed by a fully compensatory pause before the
next normal sinus beat occurs. When this happens, the
individual may feel that the heart has stopped for a second.
A VPB following each normal beat (termed ventricular
bigeminy) is a common occurrence in healthy individuals,
but pairs (couplets) or runs of three beats (triplets,
nonsustained ventricular) are not uncommon in those
with heart disorders.

ANTIARRHYTHMIC AGENTS
Figure 11 illustrates how myocardial cells generate an
action potential in phase zero through a fast influx of
sodium ions into cells. This increases the resting potential
and voltage of the cell (depolarization). During phase three
the cell returns to its resting potential with an efflux of
potassium ions. Some antiarrhythmic agents produce their
effects by decreasing the rate at which sodium enters the
myocardial cell during phase zero. Thus, generation of the
action potential of an abnormal impulse is dampened and
does not reach sufficient magnitude to produce abnormal
beats. Quinidine, disopyramide, procainamide, flecainide,
and propafenone decrease the rate at which sodium enters
myocardial cells. Beta-adrenergic blocking agents, lidocaine,
and several antiarrhythmic agents decrease the
rate of automaticity of abnormal rhythms by depressing
phase four of the action potential (as indicated by the
arrow in Fig. 3). Amiodarone and a unique beta-blocker,
sotalol, cause prolongation of the action potential (phase
two) and retard the generation of an abnormal impulse.
Most important, an increase in the absolute refractory
period(phases one and two), protects the heart from
dangerous impulse stimuli. During a 20–30 ms vulnerable
period in phase three a strong electrical stimulus
or ventricular ectopic beat can readily trigger ventricular
tachycardia and ventricular fibrillation.

A. Digoxin (Lanoxin)
Digoxin is used to treat patients with atrial fibrillation
to slow the fast heart rate. This drug may also be used to
prevent recurrent attacks of AVNRT. It is used daily for
a prolonged period to prevent recurrent attacks, but
the success rate may be low for some patients. The important
role of digoxin in slowing the heart rate in patients
with atrial fibrillation is discussed in the chapter Atrial
Fibrillation.

B. Beta-Blockers
Beta-blockers are occasionally used to treat AVNRT.
These drugs can also be used to treat bothersome VPBs
when they are associated with increased secretion of
catecholamines and in individuals with mitral valve
prolapse. These agents have a beneficial effect on
VPBs produced during or following a heart attack. Betablockers
are the only safe antiarrhythmic drugs that have
been proven to prevent sudden cardiac death and heart
attacks.
Several other drugs are used to treat more difficult
and serious heart rhythm disorders. Most of these drugs
have serious side effects, are only 60–80% effective in
controlling the disturbance, and do not prevent death.
Thus, doctors are not keen to treat premature beats unless
they are associated with serious heart disease. In such
patients, when premature beats are numerous with runs of
four or more occurring together for more than 30 seconds,
drugs are usually tried.

C. Sotalol
Sotalol is unique in that it is the only beta-blocker
that has class III antiarrhythmic effects. It is the most
effective beta-blocker available for the treatment of serious
abnormal heart rhythms, particularly the prevention of
ventricular tachycardia. This drug may prevent recurrences
of paroxysmal atrial fibrillation, although this effect is
modest.
Sotalol is hydrophilic and is eliminated by the kidney.
The action of the drug is prolonged, so it is effective when
taken once daily. It is not affected by smoking. The
recommended dosage is 80 mg once or twice daily for
4 weeks, then 160 mg once daily with a maximum dose
of 240 mg daily. The drug must not be used in patients
with a low serum potassium, and it must not be used
concomitantly with drugs that increase the QT interval
because torsades de pointes may be precipitated.

D. Amiodarone
This drug is effective in suppressing life-threatening
abnormal heart rhythms and is approved for treating
recurrent episodes of sustained ventricular tachycardia.
The drug’s major toxicity manifests deposits of granules
in the cornea, fibrosis of the lung in about 5%, and
grayish blue discoloration of the skin with prolonged
use at high doses. Neuropathy and thyroid disturbances
may also occur. Amiodarone must not be used in
combination with verapamil. Interaction may occur
when used concomitantly with quinidine, digoxin,
and oral anticoagulants such as warfarin. The drug
should be avoided in patients with a low serum potassium
and should not be used with agents that prolong the
QT interval because torsades de pointes may be precipitated.
It is also contraindicated in patients with sick sinus
syndrome.

E. Disopyramide
This drug has effects similar to quinidine. It is useful in
the emergency treatment of ventricular tachycardia when
given intravenously. Disopyramide should not be used
in patients with heart failure or poor heart muscle function
because it can precipitate heart failure. It is contraindicated
in individuals with glaucoma, kidney failure, low blood
pressure, and enlargement of the prostate because urinary
retention can be precipitated. The drug must not be used
in combination with verapamil.

F. Lidocaine
This drug is used intravenously in emergency situations
and is effective in suppressing ventricular tachycardia and
serious premature beats.

G. Mexiletine
This drug is more effective than disopyramide. It suppresses
complex abnormal heart rhythms, but it has not
improved survival rate. Mexiletine is contraindicated in
patients with low blood pressure. The dose must be
reduced if kidney failure is present. Side effects include
slowing of the pulse, stomach problems, confusional
states, double vision, and disturbance in walking (ataxia).
The drug is therefore reserved for the treatment of lifethreatening
arrhythmias.

H. Procainamide
Procainamide has similarities to the well-known quinidine.
It is of value when given intravenously in the emergency
management of ventricular tachycardia that is not responsive
to lidocaine. When used orally it has a variable
effect. It is less effective than quinidine or disopyramide
and when used for longer than six months, patients can
develop joint pains and fever (lupus erythematosus).
Although very rare, white blood cells can be damaged
(agranulocytosis) with its use. The drug should not be used
in patients with low blood pressure, severe heart failure,
and myasthenia gravis.

I. Quinidine
The use of quinidine has greatly decreased since the advent
of other antiarrhythmic agents. Quinidine suppresses
premature beats in about 60% of cases, but it is only
partially effective with life-threatening arrhythmias.
Because of rare but serious side effects, the use of the
drug is questionable. Quinidine can precipitate ventricular
fibrillation, which is the most dangerous abnormal heart
rhythm, and cardiac arrest. It does not seem reasonable to
give priority to a drug that may increase the risk of
ventricular fibrillation and death. This agent increases the
level of digoxin in the blood and when used concomitantly,
care is necessary with digoxin and anticoagulants such as
warfarin.

AUTOMATIC IMPLANTABLE CARDIOVERTER DEFIBRILLATOR
When life is severely threatened by the recurrence of
abnormal heart rhythms that have caused cardiac arrest
or recurrent sustained ventricular tachycardia, the automatic
implantable cardioverter defibrillator can play a role
in the health of selected patients. Recent advances in this
area allow a ray of hope. Dr. Saksena in New Jersey has
introduced a nonsurgical technique for implanting the
automatic cardioverter defibrillator. Clinical trials have
shown this to be highly successful.

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