Blood, Heart, and Circulation 441fibrillation. In flutter, the contractions are very rapid (200 to 300
per minute) but are coordinated. In fibrillation, contractions of
different groups of myocardial cells occur at different times, so
that a coordinated pumping action of the chambers is impossible.
Atrial flutter usually degenerates quickly into atrial fibril-
lation, where the disorganized production of impulses occurs
very rapidly (about 600 times per minute) and contraction of
the atria is ineffectual. The AV node doesn’t respond to all of
those impulses, but enough impulses still get through to stimu-
late the ventricles to beat at a rapid rate (up to 150–180 beats
per minute). Since the ventricles fill to about 80% of their end-
diastolic volume before even normal atrial contraction, atrial
fibrillation only reduces the cardiac output by about 15%. Peo-
ple with atrial fibrillation can live for many years, although this
condition is associated with increased mortality due to stroke
and heart failure. It has been estimated that 20% to 25% of all
strokes may result from thrombi promoted by atrial fibrillation.
Atrial fibrillation is the most common heart arrhythmia,
and is usually treated with antithrombotic and antiarrhythmia
drugs. Another common treatment is catheter ablation, which
destroys atrial tissue (by heating the tissue around the pulmo-
nary veins) that may contribute to the fibrillation.
By contrast, people with ventricular fibrillation ( fig. 13.34 )
can live for only a few minutes unless this is extended by car-
diopulmonary resuscitation (CPR) techniques or the fibrillation
is ended by electrical defibrillation (discussed shortly). Death
is caused by the inability of the fibrillating ventricles to pump
blood and thus deliver needed oxygen to the heart and brain.
Fibrillation is caused by a continuous recycling of elec-
trical waves, known as circus rhythms, through the myocar-
dium. The recycling of action potentials is normally prevented
by the entire myocardium entering a refractory period as a sin-
gle unit, owing to the rapid transmission of the action potential
among the myocardial cells by their gap junctions and to the
long duration of the action potential provided by its plateau
phase (see fig. 13.21 ). However, if some cells emerge from
their refractory periods before others, an action potential can
be continuously regenerated and conducted. Recycling of elec-
trical waves along continuously changing pathways produces
uncoordinated contraction and an impotent pumping action.
Circus rhythms are thus produced whenever impulses can
be conducted without interruption by nonrefractory tissue.
This may occur when the conduction pathway is longer than
normal, as in a dilated heart. It can also be produced by an
electric shock delivered at the middle of the T wave, when dif-
ferent myocardial cells are in different stages of recovery from
their refractory period. Finally, circus rhythms and fibrillation
may be produced by damage to the myocardium, which slows
the normal rate of impulse conduction.
Sudden death from cardiac arrhythmia usually progresses
from ventricular tachycardia through ventricular fibrilla-
tion, culminating in asystole (the cessation of beating, with a
straight-line ECG). Sudden death from cardiac arrhythmia is
commonly a result of acute myocardial ischemia (insufficient
blood flow to the heart muscle), most often due to atheroscle-
rosis of the coronary arteries.
Fibrillation can sometimes be stopped by a strong electric
shock delivered to the chest. This procedure is called electrical
defibrillation. The electric shock depolarizes all of the myo-
cardial cells at the same time, causing them all to enter a refrac-
tory state. Conduction of circus rhythms thus stops, and the SA
node can begin to stimulate contraction in a normal fashion.
This does not correct the initial problem that caused circus
rhythms and fibrillation, but it does keep the person alive long
enough to take other corrective measures.
A device known as an implantable converter-defibrillator
is now available for high-risk patients. This device consists of
a unit that is implanted into a subcutaneous pocket in the pec-
toral region, with a lead containing electrodes and a shocking
coil that is threaded into the heart (usually the right ventricle).
Sensors can detect when ventricular fibrillation occurs, and can
distinguish between supraventricular and ventricular tachycar-
dia ( fig. 13.34 ). The coil can deliver defibrillating shocks if
ventricular fibrillation is detected.Clinical Investigation CLUES
The physician told Jessica that she had atrial fibrillation.- What is atrial fibrillation, and how does it appear on
an ECG? - What is the major danger of atrial fibrillation, and
how did Jessica’s physician address this?
AV Node Block
The time interval between the beginning of atrial depolarization—
indicated by the P wave—and the beginning of ventricular depo-
larization (as shown by the Q part of the QRS complex) is called
the P-R interval (see fig. 13.22 ). In the normal heart, this time
interval is 0.12 to 0.20 second in duration. Damage to the AV
node causes slowing of impulse conduction and is reflected by
changes in the P-R interval. This condition is known as AV node
block ( fig. 13.35 ).CLINICAL APPLICATION
An artificial pacemaker, about the size of a locket, can
be implanted under the skin below the clavicle. This is a
battery-powered device with electrodes that are threaded
into the heart through a vein using fluoroscopy for guidance,
and used to correct for such arrhythmias as a blockage in
conduction of the impulse in the AV node or bundle of His.
There are many different types of implantable pacemakers;
some stimulate just one chamber, and some stimulate both
an atrium and a ventricle by delivering a low-voltage shock
causing depolarization and contraction. Most sense if a
heartbeat is delayed and stimulate the heart on demand to
maintain a good cardiac rate, and some can even sense if a
person is exercising and adjust the cardiac rate accordingly.