Quick and decisive management is of paramount importance in the treatment
of cardiac rhythm disturbances in the ED. Cardiac arrhythmias are
common and can present as dizziness, palpitations, syncope, or sudden
death. Arrhythmias can be caused by a primary cardiac event, such
as ischemia, by a genetic abnormality of the conduction system,
or be the result of a vast number of pathologic processes, including
sepsis, metabolic derangements, toxicologic, or traumatic.
Through understanding of cardiac anatomy and electrophysiology (EP), the
ECG, and the patient’s clinical status, decisions can be
made quickly and aggressively to stabilize the patient and uncover
the underlying diagnosis to provide definitive management.
A. Cardiac conduction system. B. Vasculature. (Reproduced
with permission from Fauci AS, Kasper DL, Braunwald E, et al: Harrison’s
Principles of Internal Medicine, 17th ed. © 2008,
McGraw-Hill, New York.)
The heart consists of three types of specialized tissue: (1) pacemaker
cells that undergo spontaneous depolarization and can initiate an
electric impulse (this property is called automaticity);
(2) Purkinje cells that conduct electrical waves more rapidly than
other cardiac cells; and (3) contractile cells, which contract when
The sinus [sinoatrial (SA)] node is the dominant
cardiac pacemaker unless disease or drugs depress its activity.
The SA node is near the junction of the superior vena cava and right
atrium. Blood supply is from the sinus node artery, which arises
from the right coronary artery in about 55% of individuals
or from the left circumflex artery in the other 45%. Sympathetic and parasympathetic
nerves are the primary controls of the heart rate and innervate
the SA node. The normal sinus discharge rate is 60 to 100 beats/min.
Specialized atrial conduction tracts (anterior, middle, and posterior
internodal tracts) propagate the electric impulse through the atria
from the SA node and the atrioventricular (AV) node, thus activating atrial
The atria and ventricles are insulated electrically from each
other by the fibrous connective tissue of the AV ring (annulus fibrosus).
Normally, electrical impulses from the atria can reach the ventricles
only by passing through the AV node and infranodal conducting system.
The AV node is under the surface of the right atrial endocardium.
The AV node receives its blood supply from the right coronary artery
in 90% of individuals or from the left circumflex artery
in the other 10%. This accounts for the common occurrence
of AV conduction disturbances with acute inferior myocardial infarctions
(MIs). The AV node is innervated by sympathetic and parasympathetic
fibers. It has two important electrophysiologic characteristics:
a slow conduction velocity and a long refractory period. The slow
conduction velocity through the AV node allows time for atrial contraction
to give an extra 10% ventricular filling. This “atrial
kick” is most important for patients with ventricular failure. The
long refractory period of the AV node protects the ventricles from excessively
rapid stimulation; very rapid heart rates decrease the diastolic filling
period and thereby reduce cardiac output. Cells near the AV node have automaticity and
will escape from the control of the SA node if its rate becomes
too slow, normally slower than 60 beats/min.
Electrical impulses leave the inferior pole of the AV node along
the bundle of His, which travels downward along the posterior margin
of the membranous portion of the intraventricular septum to reach
the top of the muscular portion. The bundle of His consists of Purkinje
cells, which are the most rapidly conducting cells of the heart.
The common bundle divides into the right and left bundle branches
(RBB and LBB, respectively). The RBB is a compact group of fibers
that travels down to the apex of the right ventricle before separating
into smaller branches. The LBB divides into two distinct pathways,
the left anterior superior fascicle (LASF) and the left posterior
inferior fascicle (LPIF).
The blood supply to the RBB and LASF is from the same sources:
about half the time from the left anterior descending artery (LAD)
and half the time from both the AV nodal artery and LAD. The LPIF
is supplied about half the time from the AV nodal artery and the
other half by the AV nodal artery and LAD. Infarction in the region
supplied by the LAD can affect the RBB and LASF but very rarely
A basic understanding of the EP of cardiac conduction is helpful
in understanding the derangements that occur to cause cardiac arrhythmias.
The three major cations involved in cardiac conduction are sodium [Na+],
potassium [K+], and calcium [Ca2+].
Conduction propagates through the heart based on the difference
in both voltage and concentration between the intracellular and
extracellular matrix. There
is a negative intracellular potential at baseline, creating a driving
force for positive ions to enter the cell. There is a greater concentration
of Na+ and Ca2+ ions outside
the cell than inside, creating a second stoichiometric force for
movement of Na+ and Ca2+ inward.
Potassium is more abundant intracellularly and has a stoichiometric
force to move outward. Cellular membrane ion pumps, specifically
the Na+/ K+ATP pump,
keep these forces at bay at rest and restore cells to baseline after
depolarization, using adenosine triphosphate to do so. Ions move in
and out of the cell by specific ion channels, using these forces
of voltage and concentration (Figure 22-1.1).
Time course of membrane potential and ion permeability changes that occur during "fast response" (left) and "slow response" (right) action potentials.
(Reproduced with permission from Mohrman DE, Heller LJ: ...
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