Aberrancy
Changed depolarization pattern of the ventricles with the result of an
abnormal wide QRS-complex, usually frequency dependent.
Accelerated junctional rhythm
This is a supraventricular rhythm resulting from a focus in or near the
atrioventricular junction. The rate ranges from 60 to 100 beats per minute.
This is an abnormal rhythm that can result from digitalis toxicity,
particularly when it occurs in combination with atrial fibrillation. It can also result
from physiologic stress and other causes of increased sympathetic nervous system tone.
Accelerated rhythm
Three or more depolarization following each other with a frequency smaller
than 100 bpm, but higher than the inherent frequency of the specific origin.
Accelerated ventricular rhythm
This is diagnosed when only ventricular escape complexes are present, and they
occur at 60 to 100 beats per minute. This rhythm is usually seen in the setting of acute
myocardial infarction. If the patient is in sinus rhythm, the rate of this rhythm tends to
be about the same as the rate of the sinus rhythm. In this case, the two rhythms will
speed up and slow down so that they alternately capture the ventricle, with characteristic
periods of fusion QRS complexes during the changes in rate.
This rhythm is usually benign. Because it occurs in the setting of acute myocardial
infarction, patients who exhibit it are already in an intensive care unit where any
malignant sequel can be treated readily.
Action potential
The cycle of repolarization of the myocard cell (phase 0, 1, 2 and 3).
Adams-Stokes attack
Unconsciousness as a result of a to fast or to slow rhythm.
Angina pectoris
Pain on the chest as a result of a shortage of oxygen in the myocard.
Anterograde
From the atrium towards the direction of the ventricle.
Aneurysma cordis
Dilatation and expansion (forming of an aneurysm) of a part of the ventricular
wall usually the left ventricle.
Arrest
Stagnation in the electrical activation of the heart or part of the heart
(atria or ventricles).
Arrhythmia
Every rhythm in which the stimulus does not originate from the SA-node
(ectopic arrhythmia), or in which non-physiological deviation in the frequency or
regularity of the sinus rhythm appear.
Asystole
This is diagnosed when no ventricular escape complexes are present. This is an agonal
rhythm that is not consistent with life. To confirm the diagnosis, you should check
another EKG lead, because fine (low amplitude) ventricular fibrillation can appear as a
flat line in one lead, but should be treated with immediate countershock. If you see these
rhythms, you should initiate Cardiopulmonary Resuscitation immediately.
Atrial couplet
This is a pair of atrial premature complexes in a row.
While it is less common in normal subjects than are atrial premature complexes, it can
still be benign. The appearance of atrial couplets should also raise the index of
suspicion for susceptibility to atrial fibrillation, atrial flutter, and supraventricular
tachycardia.
Atrial escape complex
This is a P wave that occurs later than would be expected from the sinus rate. Like all
escape complexes, it can occur only when the normal cardiac pacemaker does not function,
as is sinus arrest.
Atrial
fibrillation
This is a supraventricular rhythm resulting from multiple reentrant circuits
within either the right or left atria, or both. It is characterized by an irregularly
irregular ventricular rate that is usually rapid in young patients, but may be normal or
even bradycardic in elderly patients or patients taking medications that can cause
atrioventricular nodal blockade.
It can occur alone, but is usually associated with hypertensive cardiomyopathy, COPD, or
congestive cardiomyopathy. The new onset of either rhythm is seen in about 5% of cases of
acute myocardial infarction. The clinician may also want to check for congestive heart
failure, since worsening CHF can present with these rhythms.
Atrial
flutter
his is a supraventricular rhythm resulting from a reentrant circuit that lies
within the right atrium. It is characterized by an atrial rate of 250 to 350 beats per
minute, and a ventricular response that is usually about 75, 150, or 300 beats per minute.
Flutter waves are best found in EKG leads II, III, aVF, and V1. Sometimes they are located
at the onset or offset of the QRS complex, and are best found by comparison with the QRS
morphology in a 12-lead EKG recording obtained during sinus rhythm. Even if flutter waves
are not found, this rhythm should be suspected when the ventricular rate ranges from 140
to 160 beats per minute and there is no clear evidence of atrial activity.
It can occur alone, but is usually associated with hypertensive cardiomyopathy, COPD, or
congestive cardiomyopathy. The new onset of either rhythm is seen in about 5% of cases of
acute myocardial infarction. The clinician may also want to check for congestive heart
failure, since worsening CHF can present with these rhythms.
For emergency treatment of this rhythm, when the patient has hypotension, angina, or acute
congestive heart failure, synchronized cardioversion with appropriate
anesthesia is indicated. For short-term pharmacological control of this rhythm, drugs that
decrease AV nodal conduction (beta blockers, calcium blockers, and digoxin) may be
considered. For long-term treatment of this rhythm, consultation with a Cardiologist is
recommended.
Atrial
multiform couplet
This is a pair of atrial premature complexes, with differing P wave morphologies,
in a row.
This is unusual in normal subjects, but is itself benign. The appearance of multiform
atrial couplets, especially in patients with pulmonary disease, should raise the index of
suspicion for susceptibility to multifocal atrial tachycardia, atrial fibrillation, and
atrial flutter.
Atrial premature complex
This is a P wave that occurs earlier than would be expected from the sinus rate,
and that usually has an abnormal morphology. It can fail to conduct through the
atrioventricular node, in which case it will not result in a QRS complex. The commonest
causes of pauses are non-conducted atrial premature complexes. When it does conduct
through the atrioventricular node, it can be conducted aberrantly if it traverses the
bundle branches of the His-Purkinje system while one or both is in its relatively
refractory period. Aberrantly conducted QRS complexes are wider than normal, and have the
morphology of bundle branch block pattern.
Atrial premature complexes are a normal finding in adults of all ages. The frequency can
be increased during stress, with ingestion of caffeine, and with sympathomimetic
drugs
such as some over-the-counter cold remedies.
Atrial tachycardia
This is a supraventricular rhythm resulting from either an atrial automatic focus
or a reentrant circuit that lies entirely within the atrium. It is characterized by a rate
more than 100 beats per minute, and a P wave morphology that is usually different from
that of the sinus P wave. It can be intermittent or incessant (present more than 50% of
the time). When it is incessant, it can cause symptomatic dilated cardiomyopathy that is
reversible with control of the tachycardia.
This is an abnormal rhythm that can result from digitalis toxicity,
particularly when it occurs in combination with Atrioventricular nodal block, second
degree, Mobitz type I (Wenckebach).
For emergency treatment of this rhythm, when the patient has hypotension, angina, or acute
congestive heart failure, synchronized cardioversion with appropriate
anesthesia is indicated. For short-term pharmacological control of this rhythm, drugs that
decrease AV nodal conduction (beta blockers, calcium blockers, and diltiazem) may be
considered. For long-term treatment of this rhythm, consultation with a Cardiac
Electrophysiologist is recommended.
Atrioventricular block
Conduction disorder between atrium and ventricle.
Atrioventricular nodal block, 2:1
This rhythm is diagnosed when the entire rhythm strip shows only conduction of
every other P wave to the ventricle. Because the record does not show two consecutive P
waves that conduct to the ventricle, it is not possible to measure prolongation of the PR
interval, so that it is not possible to distinguish between Mobitz type I
and the dangerous Mobitz type II Second degree Atrioventricular nodal
block. By convention, recordings obtained at other recent times are used to make this
distinction. This degree of block is usually considered pathological when the atrial
rate
is less than 150 beats per minute or so, because the normal AV node should be able to
conduct 1:1 from the atrium to the ventricle at this rate.
Atrioventricular dissociation
This term refers to a group of three categories of rhythms in which the
atrial and ventricular rhythms are unrelated to each other. The three categories are:
Third degree (complete) heart block.
sinus arrest or sinus bradycardia with junctional rhythm or Idioventricular rhythm.
ventricular tachycardia.
Atrioventricular nodal block, first degree
This refers to an excessively long PR interval only. All P waves are conducted
through the atrioventricular node to the ventricle. By itself, it is a benign condition,
but may result from disease in the atrioventricular node, high vagal tone, or medication
that reduces conduction through the atrioventricular node.
Atrioventricular nodal block, second degree, Mobitz Type
I (Wenckebach)
This refers to a gradual prolongation of the PR interval, with occasional failure to
conduct a P wave through the atrioventricular node to the ventricle. By itself, it is a
benign condition, but may result from disease in the atrioventricular node, high vagal
tone, or medication that reduces conduction through the atrioventricular node. It is
commonly seen in athletic young patients, particularly during sleep.
This is an abnormal rhythm that can result from digitalis toxicity,
particularly when it occurs in combination with Atrial tachycardia.
It is distinguished from Second degree Atrioventricular nodal block, Mobitz type II by the
fact that the PR interval of the P wave that follows the non-conducted P wave is at least
10 msec shorter than the PR interval of the P wave that precedes the non-conducted P wave.
Typically, the QRS complex is unchanged from the patient's normal QRS morphology. By
contrast, the PR interval does not change in Mobitz type II block. Mobitz type II block is
dangerous because it can progress to complete heart block and death without warning.
Atrioventricular nodal block, second degree, Mobitz type
II
This refers to occasional failure to conduct a P wave through the
atrioventricular node to the ventricle without a change in the PR interval after the
nonconducted P wave compared with before the nonconducted P wave. This is a dangerous
condition because it can progress to complete heart block and death without warning.
Immediate consultation with a Cardiologist for placement of a temporary pacemaker is
advisable. Placement of an external pacemaker may be lifesaving if a temporary pacemaker
cannot be placed immediately.
This condition, while dangerous, is very unusual. The QRS complex is usually wide, due to
extensive disease of the His-Purkinje system, although a narrow QRS complex does not
exclude the diagnosis. The clinician should measure the change in PR interval carefully,
as described for Second degree Atrioventricular nodal block, Mobitz type I.
Atrioventricular nodal reentrant tachycardia
This is a reentrant supraventricular rhythm whose circuit is located in the
region of the atrioventricular node. It is characterized by a QRS morphology that is
normal for the patient. P waves may or may not be seen, but they follow closely after the
QRS if they are seen.
Only about 60% of narrow-complex tachycardias have this mechanism. It is important to note
that 20% of narrow-complex tachycardias are atrioventricular reentrant tachycardias, which
use a concealed accessory pathway for retrograde conduction.
The clinical significance of this rhythm depends on the rate. It stops abruptly with
effective treatment. The usual initial treatments are the Valsalva maneuver, then
intravenous adenosine. If these are unsuccessful, one can try medication that reduces
conduction through the atrioventricular node. Consultation with a Cardiac
Electrophysiologist is recommended for follow-up because this rhythm can now be cured by
catheter-mediated radiofrequency ablation.
Atrioventricular reentrant tachycardia (AVRT)
This is a reentrant supraventricular rhythm whose circuit includes both the
atrium and the ventricle, and that uses an accessory atrioventricular pathway for at least
one limb of the circuit. "Orthodromic" AVRT, which is the most common form,
proceeds antegrade (from atrium to ventricle) over the AV node, and retrograde over an
accessory pathway. "Antedromic" AVRT proceeds in the reverse direction, and has
is a wide QRS tachycardia except when the accessory pathway is located in the right
anteroseptal location very close to the His bundle. When multiple pathways are present, it
is also possible for the circuit to use two pathways as a circuit.
P waves may or may not be seen, but they usually do not follow closely after the
QRS if they are seen.
The clinical significance of this rhythm depends on the rate. It stops abruptly with
effective treatment. The usual initial treatments are the Valsalva maneuver, then
intravenous adenosine. If these are unsuccessful, one can try medication that reduces
conduction through the atrioventricular node, except that verapamil and digitalis
SHOULD NOT BE GIVEN. Consultation with a Cardiac Electrophysiologist is
recommended for follow-up because this rhythm can now be cured by catheter-mediated
radiofrequency ablation.
AV-junctional rhythm
Nodal rhythm originating in the AV-junctional area.
AV-dissociation
Atria and ventricles are independent depolarized of each other. If a
AV-dissociation is caused by a total AV-block it is preferably called a total AV-block.
AV-node
Part of the AV-junction
Bifascicular block
The conduction in the right bundle branch and in one of the left fascicles is
disturbed, or the anterior and posterior fascicle of the left bundle is blocked (=LBBB).
Biphasic wave
A wave on the EKG of which one part is negative and the other part positive.
Bifide wave
A wave on the EKG with a 'notch' (usually a notch in a P wave).
Bigeminy
An abnormal but usually harmless rhythm characterized by occurrence of one
ventricular premature complex (VPC) after each normal QRS complex. This rhythm usually
does not progress to dangerous forms of fast ventricular rhythms. Note that in this
rhythm, two PVC's never occur one right after the other.
Bipolar lead
Registration of the potential difference between two electrodes.
Bradycardia
Heart frequency of less then 60 bpm.
Three or more depolarization's following each other from the same origin with a frequency
which lay under the inherent frequency of the specific origin.
Bundle branch block
This term refers to the QRS morphology seen when either the right bundle
branch or the left bundle branch fails to conduct from the His bundle to the ipsilateral
ventricle. Right bundle branch block is characterized by an "M" pattern in V1
and wide S waves in the lateral leads (I, V6). Complete left bundle branch block is
characterized by negative forces (QS or rS) in V1 and positive forces (monophasic R wave
with no Q wave) in V6. Incomplete left bundle branch block can manifest as left anterior
hemiblock or left posterior hemiblock.
Cardiomyopathy
A large number of disorders with anatomical and functional heart muscle
diseases, which are not caused by coronary sclerosis, hypertension, valve disorders or
congenital malformations of the heart.
Cardioversion
Synchronized electro-shock.
Central terminal
Reference point with constant potential which approaches zero.
Compensatory pause
Pause after a premature complex in which the distance between the premature
complex and the following complex is more then twice the normal distance of the 'normal'
rhythm.
Cor pulmonale
Hypertrophy or overloading of the right ventricle as a result of a
disturbance, anatomic and/or functional, in the lung.
Decompensatio cordis
Heart insufficiency.
Defibrillation
Short and powerful electric impulse through the thorax and heart to end a
live threatening tachycardia.
Depression
The lowering of the ST-segment under the iso-electrical line.
Diastole
Phase of ventricular relaxation
Digitalis toxicity is suggested by a regular ventricular response
(Accelerated junctional rhythm) in combination with atrial fibrillation.
In the presence of an accessory atrioventricular pathway, atrial fibrillation can manifest
as a rapid, irregularly irregular wide complex tachycardia that can resemble ventricular
tachycardia closely. It should be suspected particularly in young patients with very rapid
tachycardia that is well tolerated hemodynamically. Close examination of the EKG
will
reveal irregularly irregular RR intervals. In this case:
It is important to obtain a 12-lead EKG before cardioversion because the location of
the pathway, and therefore the risks of a subsequent curative catheter-mediated
radiofrequency ablation procedure, can be estimated fairly accurately from the 12-lead
EKG.
DO NOT give digitalis or verapamil to try to slow ventricular response if an
accessory pathway is suspected. These drugs can accelerate conduction over
accessory pathways, resulting in even more rapid ventricular activation which can, in
turn, induce ventricular fibrillation.
There are four issues related to care of patients with this rhythm:
control of the rate of the ventricular response,
conversion of the atrial rhythm to sinus rhythm,
maintenance of sinus rhythm following conversion, and
prevention of embolic stroke from thrombi that form in the fibrillating left atrium.
Consultation with an Internist or Cardiologist is recommended for advice on these issues..
Doublet
Two premature beats following each other.
Ectopic complex
Complex which originates outside the sinus node.
Electrical heart axis
The direction of the electrical depolarization obtained from the sum of all
different vectors in the frontal plane.
Electrocardiogram
EKG, registering the electrical potentials which occur during a heart cycle
on paper.
Elevation
The rise of the ST-segment above the iso-electrical line.
Endocard
The interior wall of the heart.
Epicard
The exterior wall of the heart.
Escape interval
The interval between the first escape beat and the preceding complex of the
normal rhythm.
Escape rhythm
Rhythm of at least three ectopic complexes (escape beats). The length of the
cycle of the escape rhythm correspond with the origin of the stimulus (inherent
frequency): SA-node 50-60 bpm; Atria and AV-junction 40-60 bpm; ventricles 30-40 bpm.
Fasciculus
Fascicle, the left bundle of His divides in two fascicles, an anterior and a
posterior fascicle.
Fibrillation
Irregular, unorganized electrical activity of the atrium (atrium
fibrillation) or ventricle (ventricle fibrillation), without any mechanical activity (no
circulation of blood) of respectively the atrium or ventricle.
Fibrosis
Uncontrolled growth of connective tissue.
Flutter
Fast, regular electrical activity of the atrium (atrium flutter) or ventricle
(ventricle flutter) with a frequency up to 300 bpm.
Frequency
The number of beats per minute.
Frontal plane leads
The frontal plane leads are the leads I, II, III, aVR, aVL and aVF.
(empty)
Hidden Atrial Activation
Activation of the atrium by the sinus node can be inferred from surrounding sinus
P waves. For example, if the P wave following a ventricular premature complex occurs at
the time that would have been expected had the premature complex not occurred, then in can
be inferred that the atrium was not activated retrograde by the premature complex and that
a hidden, or obscured, P wave did occur. Such an inference can be confirmed during
invasive electrophysiologic study.
His, bundle of
Fast conducting bundle which runs from the AV-node to the cells of the
ventricles.
Hypertrophy
Thickening of the muscle wall, increased muscle mass.
Idioventricular
This is diagnosed when only ventricular escape complexes are present, and
they occur at 20 to 40 beats per minute. This rhythm is barely consistent with life. If
you see this, you should consider initiating Cardiopulmonary Resuscitation immediately,
and should move the patient to an intensive care unit as soon as possible.
DO NOT give lidocaine or any other antiarrhythmic medication for this rhythm. You
could cause asystole and death by inhibiting the only spontaneous rhythm the patient's
heart is able to generate.
Infarction
Necrotic (dead) area of the heart muscle.
Interval
A specific distance on the EKG.
Ischemia
Shortage of oxygen in a tissue, caused by insufficient blood flow towards
that tissue.
James, bundle of
Accessory bundle of conducting tissue between the atrium and the bundle of
His.
Junctional escape complex
This is a QRS with normal morphology for the patient that is not preceded by a P
wave and occurs later than would be expected from the sinus rate. Like all escape
complexes, it can occur only when the normal cardiac pacemaker does not function, as is
sinus arrest.
Junctional rhythm
This is a slow rhythm, with rates ranging from 40 to 60 beats per minute,
with QRS complexes that have the patient's normal morphology. Usually, no P waves are
seen. When P waves are present, they follow closely after the QRS complexes.
This rhythm results from the backup pacemaker capability of the atrioventricular node
during sinus arrest.
Junctional tachycardia
This is a supraventricular rhythm resulting from a focus in or near the
atrioventricular junction. The rate is greater than or equal to 100 beats per minute. See
also Accelerated junctional rhythm.
This rhythm usually results from a primary arrhythmia rather than as a response to
physiologic stimulation. The electrocardiogram usually cannot distinguish this rhythm from
the more common types of Supraventricular tachycardia, for which different treatments may
be appropriate. Consultation with a Cardiac Electrophysiologist is recommended for further
evaluation.
Junction point
J-point, point where the ST-segment begins, immediate behind the QRS-complex.
Junctional premature complex
This is a QRS complex that occurs earlier than would be expected from the sinus
rate, and that usually has a normal morphology for the patient. It can fail to conduct
retrograde through the atrioventricular node, in which case it results in a compensatory
pause. That is, the next P wave occurs at the same time as would be expected had the VPC
not occurred. More usually, it does conduct through the atrioventricular node, so that the
following P wave may occur either sooner or later than would be expected.
Junctional premature complexes are relatively uncommon. They can be seen with increased
frequency during stress, with ingestion of caffeine, and with sympathomimetic drugs such
as some over-the-counter cold remedies. They can also be misdiagnosed when the P wave of
an atrial premature complex is obscured by the preceding T wave.
Junctional premature couplet
See junctional premature complex. This is an unusual rhythm, and most likely
represents two cycles of one of the supraventricular tachycardias.
Kent, bundle of
Accessory bundle of conducting tissue between the atrium and the ventricle,
sometimes between the right atrium and right ventricle, sometimes between the left atrium
and the left ventricle.
Lead
Electrode for registering the electrical potentials.
Left anterior fascicular block
Interrupted conduction through the front part of the left bundle.
Left bundle branch block
Interrupted conduction of the left fibers behind the division of the bundle
of His.
Left posterior fascicular block
Interrupted conduction through the back part of the left bundle.
Mahaim, bundle of
Accessory bundle of conducting tissue between the bundle of His and the left
ventricle.
Membrane potential
Potential difference across the cell membrane.
Mobitz-type II
A type of second grade AV-block (Wenckebach).
Multifocal
Impulses originating from more then one focus.
Multifocal atrial tachycardia
This is a supraventricular rhythm resulting from multiple ectopic foci in the
atria. It is characterized by three or more P wave morphologies and a rate greater than or
equal to 100 beats per minute. It is seen most frequently in patients with severe
pulmonary disease. The rapid ventricular rate can be symptomatic (hypotension, angina,
congestive heart failure). Treatment includes improvement of the concomitant pulmonary
disease, and consideration of administration of verapamil. Digoxin is not effective in
treatment of this rhythm. Consultation with an Internist, Pulmonologist or Cardiologist is
recommended for further advice.
Nodal rhythm
Rhythm originating in the AV-junctional area.
Notch
An irregularity in the line of the QRS-complex.
(empty)
Parasystole
The rhythm that results from intermittent capture of the ventricle by a
ventricular focus that has entrance block. That is, it is not depolarized when the
remainder of the ventricle is activated. The rhythm is characterized by premature
ventricular complexes with variable coupling intervals (intervals from the preceding
normal QRS complex to the premature complex) and with constant intervals between the
premature complexes. Detection of the latter constancy usually requires finding the least
common denominator of the intervals between premature complexes, because of the
intermittence of ventricular capture by the focus.
This rhythm is rare. It is usually considered benign, although any premature ventricular
activation can induce malignant ventricular rhythms in the ischemic myocardium or in the
presence of a suitable myocardial substrate.
Paroxysmal
Suddenly occurring.
Pericarditis
Inflammation of the pericardia.
Precordial leads
Lead place on the chest.
Pre-excitation syndrome
Syndrome of Wolff-Parkinson-White, premature discharge of a part of the right
or left ventricle caused by an accessory bundle (bundle of Kent).
Primary Ventricular standstill
This is diagnosed when only ventricular escape complexes are present, and they
occur very slowly. This is an agonal rhythm that is not consistent with life.
"Primary" means that the condition arose on its own and is the immediate source
of difficulty. If you see this, you should initiate Cardiopulmonary Resuscitation
immediately.
Prinzmetal, syndrome of
Type of angina pectoris, occurring in rest. Is caused by a spasm of the
proximal part of the coronary artery.
Purkinje-fibbers
Network of fibers which connects the bundle branches with the myocard cells
in the ventricles.
P-wave
The depolarization of both atria.
QRS complex
The depolarization of both ventricles.
Quadrigeminy
An abnormal but usually harmless rhythm characterized by occurrence of one
ventricular premature complex (VPC) after every three normal QRS complexes. This rhythm
usually does not progress to dangerous forms of fast ventricular rhythms. Note that in
this rhythm, two VPCs never occur one right after the other.
Reciprocal complex
A QRS complex that is caused by activation of a reentrant circuit rather than by
the sinus node. This can be harbinger of atrioventricular nodal tachycardia or
atrioventricular tachycardia.
Refractory period
Period following a depolarization in which the cells can not be activated.
Repolarization
Recovery of the resting potential.
Retrograde
From the ventricle towards the direction of the atrium.
Retrograde atrial activation
A P wave that occurs because of activation of a portion of the heart below the
sinus node, including elsewhere in the atrium, the atrioventricular node (via the fast or
a slow AV nodal pathway) or the ventricle (via an accessory pathway). Retrograde P waves
typically are inverted in the inferior and right precordial EKG leads (II, III, aVF, and
V1), in which the normal sinus P wave is upright.
Right bundle branch block
Interrupted conduction of the right bundle branch.
Secondary Ventricular standstill
This is diagnosed when only ventricular escape complexes are present, and they
occur very slowly. This is an agonal rhythm that is not consistent with life.
"Secondary" means that the condition is caused by another factor, such as
severely low oxygen levels, which must be fixed before the rhythm abnormality can be
stabilized. If you see this, you should initiate Cardiopulmonary Resuscitation
immediately.
Sick sinus-syndrome
Disorder of the sinus node and atrium with sinus bradycardia, SA-block and
paroxysmal tachycardia of the atrium.
Sinus arrhythmia
Irregular sinus rhythm.
Sinus arrest
This rhythm results from failure of the sinus node to activate the atria.
When it is of short duration (less than one to two seconds), it is usually benign. When it
is of long duration (greater than or equal to three seconds), it can be life-threatening
because of the potential for longer periods of sinus arrest with asystole. It can be
caused by medications, including as beta blockers, some calcium blockers such as
diltiazem, aldomet, and perhaps digitalis. It can also be part of the sick sinus
("tachy-brady") syndrome, which is one of the leading indications for
implantation of permanent pacemakers in this country. If there is any concern about this
rhythm, consultation with a Cardiologist is recommended.
Sinus arrhythmia
This rhythm is usually a benign finding. It is characterized by variations in the
heart rate from cycle to cycle that are greater than would be expected from normal
respiratory variation. When pronounced, it can be symptomatic. If there is any concern
about this rhythm, consultation with a Cardiologist is recommended.
Sinus bradycardia
This rhythm differs from normal sinus rhythm only in that the rate is below 60
beats per minute (bpm). This can be a normal finding in young patients, particularly in
athletes. It can be caused by medications, including as beta blockers, some calcium
blockers such as diltiazem, aldomet, and perhaps digitalis. If there is any concern about
this rhythm, consultation with a Cardiologist is recommended.
Sinus node
Primary pacemaker of the heart located in the right atrium.
Sinus tachycardia
This rhythm differs from normal sinus rhythm only in that the rate is above 100
beats per minute. The differential diagnosis is extensive. Common causes are anxiety;
physiological stress such as hemorrhage, dehydration, sepsis, and fever; and
hyperthyroidism. Correction of the underlying cause, if necessary, is recommended.
ST-junction
The rather sharp-cut transition from the QRS complex and the ST segment.
Subendocardial
Located in the inside of the ventricles.
Supraventricular
Located above the ventricles, the bundle of His and higher.
Supraventricular tachycardia
This is a generic name for a variety of specific supraventricular rhythms,
including Atrioventricular Reentrant Tachycardia, Atrioventricular Nodal Reentrant
Tachycardia, and Atrial Tachycardia.
It is also used in reference to any narrow complex rhythm to distinguish it from
wide-complex rhythms that could arise in the ventricle. In addition to the specific
rhythms mentioned above, this use of the term includes atrial fibrillation, atrial
flutter, junctional tachycardia, accelerated junctional rhythm, and multifocal atrial
tachycardia.
Systolic
Phase of contraction of the ventricles.
Tachycardia
Heart frequency higher then 100 bpm.
Three or more premature beats following each other.
They can be paroxysmal (suddenly occurring) or chronic (permanent). A paroxysmal
tachycardia is characterized by a sudden beginning and a sudden ending, and can have a
duration of a second (three or more complexes) up to a few days.
Third degree (complete) heart block
This rhythm is characterized by failure of conduction from the atria through the
atrioventricular node to the ventricles. The atrial rhythm is independent of the
ventricular rhythm, unless an accessory pathway that conducts antegrade is present. It is
most easily distinguished from high-grade atrioventricular nodal block when the atrial and
ventricular rhythms are regular but have different rates. Because of weak coupling between
the chambers by the autonomic nervous system, these rates can be very close to each other
and in fact can oscillate around each other.
Complete heart block is one of three forms of atrioventricular dissociation. The other two
forms are:
sinus arrest or sinus bradycardia with junctional rhythm or Idioventricular rhythm.
ventricular tachycardia.
Of these three forms, only Complete Heart Block results from antegrade conduction block
from the atria to the ventricles.
T(a)-wave
The repolarization of both atria (not visible because this wave happen at the
same time as the depolarization of the ventricles (QRS complex) and is lost therein.
Transmembrane potential
Resting potential across the cell membrane.
Transmural
Across the total ventricular wall, from endocard to epicard.
Trigeminy
An abnormal but usually harmless rhythm characterized by occurrence of one
ventricular premature complex (VPC) after every two normal QRS complexes. This rhythm
usually does not progress to dangerous forms of fast ventricular rhythms. Note that in
this rhythm, two VPCs never occur one right after the other.
T-wave
The repolarization of both ventricles.
Unipolar
Lead in which the potential differences are registered in one point compared
to the central terminal.
U-wave
Repolarization of the purkinje fibbers, visibility of the wave is dependent
on Ca- and K concentrations.
Vector
Electrical force in a specific direction and with a specific magnitude.
Ventricular couplet
Two ventricular premature complexes in a row. This can be a normal finding, but
is more suggestive of electrical heart disease than are single ventricular premature
complexes.
Ventricular escape complex
This is a QRS that is wide and occurs later than would be expected from the sinus
rate. Like all escape complexes, it can occur only when the normal cardiac pacemaker does
not function, as is sinus arrest.
Ventricular fibrillation
This is a lethal rhythm, characterized by absence of both organized electrical
and organized mechanical activity. This rhythm is equivalent to cardiac death. If
you see this, you should initiate Cardiopulmonary Resuscitation immediately.
Ventricular premature complex
This is a wide QRS complex that occurs earlier than would be expected from the
sinus rate, and that almost always has an abnormal morphology. It fails to conduct
retrograde through the atrioventricular node in half of patients, in which case it results
in a compensatory pause. That is, the next P wave occurs at the same time as would be
expected had the VPC not occurred. When it does conduct through the atrioventricular node,
the following P wave may occur either sooner or later than would be expected.
Ventricular premature complexes are a normal finding in adults of all ages. They cause
symptoms of palpitations or "skipping" in some people. Their frequency can be
increased during stress, with ingestion of caffeine, and with sympathomimetic drugs such
as some over-the-counter cold remedies. The frequency is also increased in patients with a
tendency to develop ventricular tachycardia.
Ventricular tachycardia, General
This rhythm is diagnosed when three or more premature ventricular complexes occur
in a row at a rate of 100-120 beats per minute or faster. The major clinical distinctions
are between hemodynamically unstable versus stable ventricular
tachycardia and between sustained versus unsustained ventricular
tachycardia.
Hemodynamically unstable ventricular tachycardia is a life threatening
emergency for which the ACLS protocol should be initiated immediately. Synchronized
cardioversion is usually the treatment of choice. Awake patients should be sedated heavily
before cardioversion if at all possible.
Sustained ventricular tachycardia is defined as having a duration of 30
seconds or more, or being hemodynamically unstable. The immediate treatment is
specified by the ACLS protocol. For long-term treatment, it is important to realize that
these patients have a 20% to 40% sudden death mortality, when untreated, over the 12
months following initial presentation. Empiric treatment with antiarrhythmic drugs does
not reduce this mortality. Effective treatment with drugs and/or an implantable
cardioverter defibrillator reduces the sudden death mortality over the next 12 months to
0-2%. Therefore, consultation with a Cardiac Electrophysiologist is recommended during the
initial hospital stay to ensure adequate evaluation and treatment before discharge from
the hospital.
Ventricular tachycardia, polymorphic
This form of ventricular tachycardia is characterized by changing QRS morphology,
sometimes accompanied by slight changes in the rate. It is a particularly malignant form
of ventricular tachycardia that is thought to be intermediate between ordinary monomorphic
ventricular tachycardia, and ventricular fibrillation.
For etiology, think of proarrhythmia, as from type IA antiarrhythmic medications,
ischemia, hypokalemia, hypomagnesemia, profound bradycardia, and idiopathic prolonged QT
syndrome.
Wandering atrial pacemaker
This is a supraventricular rhythm resulting from multiple ectopic foci in the
atria. It is characterized by three or more P wave morphologies and a rate less than 100
beats per minute. It itself is benign, but reflects electrical abnormalities in one or
both atria that increase the likelihood of multifocal atrial tachycardia or other atrial
arrhythmia's.
Wenckebach block
A type of second grade AV-block.
Wolff-Parkinson-White, syndrome of
The term used to describe the presence of one or more accessory
atrioventricular pathways that conduct in the antegrade direction, with or without
retrograde conduction. Patients with this syndrome are susceptible to atrioventricular
reentrant tachycardia and atrial fibrillation.
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