Reentry—a disorder of impulse transmission
Mechanisms of reentry
Reentry requires:
At least two conduction pathways
Variable block in one of the pathways
If two pathways have similar conduction velocities, the electrical impulses will merge distally and no arrhythmia will occur (see figure).
If an event (e.g., a premature ventricular contraction [PVC]) occurs at the right time and place to make one of the two pathways refractory, the impulse will be blocked in that limb.
If the impulse from the other limb travels back up the blocked limb, it may find the previously refractory area able to conduct.
If the impulse reaches the initial branch point of the two pathways before the next normal impulse arrives from above, the arrhythmia can perpetuate itself.
Properties of reentrant arrhythmias
Reentrant arrhythmias start and stop abruptly (paroxysmally).
They are usually initiated by a premature beat.
The reentrant arrhythmias that have a discreet reentrant pathway [atrial flutter, AV nodal reentrant tachycardia [AVNRT], most ventricular tachycardia (VT)] are very regular.
Reentrant arrhythmias can be terminated by any mechanism, which makes some part of the reentrant pathway refractory, including vagal maneuvers (AVNRT), chest thump (VT), medications which slow conduction (most reentrant arrhythmias) or electrocardioversion (all reentrant arrhythmias).
The major reentrant arrhythmias
Atrial fibrillation
Mechanisms and causes (Day 5-01) (Day 5-02) (Day 5-03) (Day 5-04)
DAY 5-01
DAY 5-02
DAY 5-03
DAY 5-04
The most likely cause of atrial fibrillation is microreentry between islands of atrial muscle in the vicinity of the insertion of the pulmonary veins into the left atrium.
Atrial fibrillation requires a certain amount of atrial tissue to be present to sustain the arrhythmia (an important concept in therapeutic approaches).
Atrial pressure overload (e.g., from heart failure, hypertensive heart disease, ventricular failure, or valvular heart disease) is the clinical situation responsible for the vast majority of cases.
Heart rate
The multiple reentrant wave fronts combine to have an atrial rate of 400–600.
The ventricular response is irregular.
ECG morphology
The baseline varies from coarse, irregular fibrillatory waves to virtually flat.
The QRS complexes are narrow unless there is an intraventricular conduction defect (IVCD).
Response to vagal maneuvers or AV nodal blocking medications (i.e., IV adenosine).
These maneuvers do not affect the atrial fibrillation itself.
The ventricular response is irregularly slowed.
Atrial flutter
Mechanisms and causes (Day 5-05) (Day 5-06)
Most examples are likely due to reentry.
The common reentry pathway is counterclockwise around the tricuspid annulus and involving the interatrial septum.
Atypical forms exist, which presumably have other reentrant pathways and are often faster than typical flutter. (Day 5-07)
Atrial pressure overload (from similar causes as for atrial fibrillation) is responsible for the majority of cases.
DAY 5-05
DAY 5-06
DAY 5-07
Heart rate
The atrial rate is 220–320, more commonly 280–320, with a median of 300.
Patients receiving antiarrhythmic therapy (e.g., with quinidine, sotalol, or amiodarone) may have slower (as low as 200) flutter rates.
The ventricular response is usually a whole even number division of the atrial rate (2:1, 4:1, 8:1), although alternating 2:1/4:1 or variable ventricular responses are encountered. (Day 5-08) (Day 5-09)
One of Marriott’s laws—every absolutely regular supraventricular tachycardia with a rate of 150 is atrial flutter with 2:1 block until proven otherwise.
Rarely, atrial flutter can present with 1:1 AV conduction. (Day 5-10)
ECG morphology
The baseline in typical flutter usually demonstrates extremely regular sawtooth flutter waves in Leads II, III, aVF, or V1, although the flutter waves may be difficult to discern if the ventricular rate is rapid.
The QRS complexes are narrow unless there is an IVCD.
Response to vagal maneuvers or AV nodal blocking medications
Vagal maneuvers do not affect the atrial flutter itself.
The ventricular response is slowed, usually in whole number divisions of the atrial rate, unmasking the underlying flutter waves.
AV nodal reentrant tachycardia (AVNRT)
Mechanisms
Anatomy of the AV node.
The electrical properties of the AV node with its fast and slow pathways with different repolarization rates, facilitate reentry.
DAY 5-08
DAY 5-09
DAY 5-10
“Short R-P” form
(1) In about 90% of patients with AVNRT, the fast pathway has a longer refractory period (i.e., takes longer to repolarize) than the slow pathway.
(2) A fortuitously timed premature atrial complex (PAC) may be conducted down the slow pathway while the fast pathway is still refractory, thus setting the stage for a reentrant arrhythmia.
(3) Since the impulse travels down the slow pathway and back up the fast pathway, there is a retrograde P wave buried within the QRS complex or shortly thereafter. (Day 5-11) (Day 5-12)
“Long R-P” form
(1) In about 10% of patients, the slow pathway appears to have a longer refractory period (i.e., repolarizes more slowly) than the fast pathway.
DAY 5-11
DAY 5-12
(2) Since the impulse travels down the fast pathway and back up the slow pathway, the P wave is typically closer to the next QRS complex. (Day 5-13)
Heart rate
The AVNRT rate is usually 120–220.
The ventricular rate is almost always the same as the atrial rate.
ECG morphology—see figures.
Response to vagal maneuvers or AV nodal blocking medications—these measures frequently terminate the arrhythmia.
DAY 5-13
Ventricular tachycardia (VT)
Mechanisms and causes
Most VT (90%) is due to reentry.
The reentry pathway frequently involves the edges of a previously infarcted area of myocardium, but also may be present in any condition, which causes a myocardial abnormality.
VT rarely occurs in healthy individuals.
Heart rate
The VT rate is typically 120–220.
The atrial rhythm may remain the same as it was prior to the development of VT (70% of the time, in which case there is AV dissociation), or there may be retrograde conduction to the atrium (30%, no AV dissociation).
ECG morphology (Day 5-14)
VT demonstrates a wide QRS morphology.
For a discussion of the differentiation of wide QRS tachycardias, see the notes for Day 8.
Response to vagal maneuvers—vagal maneuvers rarely have any effect on VT.
DAY 5-14
Ventricular fibrillation (VF)
Mechanisms and causes
VF probably represents multiple chaotic reentrant pathways involving the entire ventricular muscle.
VF occurs in patients with severe ischemia, hypoxia, metabolic abnormalities, etc.
VF is obviously rapidly fatal unless defibrillated.
ECG morphology—VF demonstrates an erratic baseline with no organized activity.
Summary of reentrant arrhythmias
Sample Tracings
ECG 1
ECG 2
ECG 3
ECG 4
ECG 5
ECG 6
ECG 7
ECG 8
ECG 9
ECG 10
ECG 11
ECG 12
ECG 13
ECG 14
ECG 15
ECG 16
ECG 17
ECG 18
ECG 19
ECG 20
Reentrant Arrhythmias
ECG 1
Atrial rate:
Ventricular rate: 175
Rhythm: Atrial fibrillation with rapid ventricular response
P wave:
PR interval:
QRS complex:
Axis: 0°
Duration: 80 msec
Voltage: Normal
Morphology: Normal
ST segment: Normal
T wave: Nonspecific changes
QT interval: 270 msec
U wave:
Diagnosis: Atrial fibrillation with rapid ventricular response. Some complexes are conducted aberrantly.
ECG 2
Atrial rate:
Ventricular rate: 108
Rhythm: Atrial fibrillation with rapid ventricular response converting to sinus rhythm
P wave: Normal in sinus rhythm
PR interval: 160 msec in sinus rhythm
QRS complex:
Axis: 45°
Duration: 80 msec
Voltage: Normal
Morphology: Normal
ST segment: Normal
T wave: Normal
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