The atrioventricular block is a disturbance of the progression of activation at
any point of its path on the conduction path between the atria and ventricles:
that is, in the Aschoff-Tawara node, in the trunk of His beam or, simultaneously
in its two branches.
According to the degree of severity of this conduction disorder, three types of
atrioventricular block are distinguished:
1 ° - The simple slowing of atrio-ventricular conduction or BAV of the degree.
The atrial activation waves all come to the ventricles, but with an abnormal
delay.
2 ° - Intermittent interruption of atrioventricular conduction or 2nd degree BAV.
Not all atrial activation waves come to the ventricles, because some are blocked.
This arrest of atrio-ventricular conduction can occur both after a progressive
slowing down of this and abruptly and more or less frequently.
3° - The complete and permanent interruption of conduction atrio-ventricular or BAV of 3rd degree. Ventricular activation becomes totally
independent of atrial activation. In this case ventricular activation is ensured
by an escapement spot located below the block site
• It consists by definition in the slowing of atrio-venicular conduction.
• It's expressed by:
- An extension of the interval over 0,21 seconds, in adults (over 0.18 in the
child), remaining however normally less than 0.40 seconds.
- A numer of waves P equal to the number of QRS complexes.
- QRS complexes the most often ends, but sometimes, on the contrary, spread to
bundle branch type.
Most often it is the expression of a conduction disturbance in the
Aschoff-Tawara node (atriododal or nodal region): This conduction disorder is
not in principle linked to irreversible histo-logical alterations, but more
often than not it is related to transitory local metabolic perturbations and is
the expression of the exaggeration of the physiological process of slowing down
the characteristic conduction of the Aschoff-Tawara node (see in the lexicon:
decremental conduction). The BAV of the first degree may also depend on a
disturbance in the conduction of the beam of His. The high location of the
conduction disorder site explains the normal rule morphology of QRS complexes.
Sometimes the QRS complexes are spread to the type of bundle branch block, and
in this case, the association of the BAV of the first degree must make one think
of the possibility of a conduction disorder with a low seat, located on the
branch opposite the blocked branch ( see: bilateral branch block).
First degree is varied: we can treat:
1 - Of a pharmacological cause: digital, essentially, and in general negative
dromotropic drugs: beta-blockers, Amiodarone, Quinidine, Ajmalina, Procainamide,
Lidocaine, Disopyramide.
2 - Of an infectious cause: acute articular rheumatism, diphtheria, typhus or
viral.
3 - It is well understood, of all the causes of BAV of higher grade.
EVOLUTION is different depending on the etiology:
It is regressive when the pharmacological or infectious cause has itself
disappeared.
On the other hand, it may progress towards a higher grade block if a different
etiology is involved, particularly in the case of association with a branch
block.
There are 3 types:
1- In the Mobitz I block (Wenckebach)
2- In the Mobitz II block
3- In the high-grade atrioventricular block
• It is characterized by intermittent interruption of atrio-ventricular
conduction.
• It manifests itself with:
- The intermittent appearance of a wave P not followed by a QRS complex: the
wave P in this case is called blocked
- The number of P wave is so superior to the number of the QRS complex.
Among the 2nd grade BAVs there are different varieties depending on the way in
which the P wave is blocked:
The lengthening of the PR interval is
progressive from one complex to another until the appearance of a blocked P wave,
so the same sequence repeats itself: these are the periods of Luciani-Wenckebach.
The progressive lengthening of the PR interval followed by a block of the P wave
produces apparently paradoxical effects in the intervals between the QRS
complexes (RR intervals), since these progressively shorten until the appearance
of a very long RR interval (this interval, however, it remains less than twice
the previous RR interval). The paradoxical shortening of the RR interval is
explained by the decreasing progression of the prolongation of the PR interval:
the rate of lengthening of PR, important at the beginning, decreases later
- It may also be a more anarchic variations of the PR interval, which lengthens
or shortens unexpectedly before the blocking of the wave P: this is the atypical
Luciani-Wenckebach Block.
-The Ventricular complexes in this variety of BAV are most often of normal
morphology, but sometimes of bundle branch type.
- P-wave blocking is frequent and regular.
- On the other hand, the PR interval remains constant whether its duration is
normal or elongated. The QRS waves may be missing
-The ventricular complexes in this form of BAV are most often abnormal to bundle
branch type, rarely have a normal morphology.
The second ventricular atrioventric block can be of two types:
- type Mobitz I (or periodical of Luciani-Wenckebach)
- type Mobitz II
In the Mobitz I type, the P-Q interval is progressively lengthened until the
ventricular pulse is not conducted. Then the cycle begins again.
(See the example)
In the second-degree BAV type Mobitz II not all P are followed by the QRS. So we
will have a block 2: 1, 3: 1, 4: 1 and so on.
These two BAV varieties are not only electrocardiographically distinguished,
they are linked to different mechanisms and imply also different prognostics:
- The BAV type Mobitz I (or periodically by Luciani-Wenckebach is most often
caused by a conduction disturbance located in the Aschoff-Tawara node or in the
adjacent portion of the trunk of His beam. conduction explains the morphology
most often normal of QRS complexes, however, the conduction disturbance is not
in principle linked to irreversible isto-logical alterations, but is in most
cases in relationship with local transient metabolic perturbations, just like
BAV of the first degree When the association with a branch block exists, the BAV
of Luciani-Wenckebach must make suspect a disturbance of the conduction at lower
localization, on the branch opposite the blocked branch (see bilateral branch
block).
- The Mobitz II type BAV, in which the conduction disturbance is more severe, is
most often determined by alterations located in the lower part of the trunk or
in the two branches of the His beam. As a rule yielded alterations are
histological and irreversible. Frequent involvement of His bundle branches
explains the habitual morphology of QRS complexes, type of bundle block
The 2nd degree BAV, like Luciani-Wenckebach, can be observed in a normal subject;
its etiology, however, is confused with that of the BAV of the degree.
The aetiology of the 2nd degree BAV, type Mobitz, is, on the contrary,
superimposed on that of the 3rd degree BAV.
EVOLUTION:
The 2nd degree BAV, type Luciani-Wenckebach, most often tends to regress,
particularly when the QRS complexes are fine, it may on the contrary evolve
towards a block of higher degree if it is associated with a block appearance of
branch.
NOTE: It is clearly seen here that the essential differential character between
the Luciani-Wenckebach-type BAV and the Mobitz-type BAV is given by the fixity
or not of the conduction time of the QRS complexes conducted (PR interval).
It is characterized by complete interruption of the atrioventricular
conduction.
It manifests itself with complete independence of P waves and ventricular
complexes.
1 - Atrial activity completely dissociated from ventricular complexes is of
variable aspect:
• most often it is sinus: P waves are normal and regular. Sometimes the atrial
rhythm is accelerated, the atrial rate having a tendency to be as rapid as the
ventricular rate is slower. With the same frequency there is a sinus arrhythmia
called ventriculofasica: the interval between 2 waves P is shorter when they
vent a ventricular complex, but it is longer when there are no ventricular
complexes between them.
• sometimes a flutter or atrial fibrillation exists.
• no atrial activity is rarely seen: in this case a differential diagnosis
between full BAV, atrial paralysis and complete BSA is required. Only one
endocavitary registration allows one to conclude for a BAV: this happens if it
is able to highlight the waves of a small-meshed atrial fibrillation or of sinus
low-voltage P waves.
• a retrograde P wave can occur that follows a QRS complex, which attests to the
possibility of intermittent ventriculo-atrial conduction.
2 - QRS complexes are completely interspersed
• with a frequency slower than that of the P waves, absolutely constant, not
influenced by the effort or by the vagal maneuvers.
• with a variable morphology: the QRS complexes are much finer the higher the
BAV is located:
2.1 - Normal QRS complexes
• shorter than 0.08 seconds
• of fairly rapid frequency between 40 and 50 per minute.
• the origin of the escapement rhythm is in this case at high location, above
the bifurcation of His beam (Aschoff-Tawara node or trunk), the block being
itself at high localization.
2.2 - Wide QRS complexes
• lasting close to 0.12 seconds
• of frequency between 30 and 40 per minute
• of morphology similar to that of a blockade of a right branch (most often) or
of a left bundle branch block, and in this case we talk about right delay or
left delay. The appearance of BSD may be associated with a left or right axial
deviation of QRS that resembles the anterior or posterior hemiblock.
• the origin of this escapement rhythm is situated either below the bifurcation
of His beam, on one of its two branches, or above the bifurcation, but with a
single or two-sided branch bundle
It is noteworthy that a similar QRS morphology can be accomplished by 2 types of
blocks, with different locations: for example, an aspect of right bundle branch
block with left anterior hemiblock may occur due to existence:
a) a block having its seat on the common trunk of the beam of His, associated
with a right bundle branch block and of the anterior bundle of the left bundle,
and with an escapement focussed on the common trunk itself, beneath the block.
In this case the activation wave to reach the two ventricles takes the path of
the posterior bundle of the left branch.
b) a block having its seat on the right branch and on the two bundles of the
left branch, and with an outflow located on the posterior branch below the
block. Also in this case the activation wave to reach the two ventricles takes
the path of the posterior bundle of the left branch.
2.3 - Very large QRS Complexes:
• longer than 0.12 seconds, usually between 0.14 and 0.20 seconds.
• of slow frequency, sometimes less than 20 per minute.
• morphology very roughly reminiscent of a branch block and qualified as right
delay or left delay.
• the origin of the escapement rhythm is in this case located in a right
idioventricular outbreak, if the QRS complexes have a left-late appearance, in a
left idioventricular outbreak, if the QRS complexes have a right-delay
appearance.
3 - Alteration of repolarization. They are found when the QRS complexes are
spread out, and they are more important the more accentuated it is the widening
of the complexes themselves: the RST segment is deviated and the T wave is
inverted with respect to the QRS. The QT interval is extended,
When very important disturbances of repolarization are found, especially if
there is a giant T-wave and a QT-elongation greater than 0.60 seconds, one must
fear the onset of ventricular fibrillation.
Mechanism
The complete BAV depends on a complete interruption of conduction either at the
level of the node-Hissian region or at the level of the trunk of the HIS beam
or, more often than not, at the level of its branches.
It can depend on transient biochemical disturbances, responsible for stopping
the activation waves by creating a permanent refractory period. Most of the time,
however, depends on a complete destruction of the trunk of the beam of HIS or
its two branches, which permanently prevents any propagation of the activation
wave.
Etiology of the complete atrioventricular block (BAVC)
From the etiological point of view, the following block types are distinguished:
1 - idioventricular BCA secndario to a fibrous degeneration of the 2 branches of
the HIS beam (LENE 'GRE disease).
2 - Blockage of the acute phase of the ventricular infarct. We must distinguish
two varieties of BAV depending on the site of the infarct, front or back. Their
morphological evlutive and anatomical features contrast them:
a) When the infarction is posterior: the BAV is characterized:
- from its electrical appearance: relatively fast ventricular rate (between 40
and 60 per minute), COMPLETE QRS FINI.
- from his way of evolving: spontaneous regression in a few days.
- from the corresponding histological lesions: inflammatory and edemigenic
alterations of the Aschoff-Tawara node and of the adjacent part of the HIS beam.
These alterations are reactive with respect to nearby and therefore reversible
myocardial necrosis.
It's a specific type of abnormal heart rhythm that can lead to sudden cardiac death. It is a polymorphic ventricular tachycardia that exhibits distinct characteristics on the electrocardiogram (ECG).
Common causes for torsades de pointes include diarrhea, low blood magnesium, and low blood potassium. It is commonly seen in malnourished individuals and chronic alcoholics, due to a deficiency in potassium and/or magnesium.
Certain combinations of drugs resulting in drug interactions can contribute to torsades de pointes risk. QT prolonging medications such as clarithromycin, levofloxacin, or haloperidol, when taken concurrently with cytochrome P450 inhibitors, such as fluoxetine, cimetidine, or particular foods including grapefruit, can result in higher-than-normal levels of medications that prolong the QT interval in the bloodstream and therefore increase a person's risk of developing torsades de pointes. In addition, inherited long QT syndrome significantly increases the risk of episodes of TdP.