predominate, creating increased cardiac output and other
Premature atrial contractions (PACs) are contractions of the
atria that are triggered by the atrial myocardium but have not
originated from the sinoatrial node (SA node).
PACs typically have normal QRS complex and a normal, short,
or longer PR interval than sinus rhythm. Sometimes, non
conducted PACs occur in which there is no QRS complex
following the PAC. PACs can be unifocal arising from one
location (similar P waves in all PACs) or multifocal and arising
from several locations (different P wave morphologies for
PACs). The P wave of the PAC typically occurs earlier than the
sinus P wave and has a different morphology and axis from the
sinus P wave. It appears dissimilar from a standard sinus node
generation, with variations in height, length, and shape of the P
wave; furthermore, the P wave may be inverted or biphasic.
Pharmacologic management can be achieved using:
● Beta-adrenergic blockers at low doses are the
relatively safe and first-line treatment in
symptomatic patients if conservative measures fail.
The role of calcium channel blockers to treat PACs
is not well defined.
● Type IA, type IC, and type III antiarrhythmic
agents can all suppress the PAC origin and are
infrequently used only after careful consideration of
their pro-arrhythmogenic nature.[36][37][38]
a compensatory pause results when the ectopic impulse fails to
enter the SA node. The SA node continues to produce impulses
without any effect from the ectopic impulse. Each sinus P wave
is normal and right on time. Occasionally, we can see every P
wave produced,
Now let’s move on to the second PAC. The blue line in Figure 2
indicates that the visible P-P interval surrounding this PAC is
less than two P-P intervals. This represents a non-compensatory
pause. This is what happened to cause the non-compensatory
pause: before the SA node could complete its depolarization
process (which is relatively slow since it is based on slow
calcium channels), the PAC entered the SA node and
discharged it. The SA node then began its depolarization
process once again. We call this process a reset. Because the
time from the last normal P wave (before the reset occurred) to
the reset itself is less than a full P-P interval, the P-P interval
surrounding the ectopic beat is equal to one full P-P interval
plus that partial P-P interval (ie, less than two complete,
normal P-P intervals).
So, if the P-P interval surrounding an ectopic beat is equal to
two normal P-P intervals, we call that a compensatory pause.
And if the P-P interval surrounding an ectopic beat is less than
two normal P-P intervals, we call that a non-compensatory
pause. —-
-wandering atrial pacemaker
atropine
anti-vagal effect, organophosphate/muscarinic poisoning, and
bradycardia. an anticholinergic drug
-competitive inhibition of postganglionic acetylcholine
receptors and direct vagolytic action, which leads to
parasympathetic inhibition of the acetylcholine receptors in
smooth muscle. The end effect of increased parasympathetic
inhibition allows for preexisting sympathetic stimulation to
associated antimuscarinic side effects as described herein
—--------
Reentry, due to a circuit within the myocardium, occurs
when a propagating impulse fails to die out after normal
activation of the heart and persists as a result of
continuous activity around the circuit to re-excite the
heart after the refractory period has ended.
—---
Adenosine further classifies as a miscellaneous antiarrhythmic
drug outside the Vaughan-Williams classification scheme. It
acts on receptors in the cardiac AV node, significantly slowing
conduction time.[3] This effect occurs by activation of specific
potassium channels, driving potassium outside of cells, and
inhibition of calcium influx, disrupting the resting potential of
the slow nodal cardiac myocyte. Driving potassium outside of
the cell causes hyperpolarization of the resting membrane
potential while slowing of calcium influx causes suppression of
calcium-dependent action potentials, all requiring a longer
time for depolarization to occur and thus slowing down
conduction within these cells, which is useful in SVT. SVT is
defined as any arrhythmia originating above and including the
bundle of His and specifically excludes atrial fibrillation by the
ACC/AHA 2015 guidelines.[4] Usually narrow complex, SVT
consists of several specific arrhythmias, which at a high rate
(greater than 150 beats per minute), is difficult to diagnose.
Adenosine has a role in slowing down the heart rate enough to
assist in diagnosis. It can also terminate specific reentrant
tachycardia involving the AV node, including AV nodal
reentrant tachycardia (AVNRT), orthodromic AV reentrant
tachycardia (AVRT), and antidromic AVRT, although extreme
caution is necessary when administering adenosine for
antidromic AVRT as it should be used only if the diagnosis is
certain.
____
A junctional rhythm is an abnormal heart rhythm that
originates from the AV node or His bundle.
A junctional rhythm is where the heartbeat originates from the
AV node or His bundle, which lies within the tissue at the
junction of the atria and the ventricle. Generally, in sinus
rhythm, a heartbeat is originated at the SA node. This
electrical activity then travels through the atria to the AV node
from where it reaches the Bundle of His from where the
electrical signals travel to the ventricles through the Purkinje
fibers.
The terminology used to identify the type junctional rhythm
depends on its rate and is as follows:
● Junctional bradycardia: rate below 40 beats per
minute
● Junction escape rhythm: rate 40 to 60 beats per
minute
● Accelerated junctional rhythm: rate of 60 to 100
beats per minute
● Junctional tachycardia: rate above 100 beats per
minute
Go to:
Etiology
When the electrical activity of the SA node is blocked or is less
than the automaticity of the AV node/His bundle, a junctional
rhythm originates. Numerous conditions and medications can
lead to a diseased SA node and lead to the AV node/His bundle
taking over due to the higher automaticity of the ectopic
pacemaker.[7][8][9]
Accelerated junctional rhythm
An accelerated junctional rhythm (rate >60) is a narrow
complex rhythm that often supersedes a clinically
bradycardic sinus node rate (see images below). The
QRS complexes are uniform in shape, and evidence of
retrograde P wave activation may or may not be present.
The junctional rhythm initiates within the AV nodal
tissue. Accelerated junctional rhythm is a result of
enhanced automaticity of the AVN that supersedes the
sinus node rate. During this rhythm, the AVN is firing
faster than the sinus node, resulting in a regular narrow
complex rhythm. These rhythms may demonstrate
retrograde P waves on ECG findings, and the rates can
vary from 40-60 beats per minute.
Changes in autonomic tone or the presence of sinus
node disease that is causing an inappropriate slowing of
the sinus node may exacerbate this rhythm. Young
healthy individuals, especially those with increased
vagal tone during sleep, are often noted to have periods
of junctional rhythm that is completely benign, not
requiring any intervention.
First degree. In first-degree AV block, the P waves always precede
the QRS complexes, but there is a prolongation of the PR interval.
That is, the PR interval will be greater than 200 milliseconds in
duration without any dropped beats. There is a delay, without
interruption, in conduction from the atrium to the ventricle. In
other words, while the impulse is slowed, it is still able to get
through to the ventricles. All atrial activation is eventually
transmitted to the ventricles. The delay is typically due to a minor
AV conduction defect occurring at or below the AV node. If the PR
interval is more than 300 milliseconds, it is considered “marked”
first-degree AV block and the P waves may be buried in the
preceding T wave.
● Causes. There are multiple causes of first-degree AV
block, including simply being a normal variant. Other
causes include inferior myocardial infarction (MI),
increased vagal tone (e.g., athletes), status post-cardiac
surgery, myocarditis, hyperkalemia, or even
medication-induced (e.g., beta-blockers,
non-dihydropyridine calcium channel blocks,
adenosine, digitalis, and amiodarone).
● Clinical significance. This is a benign entity that does
not result in any hemodynamic instability. No specific
treatment is required.
Second degree (incomplete). Second-degree or incomplete AV
block occurs when there is intermittent atrial to ventricle
conduction. That is, the P waves are sometimes related to the QRS
complexes. It often occurs in a regular P:QRS pattern with ratios of
2:1. 3:2, 4:3, 5:4, and so forth. Second-degree AV blocks can be
further classified into Mobitz type 1 (Wenckebach) or Mobitz type
2, which can be distinguished by examining the PR interval.
Second degree, Mobitz type 1 (Wenckebach). In second-degree
Mobitz type 1 AV block, there is a progressive prolongation of the
PR interval, which eventually culminates in a non-conducted P
wave. It is often evident by clustering of QRS complexes in groups
that are separated by non-conducted P waves. The greatest increase
in PR interval prolongation is often between the first two beats of
the cycle. While the PR interval continues to prolong with each
beat of the cycle, the subsequent PR lengthening is progressively
shorter. Even though the PR interval is progressively increasing in
duration, the PP interval remains relatively unchanged. One way to
confirm the presence of this is by noticing that the PR interval after
the dropped beat is shorter than the PR interval that came before
the dropped beat. In other words, the PR interval before the
dropped beat is the longest of the cycle, and the PR interval after
the dropped beat is the shortest as the cycle starts over.
● Mechanism. This is usually a result of a reversible
conduction block at the level of the AV node. In fact,
studies have shown that the site of block is likely at the
crest of the AV node, where the atrium and AV node
meet. There is typically a functional suppression of AV
conduction. The AV nodal cells seem to progressively
fatigue until they fail to conduct an impulse to the
ventricles and a dropped beat occurs.
● Causes. There are multiple causes of second-degree
Mobitz type 1 (Wenckebach) AV block, including
reversible ischemia, myocarditis, increased vagal tone,
status post-cardiac surgery, or even medications that
slow AV nodal conduction (e.g., beta-blockers,
non-dihydropyridine calcium channel blocks,
adenosine, digitalis, and amiodarone).
● Clinical significance. Differentiating between
second-degree Mobitz type 1 (Wenckebach) and Mobitz
type 2 AV blocks is important as the management and
treatment is different. Mobitz type 1 is often a benign
rhythm. Most patients are asymptomatic, and there is
tends to be minimal hemodynamic disturbance. The risk
of Mobitz type 1 (Wenckebach) progressing to
third-degree (complete) heart block is much lower than
Mobitz type 2. Patients that are asymptomatic do not
require treatment and can be monitored on an outpatient
basis. Patients that are symptomatic typically respond to
atropine and rarely require permanent cardiac pacing.
Medication-induced impairment of AV conduction is
often reversible after stopping the offending agent.
Second degree, Mobitz type 2. In second-degree Mobitz type 2
AV block, there are intermittent non-conducted P waves without
warning. Unlike Mobitz type 1 (Wenckebach), there is no
progressive prolongation of the PR interval; instead, the PR
interval remains constant, and the P waves occur at a constant rate
with unchanged P-P intervals. Because the P waves continue to
occur at normal intervals, the R-R interval surrounding the dropped
beat is simply a multiple of the preceding R-R interval and remains
unchanged.
● Mechanism. Whereas in Mobitz type 1 there was a
reversible block at the level of the AV node, in Mobitz
type 2 the block occurs further along the electrical
conduction system below the AV node. It can occur at
the level of the His Bundle, both bundles branches, or
the three fascicles (i.e., the left anterior fascicle, left
posterior fascicle, and right bundle branch).
● In this case, the cells don’t progressively fatigue, but
rather abruptly and unpredictably fail to conduct a
supraventricular impulse. This is often the result of
 structural damage to the conduction system, such as
from MI, fibrosis, or necrosis. Many patients have a
pre-existing left bundle branch or bifascicular block,
and the remaining fascicle intermittently fails to
conduct causing the second degree AV block.
● Because the defect occurs below the AV node and often
times distal to the His Bundle, it produces wide,
bizarre-appearing QRS complexes. In the remaining
cases, the defect is located within the Bundle of His,
resulting in the normal, narrow QRS complexes. There
can be a fixed P:QRS relationship (e.g., 2:1, 3:1) or no
pattern at all.
● Causes. Common causes of second-degree Mobitz type
2 AV block include anterior MI, causing septal
infarction with necrosis of the bundle branches. Other
causes include idiopathic fibrosis of the conducting
system, autoimmune (e.g., systemic sclerosis or
systemic lupus erythematosus) or inflammatory (e.g.,
myocarditis, Lyme disease, or rheumatic fever)
conditions, infiltrative myocardial disease
(hemochromatosis, sarcoidosis, or amyloidosis),
electrolyte imbalance (e.g., hyperkalemia),
medication-induced (e.g., beta-blockers,
non-dihydropyridine calcium channel blockers,
digitalis, adenosine, or amiodarone), or status
post-cardiac surgery (e.g., mitral valve repair).
● Clinical significance. Mobitz type 2 AV block can be
associated with severe bradycardia and hemodynamic
instability. It has a greater risk of progressing to
third-degree (complete) heart block or asystole.
Because the onset of dropped beats can occur abruptly
and unexpectedly, hemodynamic instability and the
consequential syncope and potential sudden cardiac
death can occur at any moment. Thus, patients require a
permanent pacemaker. While Mobitz type 1 can
improve with atropine, giving atropine in the setting of
Mobitz type 2 can worsen the block and increase the
risk of complete heart block or asystole.
Note in cases in which every other QRS complex is dropped, there
are never two consecutive PR intervals. Therefore, there is not
enough information to evaluate the PR interval to further classify it
as either second-degree Mobitz type 1 (Wenckebach) or Mobitz
type 2 AV block. The site of block is also indeterminate.
● Mechanism. Third-degree heart block is the end result
of progressively worsening second-degree AV block. It
can be from Mobitz type 1 if the AV nodal cells fatigue
to a point in which they no longer conduct impulses
through to the ventricles; or from Mobitz type 2, where
there can be an abrupt and complete conduction failure
throughout the His-Purkinje system. Because
third-degree heart block can occur above or below the
AV node, two different rhythms can take over. If it
occurs above or at the crest of the AV node, a junctional
rhythm will take over and drive the ventricles. The
resulting QRS complexes will be narrow and occur at
the intrinsic rate of the AV node (40 to 55
beats/minute). Whereas if the block occurs below the
AV node, a ventricular pacemaker must take over. In
such cases, the QRS complexes will be wide and at the
intrinsic rate of the ventricular pacemaker (20 to 40
beats/minute).
● Causes. Complete heart block is often the result of the
same causes as Mobitz type 1 and Mobitz type 2. Other
causes include inferior MI, degeneration of the
conduction system, and AV-nodal blocking agents such
as beta-blockers, non-dihydropyridine calcium channel
blockers, adenosine, digitalis, and amiodarone.
● Clinical significance. Patients with complete heart
block are at great risk of developing asystole,
ventricular tachycardia, and sudden cardiac death.
Insertion of a permanent pacemaker is required.
AV dissociation. AV dissociation occurs when there is no
relationship between the P waves and QRS complexes; however,
the QRS complexes occur at a faster rate than the P rate. Unlike
AV block, in which failure of an intrinsically more rapid atrial
rhythm to conduct antegrade and supersede a slower ventricular
rhythm is abnormal, failure of a rapid ventricular rhythm to
conduct retrograde and supersede a slower atrial rhythm does not
necessarily imply damage to the conducting system. In fact, AV
dissociation with more rapid ventricular rates is typically due to
unusual ventricular irritability.

Second degree, high-grade. High-grade AV block is a form of

second-degree (incomplete) heart block that can commonly be
confused with third-degree (complete) heart block. It occurs when
there are two or more consecutively blocked P waves. This
conduction disturbance can be particularly dangerous as it can
progress to complete heart block. The anatomic region involved is
almost always below the AV node as in Mobitz type 2. The P:QRS
is 3:1 or higher and the ventricular rate is typically very slow. What
differentiates high-grade AV block from the third-degree
(complete) heart block is that there remains some relationship
between the P waves and QRS complexes. In other words, there is
still some AV conduction taking place.

Third-degree (complete). In third-degree, or complete, heart

block there is an absence of AV nodal conduction, and the P waves
are never related to the QRS complexes. In other words, the
supraventricular impulses generated do not conduct to the
ventricles. Instead, if ventricular conduction occurs, it is
maintained by a junctional or ventricular escape rhythm. There is a
complete dissociation between the atria and ventricles. The atria
and ventricles conduct independent of each other. The P waves
(atrial activity) are said to “march through” the QRS complexes at
their regular, faster rate. The QRS complexes (ventricular activity)
also occur at a regular, but slower rate. There are two independent
rhythms occurring simultaneously.