Case: 25 year old female having a diagnosis of cyanotic congenital
heart disease presented with acute lower respiratory tract infection. On
examination she had central cyanosis, clubbing, kyphoscoliosis, dextrocardia,
situs inversus, pulmonary stenosis, ventricular septal defect, double outlet
right ventricle, right ventricular hypertrophy and transposition of great
arteries.
Fig-1: ECG of a 25 year old
female having dextrocardia, situs inversus and congenital cyanotic heart disease.
ECG showed tachycardia
(ventricular rate 100 beats/minute), inverted p wave in all leads except aVR, V1
and V2, normal PR interval, narrow QRS complex and T wave inversion in all
leads. These ECG findings are in favour of accelerated junctional rhythm.
Answer:
Accelerated junctional rhythm
Discussion:
Accelerated junctional rhythm
(AJR) occurs when the rate of an AV junctional pacemaker exceeds that of the
sinus node. This situation arises when there is increased automaticity in the
AV node coupled with decreased automaticity in the sinus node. Causes of AJR
are digoxin toxicity, use of beta-agonists, e.g. isoprenaline, adrenaline, Sick
sinus syndrome, myocardial ischaemia, myocarditis (acute rheumatic fever, lyme
disease, Diphtheria) and metabolic states with increased adrenergic tone.
Certain drugs which can cause bradycardia such as beta blockers, calcium
channel blockers and antiarrhythmic agents can also induce AJR.
Junctional rhythms are classified
by their rate as 1) Junctional Escape Rhythm: 40-60 bpm 2) Accelerated
Junctional Rhythm: 60-100 bpm and 3) Junctional Tachycardia: > 100 bpm.
They may also be classified by
aetiology as automatic Junctional Rhythms (e.g. AJR) = Due to enhanced
automaticity in AV nodal cells or re-entrant Junctional Rhythms (e.g. AVNRT), due
to re-entrant loop involving AV node.
Fig-2: Example of an
accelerated junctional rhythm (courtesy ECG library)
ECG Features of AJR
·
Narrow complex rhythm; QRS duration <
120ms (unless pre-existing bundle branch block or rate-related aberrant
conduction).
·
Ventricular rate usually 60 – 100 bpm.
·
Retrograde P waves may be present and
can appear before, during or after the QRS complex.
·
Retrograde P waves are usually inverted
in the inferior leads (II, III, aVF), upright in aVR + V1.
·
AV dissociation may be present with the
ventricular rate usually greater than the atrial rate.
·
There may be associated ECG features of
digoxin effect or digoxin toxicity.
Periods
of junctional rhythm are not necessarily associated with an increase in
mortality. If an obvious cause is present, such as complete heart block or sick
sinus syndrome, then the morbidity or mortality is directly related to that and
not to the junctional rhythm mechanism, which is serving as a "backup
rhythm" during the periods of bradycardia. Accelerated junctional rhythms
may be a sign of digitalis toxicity.
ECG
features may be mistaken for that of dextrocardia as this patient is having
dextrocardia and situs inversus. In dextrocardia inverted P wave is seen only
in Lead-1 and upright P in aVR. Other features are right axis deviation, positive
QRS complexes (with upright P and T waves) in aVR, inversion of all complexes (global
negativity) in Lead I and absent R-wave progression in the chest leads.
Complications
Complications
of junctional rhythm are usually limited to symptoms such as dizziness,
dyspnea, or presyncope. Exacerbation of cardiac comorbidities, such as
congestive heart failure and rate-related cardiac ischemia, may occur.
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