British Heart Journal, 1976, 38, 1363-1366.

Pseudo second degree atrioventricularblock with bradycardiaSuccessful treatment with quinidine

Raja W. Dhurandhar, F. J. Valen, and John PhillipsFrom the Departments of Cardiology of Touro Infirmary, Veterans Administration Hospital, and TulaneUniversity School of Medicine, New Orleans, Louisiana, U.S.A.

Pseudo second degree atrioventricular block resulting from blocked His premature beats was successfullytreated with quinidine. The diagnosis was proved by His bundle electrogram which showed both blocked andconducted His premature beats. The blocked His prematures produced second degree atrioventricular blockby making the atrioventricular junction refractory. Quinidine abolished both conducted and blocked Hisextrasystoles. There has been no recurrence of arrhythmia during a one-year follow-up.

Langendorf and Mehlman (1947) suggested thatnon-conducted junctional premature beats mightproduce second degree atrioventricular block byblocking the sinus impulse following the prematurebeat. They suggested that the block was caused byjunctional extrasystoles which were concealedbecause of both anterograde and retrograde block.Rosen, Rahimtoola, and Gunnar (1970) showed,with His Bundle recordings, second degree atrio-ventricular block resulting from blocked His pre-mature beats. Since there was no intrinsic abnor-mality ofthe atrioventricular conduction, they calledthe resulting block, 'pseudo-block'.We report here a patient with bradycardia re-

sulting from pseudo second degree atrioventricularblock caused by blocked His premature beats: hewas successfully treated with quinidine.

Case report

A 54-year-old man reported to the hospital com-

plaining of tiredness and weakness. There was ahistory of heavy alcoholic intake, but the patienthad discontinued drinking a few months before.There was no history of palpitation or dizziness.Physical examination revealed an irregular pulse,with a basic rate of about 70 beats a minute but withperiodic slowing to almost 30 beats a minute. Theblood pressure was 120/80 mmHg (16-0/10-6 kPa).There was no evidence of heart failure. The heartsize was normal, no gallop rhythm was heard, and

there were no murmurs. The remainder of thephysical examination was normal. The electro-cardiogram showed supraventricular prematurebeats with aberration and episodes of apparentMobitz type II block (Fig. la). Apart from thearrhythmia, the electrocardiogram was normal.The patient was admitted for further evaluation andtreatment of the arrhythmia. Initially he was giventincture of belladonna, 1 ml, four times a day. Thepremature beats as well as periods of apparentsecond degree atrioventricular block were unin-fluenced by this therapy. His bundle recordingswere then made to clarify the nature of thearrhythmia.

Electrophysiological studiesThe His bundle electrogram was recorded simul-taneously with lead II of the surface electrocardio-gram at a paper speed of 100 mm/s. Several hundredcardiac cycles were analysed. The majority of thebeats recorded were sinus beats, with normal AHand HV intervals. The QRS complex of these sinusbeats was normal in duration. Premature beats oc-curred at an average frequency of 3 to 5 per minute.These beats could be separated into two types ac-cording to the behaviour of the QRS complex.In the first type, there was a minor change in QRSmorphology but without significant increase inits duration. The second type showed wide QRScomplexes resembling ventricular ectopic beats.The simultaneous His electrogram, however,

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Pseudo second degree AV block with bradycardia 1365

showed a consistent presence of a His spike pre-ceding the V deflection in both types of prematurebeats localizing their origin to the His bundle(Fig. Ic, d). These two types ofpremature beats wereHis extrasystoles, one type with slight and theother with more aberrant ventricular conduction.Periods of second degree atrioventricular block withnon-conducted normal P waves occurred atfrequency of about 10 a minute. The surfaceelectrocardiogram showed that the block was typeII in nature and occurred without a change in PRinterval of the preceding sinus beats. At no timewas more than one beat blocked in succession. Hisbundle recordings during these periods showedspikes preceding the blocked A deflection (Fig. lb).The latter corresponded to the non-conductednormal P waves. As the patient had conducted Hispremature beats throughout the recording, it isreasonable to conclude that these spikes representedHis premature beats with both retrograde andanterograde block. These spikes will be designatedas H'. H'-A interval varied between 94 and 304 mswith an average interval of 212 ms. Every blockedsinus beat was preceded by H'. The behaviour oftheHis premature beat was determined primarily by theinterval between the H spike of the preceding sinusbeat and the H'. The His extrasystoles with shortH-H' intervals were blocked, while those with longH-H' intervals were conducted with slight aberra-tion. The H-H' interval of the premature beats withgreater degree of aberration fell between these 2groups. These three types of His premature beatscould clearly be separated into three groups, de-termined by the length of the H-H' interval (Fig.2).

Hospital courseQuinidine sulphate, 200 mg, four times a day wasgiven in an attempt to suppress the premature beats.Within 24 hours, the premature beats as well asperiods of pseudo atrioventricular block were com-pletely abolished and did not recur during a seven-day period of observation with continuous electro-cardiographic monitoring (Fig. 3). Quinidine wasthen stopped, and within 12 hours the prematurebeats as well as the pseudo second degree atrio-ventricular block reappeared. The arrhythmia con-tinued for 36 hours until quinidine therapy was re-started, at which time the arrhythmia again dis-appeared. During a one-year follow-up underquinidine therapy, there has been no recurrence ofthe arrhythmia.

Discussion

This case is an interesting example of successful

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F I G 2 The effect of timing of H' on conduction tothe ventricles. Abscissa: H-H' intervals; Ordinate:preceding H-H intervals Note that His prematurebeats with short H-H' interval are blocked while thosewith long H-H' interval are conducted with slightaberration. His prematures with obvious aberrationfall in between these two groups. The preceding H-Hintervals do not appear to influence the behaviourof the His extrasystoles.

treatment of apparent second degree atrioventricularblock with quinidine, a drug which normally wouldbe considered contraindicated in atrioventricularblock. It is important to recognize the 'pseudo'nature of the block. The diagnosis should be sus-

pected when a patient presents with apparenttype II atrioventricular block with narrow QRScomplexes but who also shows junctional prematurebeats elsewhere in the electrocardiogram. The usual

On quinidine Lead II

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dine therapy was started The premature beats as well

as periods of second degree atrioventricular block are

no longer present.

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settings for atrioventricular block, such as myo-cardial infarction and digitalis toxicity, may not bepresent. The presence of His premature beatsshowing both retrograde and anterograde blockshould be shown by His electrogram before em-barking on a trial of quinidine.

In our patient, the reason for occurrence of Hispremature beats was not clear. They did not appearto be re-entrant beats, as the coupling intervalvaried. The premature beats occurred irregularlyand did not appear to arise from a parasystolic focus.Blocked premature beats may arise from any partof the His-Purkinje system but the presence of con-ducted premature beats preceded by a His spikelocalized their origin to the His bundle. The intervalbetween the H deflection of the preceding sinus beatand the H' determined the conduction of the pre-mature beats to the ventricles. With shorter H-H'intervals the premature beats showed both retro-grade and anterograde block, and consistentlyblocked the following sinus impulse by concealed

conduction within the atrioventricular junction. Wedid not encounter any sinus beats conducted to theventricles with prolonged AH interval following theblocked H', as described by Rosen et al. (1970). Theunique success of quinidine in abolishing thesignificant bradyarrhythmia in this patient elimi-nated the need for implanting a permanent pace-maker.

ReferencesLangendorf, R., and Mehlman, J. S. (1947). Blocked (non-

conducted) A-V nodal premature systoles imitating firstand second degree A-V block. American Heart Journal,34, 500.

Rosen, K. M., Rahimtoola, S. H., and Gunnar, R. M. (1970).Pseudo A-V block secondary to premature nonpropagatedHis bundle depolarizations. Circulation, 42, 367.

Requests for reprints to Dr. R. W. Dhurandhar,Touro Infirmary, 1401 Foucher Street, NewOrleans, Louisiana 70115, U.S.A.

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