Biomedical subjects
Publications and source records attributed to G Oreto.
This presentation reflects an atypical manifestation of sinoatrial block in a patient with chronic renal failure and hyperkalemia (7.8 mEq/L). An allorhythmic distribution of P-P intervals permits the interpretation of sinoatrial block complicated by sinoatrial reciprocation.
The retriggerable Refractory Period (RP) is an anti-interference device that causes prolongation of the RP in the presence of rapid false signals. The device starts functioning when a suprathreshold impulse manifests during the second half of the RP of the pacemaker; in such a case the RP itself is retriggered, i.e., re-starts from the moment in which the retrigger occurs. As a consequence, the time during which the pacer cannot be recycled is prolonged. We report a case of unusual pseudo-malfunction caused by the retriggerable RP observed in a patient paced with a Lit 222 Sorin VVI pacemaker. Spontaneous QRS complexes coupled up to 480 ms appeared as not senses, i.e. did not reset the pacemaker, whereas complexes occurring at 510 ms or more from the spike provoked a normal recycling, and complexes coupled at 490-500 ms resulted in partial recycling. This pattern has been interpreted assuming that a spurious signal (probably an afterpotential) occurs shortly after the paced stimulus. Such a signal falls in the retriggerable RP, resulting in prolongation of the RP. Spontaneous QRS, thus, cannot be sensed until 480 ms from the paced impulse. The chest wall stimulation has clarified the principles governing the functioning of the retriggerable RP. When the RP is retriggered three times in the course of a single pacemaker cycle, the pacer varies its mode of functioning, being the pacing rate increased to a value identical to the magnet rate. Furthermore, the RP is extremely prolonged, occupying the 90% of the pacing interval; only impulses occurring during the last 80 ms, thus, are able to reset the PM.(ABSTRACT TRUNCATED AT 250 WORDS)
A patient with a malfunctioning pacemaker due to lead insulation defect is reported. High voltage stimuli were always effective, while when the pulse amplitude was reduced to 3.8 volt stimuli were uneffective except when occurring after extremely long asystolic pauses. An advanced exit block (up to 7:1) thus occurred. Late lowering of the myocardial threshold of excitability could be explained by slow spontaneous diastolic depolarization occurring in myocardial fibers surrounding the tip of the electrode.
We report an example of ventricular fusion of a sinus impulse conducted with bundle branch block with an ectopic impulse arising on the ipsilateral side of the blocked bundle branch. The manifestation simulates the normalization which occurs during the relatively slow phase of a tachycardia dependent left bundle branch block.
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We have observed a case of ventricular parasystole in which the ectopic beats occurred often in couplets. The analysis of the interectopic intervals suggests that the first beat of the couplet is parasystolic in origin, whereas the second one is due to a re-entry which takes place in the myocardium surrounding the parasystolic focus. Moreover, our observations lead us to speculate that an occasional supraventricular beat could cause an exit block of the parasystolic focus through a concealed re-entry.
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We report a case of ventricular parasystole in which the long interectopic intervals are always less than a multiple of the short interectopic intervals. Assuming a regular ectopic discharge, the above said phenomenon could theoretically be due to relative prolongation of the short interectopic intervals caused by delayed ectopic-ventricular conduction of the second consecutive conducted impulse (a Wenckebach-like phenomenon). Nevertheless, this hypothesis may be ruled out in this case by the analysis of a long tracing. The unusual relationship between the interectopic intervals may be explained assuming the modulation of the parasystolic activity by sinus beats. Experimental work has shown that despite the protection (or entrance) block, the sinus or dominant rhythm may affect the automaticity of a parasystolic focus by means of electrotonic influence. It has been pointed out that sinus impulses falling in the first part of the ectopic cycle delay the next ectopic discharge, while relatively late sinus beats (falling in the last 30-40% of the ectopic cycle) are able to anticipate the delivery of the parasystolic impulse. The phenomenon of modulation is marked by a characteristic biphasic phase-response curve. In the reported case a phase-response curve has been obtained, which explains the parasystolic cycle variations according to the phase of the cycle in which the sinus beats fall. The obtained curve is quite similar to those observed experimentally, therefore the diagnosis of modulated parasystole appears to be very likely.(ABSTRACT TRUNCATED AT 250 WORDS)
We report a case of oversensing observed in a patient with a VVI pacemaker. This phenomenon was provoked by an inactive lead whose tip was in close apposition with the tip of the stimulating electrode. Potentials of large amplitude arose from the contact between these two catheters, causing pacer suppression. These false signals have been revealed both by intracavitary recordings and by standard ECG. In the latter they assumed a P-like shape. Withdrawal of the temporary lead restored normal pacing.
We have analyzed an electrocardiogram showing many unifocal ventricular extrasystoles with wide variations of the coupling intervals. Ventricular bigeminy was frequent but in many instances more than one sinus beat occurred between two consecutive extrasystoles. In such a case the intervening sinus beats occurred indifferently both in odd and even numbers. Moreover, extrasystoles preceded by an even number of sinus beats had a relatively long coupling interval whereas extrasystoles that followed and odd number of sinus beats showed shorter coupling intervals. An opposite pattern of the coupling interval was observed with the extrasystoles that followed an interpolated premature ventricular depolarization. In such a case the coupling interval was long after an odd number of sinus beats and vice versa. This mechanism may be interpreted as due to concealed ventricular bigeminy caused by a ventricular ectopic focus which is surrounded by two different zones of block: a proximal zone of 2:1 block, and a distal one in which the block occurs irregularly. Unlike what appears in typical concealed bigeminy, characterized by only odd numbers of sinus beats between consecutive extrasystoles the intervening sinus complexes are indifferently in odd and even numbers. The constant relationship between the coupling interval and the number (odd or even) of sinus beats by which the extrasystole is preceded, allows us to recognize the presence of an atypical form of concealed bigeminy.
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We describe the electrocardiogram of a patient who had a chaotic atrial rhythm with partial A-V block. Only the late P waves (R-P greater than 1 sec.), and the early ones (with one R-P interval between 44 and 52 hundredths of a second) were conducted to the ventricle. On the contrary, no P waves with coupling intervals between 52 and 100 hundredths of a second reached the ventricles. Careful analysis of the tracing showed that the conduction of the early P waves could not depend upon the atrial pacemaker site, or upon concealed conduction of preceding atrial impulses. The existence of a "gap" phenomenon although unlikely, could not be excluded. Supernormal A-V conduction, or early diastolic decrease of the vagal tone due to hemodynamic mechanism could be responsible for the early ventricular captures observed in this patient.
This case is an example of ventricular parasystolic tachycardia associated with variable expressions of ectopic-ventricular (E-V) exit block. The exit block manifested with 2:1, 3:2, 4:3 and higher ratios of E-V conductions, interspaced with periods of 1:1 conduction. Concealed E-V conduction of the ectopic impulse could also be deduced.
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This report concerns a patient affected by Sick Sinus Syndrome, whose ECG showed many episodes of second degree sino-atrial (SA) block. The long pause was always less than twice the normal PP interval, but the diagnostic criteria for Wenckebach SA block were not met. The atrial cycle, indeed, did not shorten progressively before the block. Furthermore even Schamroth's diagram, obtained by plotting the length of each PP cycle against the length of the following cycle, was not suggestive of Wenckebach SA block. In type 2 (Mobitz) second degree SA block, the long pause may appear slightly shortened if first degree SA block is also present. In such a situation the SA conduction time is longer than normal, but when a sinus impulse is blocked, i.e. does not reach the atrium, the following sinus impulse may travel the SA junction in a shorter time. The first P wave after the block thus occurs earlier, thereby reducing the duration of the long pause. By the same mechanism, the PP cycle that follows the long pause appears longer than expected. Both these phenomena have been observed in the reported case. First degree SA block appears to be likely when the standard ECG shows the following features: 1) the 2nd degree SA block is not classifiable as type 1 (Wenckebach); 2) the pause that includes the blocked sinus impulse measures always less than twice the sinus cycle; 3) the PP interval that follows the prolonged pause is slightly longer than the one that precedes the pause.
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