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Four: Two sinoatrial block due to hyperkalemia with electrotonic influence of AV junctional impulses upon the sinus node
168
Journal of Electrocardiology
Vol. 26 No. 2 April 1993 R
NA Distal His bundle Proximal RBB Middle RBB Distal RBB Posterior radiation of LBB* Anterior radiation of LBB* Ventricular septum* No. of cases
LAD
-
8 1 1
6 1 7
2 9 1 10
rSR’ RAD
NA
LAD
2 4
3 1 15 2 1 1 3 21
1 1 5 2 2 9 2 9
4 4 1 6
rSR’ RAD 6 4 4 2 6
QR
K
NA
-
1 1 3
1 3
1 1 2 2
LAD -
RAD -
4 4 4
1 1 1
NA = normal axis; LAD = left axis; RAD = right or northwest axis; RBB = right bundle branch; LBB = left bundle branch. *LBB and ventricular septem lesions are double counted to RBB lesion.
method for the conduction system study. The results are shown above. The variations of the QRSvr morphology in an RBBB depends on the interrupted sites in the right bundle branch, that is, Rvr corresponds with a proximal lesion to the first septal fascicle of the right bundle branch, which originates as a rule from the middle right bundle branch, and rSR’ corresponds with a distal lesion to the fascicle in the normal QRS axis group. Associated left axis deviation with RBBB modifies the rule by a proximal shift of the interrupted sites in the right bundle branch through a delay in conduction at the left side of the septum, whereas a loss of myocytes in the upper septum lowers the initial rvl. Therefore, knowledge of the QRSvr morphology helps to diagnose the interrupted site in the right bundle branch with fairly good accuracy.
Four:Two Sinoatrial Block Due to Hyperkalemia With Electrotonic Influence of AV Junctional Impulses Upon the Sinus Node G. Satullo, G. Sergi, G. Busa, A. Coglitore, L. Cavallaro, G. Oreto, Servizio di Cardiologia, Ospedale Papardo, Messina, Italy This presentation reflects a rather uncommon manifestation of hyperkalemia, namely the influence exerted by an atrioventricular (AV) junctional rhythm upon the sinoatrial node in the absence of any manifest atria1 activation. In a patient with Addison’s disease and hyperkalemia manifested with type II sinoatrial block with 4: 2 conduction ratio the following occurred: the sinus P waves occurred in pairs and the pairs were separated from each other by pauses with a duration that was approximately 3 times the basic sinus cycle length. At the end of the long pauses occasioned by the block, AV junctional escape beats occurred, but the AV junctional impulses did not result in retrograde atria1 activation. Calculation demonstrated a relationship between the duration of the escape intervals and the sinus cycle length; namely short escape intervals (~2.2 seconds)
were associated with relatively short sinus cycles. This suggested an influence of AV junctional impulses on the sinus node. And since no manifest retrograde atria1 activation occurred, the influence of the AV junctional rhythm upon the sinus node was probably mediated by conduction of the impulses across the crista terminalis, with further electrotonic influence on the sinus pacemaker cells. Laboratory research has demonstrated that AV junctional impulses may indeed affect the sinus node without the occurrence of any manifest atria1 depolarization (Sanchis J: J Cardiovasc Electrophysiol 1: 3 18, 1990). This is the opposite of the so-called sinoventricular conduction, namely the direct transmission of the sinus impulse to the ventricles without depolarization of the entire atria1 mass.
Comparison of the Diagnostic Information of Exercise 12-Lead ECG and Body Surface Map Measurements Gy. Kozmann, I. Preda, I. Balogh, Research Institute for Material Science and Postgraduate Medical University, Budapest, Hungary The extent and basic mechanism of the diagnostic information loss of the 12-lead exercise ECG (XECG) measurements with respect to exercise body surface mapping (XBSPM) was studied in a population of 50 coronary artery disease patients. Exercise body surface mapping data were taken by the 32 electrode limited lead XBSPM system at the peak effort of a symptom or submaximal heart rate limited exercise test. The complete thoracic surface potential distribution was estimated by the method suggested by R. L. Lux. The exercise induced XBSPM response was characterized by the amplitude and the anatomic location of the maximal ST depression measured 60 ms from the J point. From the same set of data, the signals of the 12-lead array were selected and similar criteria were used to characterize the maximal XECG ST response observable. The maximal depression measured by XBSPM was plotted against the maximal ST depression detected by the 12-lead system.
Journal of Electrocardiology
Vol. 26 No. 2 April 1993 R
NA Distal His bundle Proximal RBB Middle RBB Distal RBB Posterior radiation of LBB* Anterior radiation of LBB* Ventricular septum* No. of cases
LAD
-
8 1 1
6 1 7
2 9 1 10
rSR’ RAD
NA
LAD
2 4
3 1 15 2 1 1 3 21
1 1 5 2 2 9 2 9
4 4 1 6
rSR’ RAD 6 4 4 2 6
QR
K
NA
-
1 1 3
1 3
1 1 2 2
LAD -
RAD -
4 4 4
1 1 1
NA = normal axis; LAD = left axis; RAD = right or northwest axis; RBB = right bundle branch; LBB = left bundle branch. *LBB and ventricular septem lesions are double counted to RBB lesion.
method for the conduction system study. The results are shown above. The variations of the QRSvr morphology in an RBBB depends on the interrupted sites in the right bundle branch, that is, Rvr corresponds with a proximal lesion to the first septal fascicle of the right bundle branch, which originates as a rule from the middle right bundle branch, and rSR’ corresponds with a distal lesion to the fascicle in the normal QRS axis group. Associated left axis deviation with RBBB modifies the rule by a proximal shift of the interrupted sites in the right bundle branch through a delay in conduction at the left side of the septum, whereas a loss of myocytes in the upper septum lowers the initial rvl. Therefore, knowledge of the QRSvr morphology helps to diagnose the interrupted site in the right bundle branch with fairly good accuracy.
Four:Two Sinoatrial Block Due to Hyperkalemia With Electrotonic Influence of AV Junctional Impulses Upon the Sinus Node G. Satullo, G. Sergi, G. Busa, A. Coglitore, L. Cavallaro, G. Oreto, Servizio di Cardiologia, Ospedale Papardo, Messina, Italy This presentation reflects a rather uncommon manifestation of hyperkalemia, namely the influence exerted by an atrioventricular (AV) junctional rhythm upon the sinoatrial node in the absence of any manifest atria1 activation. In a patient with Addison’s disease and hyperkalemia manifested with type II sinoatrial block with 4: 2 conduction ratio the following occurred: the sinus P waves occurred in pairs and the pairs were separated from each other by pauses with a duration that was approximately 3 times the basic sinus cycle length. At the end of the long pauses occasioned by the block, AV junctional escape beats occurred, but the AV junctional impulses did not result in retrograde atria1 activation. Calculation demonstrated a relationship between the duration of the escape intervals and the sinus cycle length; namely short escape intervals (~2.2 seconds)
were associated with relatively short sinus cycles. This suggested an influence of AV junctional impulses on the sinus node. And since no manifest retrograde atria1 activation occurred, the influence of the AV junctional rhythm upon the sinus node was probably mediated by conduction of the impulses across the crista terminalis, with further electrotonic influence on the sinus pacemaker cells. Laboratory research has demonstrated that AV junctional impulses may indeed affect the sinus node without the occurrence of any manifest atria1 depolarization (Sanchis J: J Cardiovasc Electrophysiol 1: 3 18, 1990). This is the opposite of the so-called sinoventricular conduction, namely the direct transmission of the sinus impulse to the ventricles without depolarization of the entire atria1 mass.
Comparison of the Diagnostic Information of Exercise 12-Lead ECG and Body Surface Map Measurements Gy. Kozmann, I. Preda, I. Balogh, Research Institute for Material Science and Postgraduate Medical University, Budapest, Hungary The extent and basic mechanism of the diagnostic information loss of the 12-lead exercise ECG (XECG) measurements with respect to exercise body surface mapping (XBSPM) was studied in a population of 50 coronary artery disease patients. Exercise body surface mapping data were taken by the 32 electrode limited lead XBSPM system at the peak effort of a symptom or submaximal heart rate limited exercise test. The complete thoracic surface potential distribution was estimated by the method suggested by R. L. Lux. The exercise induced XBSPM response was characterized by the amplitude and the anatomic location of the maximal ST depression measured 60 ms from the J point. From the same set of data, the signals of the 12-lead array were selected and similar criteria were used to characterize the maximal XECG ST response observable. The maximal depression measured by XBSPM was plotted against the maximal ST depression detected by the 12-lead system.