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Unstable intraventricular block
422
dMERICAN
The ventricular showed configurations showed S-T segment configuration in the damage.
HWRT
.JOUWi;,\T:
extrasystoles which appeared spontaneously after coronary occlusion which indicated that they originated within the damaged area. They changes which were the same as in the supraventricular complexes. Their electrocardiogram may therefore serve RR a. localizing sign in myocardial bUTHORS.
Sabathie, L. G., Gaapary, F. V., and Rojas, argent. de Bardiol. 11: 297, 1945. Fourteen cases of electrocardiographically. for these cases, classifying
R. A.:
Unstable
Intraventricular
nonpermanent intraventricular block were The denomination of ( i unstable ’ ’ intraventricular them as transitory or intermittent according
Block.
Rev.
studied clinically and block was adopted to the circumstances.
In the mechanism of production of these blocks the modificat,ion of the refractory periods in both branches of the His bundle are of fundamental importance; the role of the precipitating factors, such as increased heart rate and vagal action, is also pointed out. -4I'THORS.
Leys,
D. G.:
Heart
The evidence patient had severe pulse was reported jerks without other
Block
Following
Diphtheria.
Brit.
Heart
J. 7: 5i,
1945.
that this case of complete heart block was due to diphtheria is: (1) the diphtheria with neuritis at the age of 10 years; (2) subsequently a slow at the age of 22 years; and (3) she has complete absence of all tendon evidence of nervous syst,em disease. AUTHOR.
abmez, out
B. H., and Evidence
YBpex, C. G.: Pennauent of Organic Heart Disease.
Auricular Fibrillation Arch. Inst. Cardiol.
in Two Brothers WithMex. 14: 251, 1945.
The authors present two cases of auricular fibrillation in brothers without cardiac injury and without other evident cause. In other similar observations there also are no explanations to justify the alteration of the cardiac rhythm.
apparent published,
AUTHORS.
Pruitt,
R. D., Barnes, A. R., Essex, Lesions in the Deeper Layers
H. E.: Electrocardiographic of the Myocardium. Am.
Changes Associated With J. M. SC. 210: 100, 1945.
Myocardial injuries were produced in dogs by mechanical means. Damage to the endocardium and deeper layers of the myocardium of the apical portion of the left ventricle was attended by certain changes in the configuration of the QRS complex in a precordial lead designated apical IVR. Most constant among these changes was a reduction in the height of the R wave. The development of a Q wave or a notch low on the upstroke of the R wave were alternative types of change. These changes in the QRS complex might be derived from: (I) injury to, or destruction of, the myocardial fibers adjacent to the endocardium; or (2) damage to Purkinje’s network or the larger subdivisions of the left branch of the bundle of His. Although in each of the twenty-two experiments under analysis there was accomplished an extensive destruction of those tissues in which portions of Purkinje’s system are supposed to lie, in twenty experiments the width of the QRS complex remained unchanged. The speed at which the excitatory impulse was propagated apparently remained essentially unchanged, even though its course, as indicated by the form of the QRS complex, was altered. Also, a lesion high on the septum apparently not only is attended by a widening of the QRS complex, but also it is the only lesion likely to produce this effect. Our results indicate that surface lesions exert a dominant in&ence on the level of the RS-T segment. We have suggested that this circumstance may prevail not because the traumatized subendoeardial fibers fail to produce currents of injury, but because the resulting injury potentials are masked by the normal action currents arising in the uninjured superficial fibers in response to the excitatory process. Changes in the T wave following injuries to the deeper layers of the myocardium The most frequently recurring alternation was an inversion of the T wave were inconstant. in a lead designated apical IVR. AUTHORS,
dMERICAN
The ventricular showed configurations showed S-T segment configuration in the damage.
HWRT
.JOUWi;,\T:
extrasystoles which appeared spontaneously after coronary occlusion which indicated that they originated within the damaged area. They changes which were the same as in the supraventricular complexes. Their electrocardiogram may therefore serve RR a. localizing sign in myocardial bUTHORS.
Sabathie, L. G., Gaapary, F. V., and Rojas, argent. de Bardiol. 11: 297, 1945. Fourteen cases of electrocardiographically. for these cases, classifying
R. A.:
Unstable
Intraventricular
nonpermanent intraventricular block were The denomination of ( i unstable ’ ’ intraventricular them as transitory or intermittent according
Block.
Rev.
studied clinically and block was adopted to the circumstances.
In the mechanism of production of these blocks the modificat,ion of the refractory periods in both branches of the His bundle are of fundamental importance; the role of the precipitating factors, such as increased heart rate and vagal action, is also pointed out. -4I'THORS.
Leys,
D. G.:
Heart
The evidence patient had severe pulse was reported jerks without other
Block
Following
Diphtheria.
Brit.
Heart
J. 7: 5i,
1945.
that this case of complete heart block was due to diphtheria is: (1) the diphtheria with neuritis at the age of 10 years; (2) subsequently a slow at the age of 22 years; and (3) she has complete absence of all tendon evidence of nervous syst,em disease. AUTHOR.
abmez, out
B. H., and Evidence
YBpex, C. G.: Pennauent of Organic Heart Disease.
Auricular Fibrillation Arch. Inst. Cardiol.
in Two Brothers WithMex. 14: 251, 1945.
The authors present two cases of auricular fibrillation in brothers without cardiac injury and without other evident cause. In other similar observations there also are no explanations to justify the alteration of the cardiac rhythm.
apparent published,
AUTHORS.
Pruitt,
R. D., Barnes, A. R., Essex, Lesions in the Deeper Layers
H. E.: Electrocardiographic of the Myocardium. Am.
Changes Associated With J. M. SC. 210: 100, 1945.
Myocardial injuries were produced in dogs by mechanical means. Damage to the endocardium and deeper layers of the myocardium of the apical portion of the left ventricle was attended by certain changes in the configuration of the QRS complex in a precordial lead designated apical IVR. Most constant among these changes was a reduction in the height of the R wave. The development of a Q wave or a notch low on the upstroke of the R wave were alternative types of change. These changes in the QRS complex might be derived from: (I) injury to, or destruction of, the myocardial fibers adjacent to the endocardium; or (2) damage to Purkinje’s network or the larger subdivisions of the left branch of the bundle of His. Although in each of the twenty-two experiments under analysis there was accomplished an extensive destruction of those tissues in which portions of Purkinje’s system are supposed to lie, in twenty experiments the width of the QRS complex remained unchanged. The speed at which the excitatory impulse was propagated apparently remained essentially unchanged, even though its course, as indicated by the form of the QRS complex, was altered. Also, a lesion high on the septum apparently not only is attended by a widening of the QRS complex, but also it is the only lesion likely to produce this effect. Our results indicate that surface lesions exert a dominant in&ence on the level of the RS-T segment. We have suggested that this circumstance may prevail not because the traumatized subendoeardial fibers fail to produce currents of injury, but because the resulting injury potentials are masked by the normal action currents arising in the uninjured superficial fibers in response to the excitatory process. Changes in the T wave following injuries to the deeper layers of the myocardium The most frequently recurring alternation was an inversion of the T wave were inconstant. in a lead designated apical IVR. AUTHORS,