bilateral bundle-branch block critical rates in ventricular conduction
TRANSCRIPT
Bilateral bundle-branch block Critical rates in ventricular conduction
Harry Vesell, M.D. Jerome A. &hack, M.D. Oscar Tannenbaum, M.D.
New York, N. I’.
A condition of unstable conduction in the cardiac bundle-branch system at
a critical heart rate is well known. Inci- dence, mechanism, pathology, duration, and some clinical aspects have been dis- cussed previously. 1-6 The purpose of this paper is to describe the occurrence of un- stable conduction at a critical rate in bi- lateral bundle-branch or intraventricular block, with shifts from double to single block and vice versa-“bloc A bascule”7; and to report observations in two cases, one with autopsy findings.
Case reports Case 1. M. P., a 78-year-old white man, was ad-
mitted to Beth Israel Hospital on Feb. 6, 1956, because of intermittent chest pain and shortness of breath which had been present for 1 month. On examination he appeared to be acutely ill, dyspneic, and cyanotic. The heart was markedly enlarged. The heart sounds were faint and irregular. A Grade 2 to 3 (maximum of 6) holosystolic murmur was audible over the area of the aortic valve. The aortic second sound was louder than the pulmonic second sound but not abnormal. The blood pressure was 160/100 mm. Hg. Respirations were 28 per minute. RBles were heard in the right posterolateral lung field. The liver was moderately enlarged and tender. There was bilateral, Grade 4, pitting pretibial edema.
Laboratory data. The venous pressure at the antecubital space was 260 mm. of saline; it rose to 420 mm. on pressure over the right upper quadrant of the abdomen. The circulation time (arm to tongue with Decholin) was 23 seconds. The hemogram and erythrocyte sedimentation rate were normal. The
blood nonprotein nitrogen was 38 mg., serum al- bumin 4.72 Gm., globulin 1.54 Gm., cholesterol 250 mg., esters 176 mg., and total serum bilirubin 1.75 mg. per 100 ml. Alkaline phosphatase was 17.8 Bodansky units, thymol turbidity was 2.2 units, and cephalin flocculation was 2 plus in 48 hours. Serum electrolytes were: sodium 113.8, potassium 3.8, and chlorides 93.5 mEq. per liter. Calcium was 8.8 mg., and phosphorus 3.8 mg., per 100 ml. Pro- thrombin time was 15.2 seconds, with a control of 14.1 seconds. A serologic test for syphilis was nega- tive. An x-ray film of the chest revealed marked enlargement of the cardiac silhouette to the right and left. There was considerable increase in the bronchopulmonary vascular markings, which sug- gested severe pulmonary congestion. S-ray exami- nation of the skull showed definite evidence of Paget’s disease. The diagnosis was hypertensive and arteriosclerotic heart disease, old myocardial infarction, congestive heart failure, Class IVE,” and Paget’s disease. The patient was treated with complete bed rest, a low-sodium diet, digoxin, Mercuhydrin, and sedatives. At the time of the first electrocardiogram, on Feb. 7, 1956, he received 1 mg. of digoxill orally that day, 0.5 mg. twice a
day for the next 2 days, then 0.25 mg. daily. He responded well to treatment, and after 6 weeks was discharged, greatly improved.
Electrocardiograms. The first electrocardiogram (Feb. 7, 1956) (Fig. 1) showed a regular sinus rhythm, P waves of normal configuration, P-R interval of 0.22 second, and QRS of 0.16 second in duration, with large R waves in Lead I and deep S waves in Lead III. R was 30 mm. in Lead aVL, which suggested the presence of left ventricular hypertrophy. An S wave was not present in Lead I but the R-T junction was depressed 2.5 mm., and in Lead III the S-T was elevated 5.0 mm. In Lead V1 the intrinsicoid deflection time, to R’ peak, was 0.12 second; and in Leads aVL and Vc. to R peak, 0.09
From the Cardiographic Laboratory and Mrdical Service, Heth Jsrael Ilospital. New York. S. \ Keceiwd for publication .Iuly 12. 1961.
162
Bduterul BBB: critical rates in ventriculur conduction 163
and 0.10 second, respectively. This evidence of delayed arrival of the activation potential over the free wall of both left and right ventricles laterally with normal activation time in between, 0.055 second in Lead VJ, was indicative of bilateral bundle- branch (intraventricular) block (see later). The cardiac rate was 87 to 89.5 per minute.
In the second electrocardiogram (Feb. 10, 1956) (Fig. 2) the P-R interval was 0.22 to 0.24 second. QRS was slightly less wide, 0.13 to 0.14 second. The appearance of the standard limb leads was similar to that in the previous tracing except for the pres- ence now of prominent slurring in the descending limb of Rr, aild greater displacements of RS-T ii Leads I and III. elevation of 8.0 mm. in Lead III as compared to 5.0 mm. previously. In Lead VI the intrinsicoid deflection time was still long, 0.11 second, but in Leads VY through VG it was reduced to 0.04 to 0.05 second, and a deep S wave appeared in Leads Vs through Vs, 20 mm. in Lead V,. The T waves showed considerable change in shape in Lead VI, and in Leads Vi, and 176 they became up- right although they had been deeply inverted in these two leads in the previous tracing. In Leads V:( and VI, T xvas no longer opposite in direction to the major QRS deflection. The normal intrinsicoid deflection time now in Leads Vj, VC, and ~VL with the reduction of the QRS interval was good evi- dence that the left bundle-branch block had dis- appeared electrocardiographically. The persistently late intrinsicoid deflection in Lead VI indicated that right bundle-branch block \vas still present. The cardiac rate in the second tracing was 77 to 79. It appeared that the slowing from 87 to 89 contri- buted to the change in block, with the critical rate between 79 and 87.
The third, fourth, and fifth electrocardiograms were taken on Feb. 1.5, 23, and 28, 1956. P-R inter- vals were slightly longer but constant at 0.24 to 0.26 second; the QRS duration was 0.15 to 0.16 second. The intrinsiroid deflection time in Lead VI was 0.11 second, and in Lead Vg it was 0.05 second. The heart rates were 65 to 70 per minute. On Oct. 20, 1956, when the electrocardiogram showed only single right bundle-branch block, the right and left pre- cordial leads were recorded simultaneously on a multichannel electrocardiograph. Attempts were made to increase the cardiac rate by Master’s two- step exercise test, amyl nitrite, and atropinc, gr. l/75 subcutaneously. The heart rate did not rise
above 80 per minute, and no change to bilateral bundle-branch block was registered. The peak of R’ in Lead V1 was synchronous \vith the nadir of S in Lead Vg.
The second and final hospitalization was on June 3, 1957. During the previous 14 months he had received digitalis leaf, 0.1 Gm. daily, and occasional injections of Mercuhydrin. He appeared to do quite well until 5 days before this hospitalization, when he developed increasing shortness of breath.
Physical examination revealed a heart rate of 30 and irregular, occasional audible atria1 sounds, blood pressure of 200/100 ~nm. Hg, distended neck veins at 90 degrees, bilateral basal &es, enlarged liver, and slight ankle edema. The laboratory fmd- illgs were not significantly different from those of the previous hospitalization. However, the electro-
cardiogram now showed complete A-\’ block (l:ig. 3) with changes in the configuration of QRS due either to (1) changes in the degree of block in the two bundle branches, if the complete .A-\’ block were produced by alterations in the A-Y Ilode or bundle of His with the ventricular pacemaker aris- ing lower in the main bundle, or to (2 1 a change to an idioventricular pacemaker, if each of the bi- lateral bundle-branch blocks had become complete. On June 8, 1957, 4 days before death, there was a return of A-V conduction, with the P-R 0.24 second and the atrial and ventricular complexes similar to those of Feb. 1.5, 1956 (Fig. 2) except for a slight11 smaller degree of right bundle-branch block.
He failed to respond to the usual cardiac therapy and died, 9 days after admission to the hospital. At necropsy, the heart was enlarged and lveighed 700 grams. The left ventricle was dilated and hyper- trophied, 1.9 cm. in thickness. There was generalized arteriosclerosis; the aorta and pulmonary arteries were affected. The right coronary artcry was larger than the left, and its ostium was surrounded b> atheromatous plaques. :\ conus artery* was present. Xtheromatous and calcific foci with narrowing of the lumina, some eccentric, were present in both right and left coronary arteries and their nlaitl branches. On microscopic examination the myo- cardium of the ventricles, including the inter- ventricular septum, showed many areas of hyper- trophic muscle fibers, areas of fibrosis, and foci of hyalinization.
Case 2. I. T., a 72-year-old white ma11, \vas atl- mitted to the Beth Israel Hospital on May 19, 1957, with a 2-da\ history of recurrent epigastric pain, which occasionally radiated to the left precordial area, and difficulty in breathing. There had been two previous admissions to this hospital, mainI>. for neurological complaints; the diagnosis was cere- bral arteriosclerosis and probable chromophobe adenoma of the pituitary gland, with panhypo- pituitarism and extrasellar extension with invol\-e- ment of the hypothalamus.
Cardiac complaints started in 1951, 6 years prior to the third and final hospitalization, when he suf- fered a myocardial infarction. This was followed bq angina pectoris, dyspnea on slight effort, and inter- mittent ankle edema. For several years he received digitoxin and IXamox.
On examination on May 19, 1957, hc appeared to be chronically il l and was suffering from mild pain in the epigastrium. The heart sounds at the apex seemed to be normal. Triple rhythm was not heard. .\ Grade 3, harsh holosystolic murmur \vas present at the apex, well transmitted over the precordium and to the neck. The pulmonic second sound was accentuated. The blood pressure was 121/76 mm. Hg. Moderately loud coarse r5les were heard throughout both lung fields, more at the bases, on inspiration and expiration, and not cleared by coughing. The liver was slightly enlarged. There was no edema and no tenderness of the cab-es.
Laboratory data. The routine urinalysis and blood coun( were normal. Hematocrit uxs 46 per cent, and the er),throcyte setlilllrlltation rate was 77 111~11. per hour. The blood carbon dioxide was 30.2 \ ol- umes per cent; serum sodium was 134.6, potassium 5.4, and chlorides 94.7 mEq. per liter. The pro-
164 Tlesell, Schack, and Tannenbaunr
Fig. 1. Case 1. Feb. 7, 1956. Nilateral bundle-branch block. Intrinsicoid deflec- tion is late in Leads \-, and \IG but not in I.ead V1. Heart rate of 87 to 89.
thrombin time 1~1~s 13.8 seconds, and transantiiiasc (G.O.T.) was 22 units. Venous pressure in the ante- cubital space was 105 mm. of saline, and the arm- to-tongue circulation time with 1)echolin was 30 seconds. A4 chest film revealed the heart to I-x generally enlarged, with congested lung fields and obliteration of the left costophrenic sinus. The diagnosis was arteriosclerotic heart disease, old myocardial infarction, coronary insufficiency, car- diac failure, especially of the left side, and chroiiic bronchitis.
Electrocavdioguan~s. On July 17, 1953, the elec- trocardiogram showed a pattern of right bundle- branch block and infarction of the anterior and diaphragmatic walls of the left ventricle. The heart rate was 60 to 70 per minute, P-R was 0.15 second, and QRS was 0.12 second. The R in Leads \,.a and 1,‘~ was 27 mm., with the peak 0.065 second from the onset of QRS. Tracings on April 22 (Fig. 4) and April 23, 1957, were at cardiac rates of 90 and 95. P-R was 0.16 and 0.15 second, and QRS was 0.11 second. These two tracings showed features of bi- lateral bundle-branch block in the late intrinsic&l deflections over both right and left precordium (Lead Vi, 0.11 second) (Lead Vo, 0.095 second) but not in between (0.05 second in Leads V? and \‘a); also late in Lead a\‘L (0.09 second). There were broad Q waves. 0.0-L to 0.05 second in I<eads I, 1 I. III, a\‘~., and \‘,; throctgh I’,,, ordinarily- charactrr-
istic of iilfarction of the anterior aiitl posterior walls, and, in the presence of left bundle-branch block, iuggestiv-e of infarction of the interventriculat septum.” I’ The initial notching of the S wave ill lead ;I\.~ and the early deep notching of S in Lead \.i just to the right of the transitional zone are also considered to be signs of septal or anteroseptal iit- f;Lrclion, ii i the presence of left bundle-branch bl0cl;.~~~‘3 Electrocardiograms on hlay 1, 2, and 6. 1957, at cardiac rates of 85, 9-l. and 91 also showed these changes of bilateral bundle-branch block. On June 8, 1957, the heart rate had increased from 98 to 115 per mitiute; P-R was 0.15 second. There tvvits some reduction iti the voltage of QRS in all leads. and its duration was 0.12 second. The Q wa\-es iit Leads I, aVt., and 1:: through Vti were smaller. The intrinsicoid deflection in Lead 1’6 was less delayed& 0.08 as compared to 0.095 second previously. This suggested less block in the left bundle-branch systcni with the faster cardiac rate.
Leads \.i and \‘,; and other leads were takeii simul- taneously on a multichannel recorder on hIay 20 and June 8, 1957. Cardiac rates were 82 and 11.3: P-R was 0.15 and 0.14 second. The onset of QRS was synchronous or 0.005 second, or less, earlier in Lead CT1 than in Lead Vr. The QRS interval was 0.119 to 0.120 second in each lead. QRS configur,i- tioit was rR’ in Lead \‘I. and QRs in Ixad Va. ‘lhe tiinc of the intrinsic&l clcflectioil, begiiining 0i
Bilateral BBB: critical ratrs in wntriculnr conduction 165
QKS to K’ peak in Lead I,‘,, was 0.11 second, and to R peak 0.09 second in Lead VS, and 0.05 second in I*eads Y:! and 1’::. In Leads Vr and V3 there was a deep S wave of - 12 and - 10.5 nun., synchronous u ith R’ in Lead Vi and R in Lead V,. The late acti- 1 .ttiorl time over the right and left precordium but not in between was indicative of bilateral bundle- branch or intraventrirular block.
Discussion
The frequent occurrence of single right or left bundle-branch block makes it like11 that the combination of the two-bilateral bundle-branch block-is not rare. Histo- logic lesions are often found in both bundles in the same individual when the electro- cardiograms reveal only- the pattern of single bundle-branch block.14 Electrocardi- ographicall\r, the diagnosis of true bilateral bundle-branch block is made when the patterns of right and left bundle-branch l)lork occur alternately or intermittently, in the same patient, together with changes in the P-R interval. The QRS configura- tion, ho\vever, appears to be affected only, 1)~ the side on which the 1:locking is greater:
the block on the contralateral side ap- parently does not affect the shape of the QRS but prolongs the X-V conduction time. The intrinsicoid deflection on the side of lesser block is not delayed. This classic type of bilateral bundle-branch block has been produced experimentally.‘5’” It has been reported in human beings, but Rosenbaum and Lepeschkin” had been able to find in the literature only 7 proved cases of true bilateral bundle-branch block with full electrocardiographic documen- tation. They have discussed this Tlye I of bilateral bundle-branch block at length.
-4 second type of bilateral bundle-branch block was described by J. R’larion Bryant.” Criteria were: initial septal ventricular activation from right to left, terminal activation in the right free ventricular wall, and slight or greater prolongation of QRS. He observed this t>-pe of bilateral bundle-branch block also in 10 of 100 healthy young people.
.I third type of bilateral bundle-branch or iIItraveiltric-ul;~r block is the one with
Vi c v.,. . .
Fig. 2. Case 1. Tracings recorded 3 days after those in Fig. 1. Intrinsicoid dc- Awtion is not late in Izads Vi an(l \‘E. Heart rate of 77 to 79. See text.
166 Vcsell, &hack, and 7’annenbaum
Fig. 3. Case 1. June 6. 1957. Complete atrioventricular heart block.
which the present report is concerned. The electrocardiographic pattern consists of the presence of a broad QRS with the intrinsicoid deflection occurring late si- multaneously over the right and left pre- cordium, but not in the intermediate area. There may be little or no increase in dura- tion of the P-R interval. This late ap- pearance of the intrinsicoid deflection simultaneously on the right and left sides though not in between is unusual and seemingly not in accord either with the standard theory of conduction in the bundle-branch system or with vectorcardi- ographic principles based on the concept of a single cardiac dipole.1g Such bilateral block may be explained by the presence of an intraventricular parietal or focal block responsible for retardation or pro- longation of QRS on one or both sides (i.e., a local block in the free wall of the right or left ventricle or in both). True classic c’errtr-al bundle-brarrch block 11~5 I)e preserrt in one or both ventricles, conr- plete on one side, incomplete on one or both sides.
Parietal localization of a block which caused prolongation of QRS had been described many years ago as arborization block by Oppenheimer and Rothschild,2fl although not accepted by others.21J2 *A possible parietal localization had also been suggested by Katz.23 More recently, Seg- erq7 and Boyadjian and Van Doren”-l have described the type of block under discussion; and it has been labeled false bilateral bundle-branch block by Laham,“” and doppelseitiger dilatation by Hilmer.26 SanabriaZ7 too proposed a parietal locali- zation for the block even in ordinarv single bundle-branch block, when in a series of 6 cases he was unable to find a histologic lesion of the main bundle branches to account for the bundle-branch block. C-on- trariwise, Lenegre”* had been able to show electrocardiographic and anatomic corre- lation in 46 cases of bundle-branch block. He was kind enough to show t-he slides of some ol these lo one of us (I-f. I’.). Lev AINI associates2Y have also found good correla- tion. Uanhaim jibus hnve been invoked to explain bilateral missed block- ~--complete
Bilateral BBB: critical rates in wntricdar conduc-tion 167
anatomic destruction of both main bundle branches without A-V block.30 Dodge and Grant31 suggested that in ordinary right bundle-branch block the site of the block was parietal since the initial 50 to 80 per cent of the QRS complex in peripheral leads in clinical right bundle-branch block aas identical with the control QRS in his series of 80 cases, each with controls. Cont.rariwise, experimentally, damage by pressure or incision, distal to the main right or left bundle branch,r5 and damage by direct application of chemicals to large areas of the endocardium32 were not able to increase the duration of the QRS inter- val even though the configuration of QRS was affected. In dogs, Sodi-Pallares and associates3” demonstrated total extirpation of the blocked free wall in experimental bundle-branch block without modification of the general morphology of the tracings. He stated, “The forces across the I-1’ septum in cases of bundle branch block are very important and they give a satis-
factory explanation of the unipolar mor- phologies.” On the other hand, Alzamora Castro3” has interpreted his own experi- ments as favoring the concept of parietal block. He injected cocaine and other substances into a coronary artery in dogs, and thus produced focal or parietal block in the territory irrigated by the vessel into which the injection had been made, with prolongation of QRS and a configuration which resembled those of incomplete and complete bundle-branch block. Peri-infarction block as described b\, Bayley3” may be considered a focal parietal block. Bryant,rY too, has described parietal ventricular block. This occurred ii1 a patient during hypothermia. His illustration, Figure 34, shows a late R’ ill Lead Vi and also in Lead Vi. .lbsence of intermediate leads (Leads \I? and V,) was in part a basis for criticism by Sodi-Pal- hues, who suggested that the right atrium and ventricle may have occupied the whole anterior aspect of the heart, because of
1:ig. 4. Case 2. Bilateral bundle-branch bloc-k. Intrinsicoid deflection is late in Leads \‘1 and VG, but not in Leads \*:{ and V4. See text.
168 Resell, &hack, and Tannertbaum
similarities to right atria1 and right ven- tricular electrocardiographic morphologies3”
Recently, by recordings of transmem- brane action potential of single fibers of the bundle and of single peripheral Pur- kinje fibers, and by use of appropriately timed extrasystoles, Hoffman and Crane- fieId3’ were able to demonstrate blocks pe- ripherally at the junction of specialized fibers with the ventricular muscle cells. Whether such blocks at this site increased the duration of QRS beyond normal was not indicated. Finally, Anselmi and as- sociates3* found that in experimental com- plete bundle-branch blocks the contribu- tion of the free wall of the blocked ven- tricle to QRS was nil. However, a contri- bution became important in proportion to the decrease in the degree of bundle- branch block, and was added at the end of the septal forces in incomplete bundle- branch block. Thus, in spite of much evi- dence against a contribution of potential from the free wall of the blocked ventricle prolonging QRS in bundle-branch block, especially in experimental settings, there is also considerable evidence that in certain clinical conditions and in some experiments this may occur.
The electrocardiogram of our first pa- tient (Fig. 1) was interpreted as repre- senting two combined bundle-branch or intraventricular blocks. One was central, either complete left bundle-branch block or incomplete left bundle-branch block plus a parietal left-free-wall block-major because of the broad QRS, 0.16 second, and the more extensive changes charac- teristic of left bundle-branch block; and temporary, since 3 days afterward the intrinsicoid deflection was no longer late over the left precordium. The initial 0.04- second ventricular septal forces were di- rected from right to left, and the absence of a Q wave in Leads I and aVI. and over the left precordium were in accord with this type of block. I1 The verv tall R in Lead aVL, with QRS duration greater than 0.14 second, was evidence of left ventricular hypertrophy. The second block was a right bundIe-branch block, manifest in the late R’ in Lead V1 and not in Lead V,. This block may be central and in- complete, or peripheral. It was the minor block, since it was found in a small area of
the right precordium-onl\- in Lend \.,, on Feb. 10, 1956. It was the more persistent one. When right bundle-branch block alone was recorded (Feb. 23, 1956), a broad Q wave with a notch in its descending limb was present in Leads I’1 and IT?, rvith cove-plane T waves. This strongly sug- gested the presence of anteroseptal infart~- tion, evidence of which, with extensive myocardial fibrosis, was found at necropsy.
In the tracing of Feb. 28, 1956, the P-R interval was 0.30 second, with single right bundle-branch block. On June 4, 1957, complete A-V heart block was recordctl with increase in the QRS interval to 0.20 second and changes in QRS contour (1;ig. 3). The separate appearances of unilateral bundle-branch block, of combination bun- dle-branch block, of increasing A-V block, and, finally, of complete A-V block with changes in QRS contour, support the diag- nosis of bilateral bundle-branch block. Evidence of acute anteroseptal myocardial infarction, and the necropsy findings of areas of fibrosis and hyalinization in the interventricular septum and ventricles sug- gested that, at least from the time of elec,- trocardiographic signs of bilateral bundle- branch block (intrinsicoid deflection late over right and left precordium ant1 11ot iI1 between), part of the ventricular block expressed in the electrocardiogram was due to a parietal lesion--possibly peri- infarction block. The disappearance in the electrocardiogram of the left bundle-branch block when the heart rate slowed was if) conformity with the behavior of unstable single bundle-branch block at critical rates.’ Segers7 has noted the greater frequency oi such intermittence in bilateral bundle- branch block. Because of the presence of significant lesions in both main bundle branches, intermittence might be expected to occur about twice as often in bilateral bundle-branch block as in unilateral ill- volvement. Alternations of double bundle and single bundle-branch block he called bloc ci bascule (seesaw). The phlrsiologic mechanism of unstable block at a critical heart rate could apply whether the lesion was in a main bundle branch or periph- erally in the Purkinje fibers, or Purkinja- myocardinque synapse. The component of QRS widening, if any, due to left vcntric- alar hypertrophy should be stable.“’
Hilaternl nm: criticd rates in zrentricul~r conduction 160
In our second case the bilateral intra- ventricular blocks were interpreted as con- sisting, first, of a major and more perma- Ilent central right bundle-branch block, indicated by the broad QRS, the initial 0.Wsecond ventricular septal activation from left to right, and the intrinsicoid de- flection late in Lead VI. This had been re- corded singly 4 years before double bundle- branch block. The block became bilateral with the increase in QRS interval from 0.12 to 0.15 second. The time of the in- trinsicoid deflection in Lead VI remained at 0.10 second, but in Lead Vc it increased to 0.95 second from 0.65 second. Some of this increase was due to widening of Q or QS in the left precordial leads-from 0.03 lo 0.05 second in Lead Vg. The broad Q waves in Lead I and the left precordial leads, and the late R peak (0.095 second) in Lead V6, which represented late and nearly terminal electrical forces pointing toward the anterolateral region of the left ventricle, strongly suggested the presence of peri-infarction block, responsible for focal conduction delay in the anterolateral left ventricle.3g -4 wide angle greater than 100 degrees was thus present between the mean initial and late QRS vector in the irontal plane, an important criterion for the diagnosis of peri-infarction block.3s The small terminal S in Lead Ve repre- sented late right ventricular forces due to the right bundle-branch block. R’ in Lead V1 was late in comparison to the centrally unblocked left ventricular forces. In this case a single bundle-branch block was noted at the slower cardiac rate of 60 to 70 per minute, and bilateral bundle- branch block at a rate of 85 to 98 per minute. At a stiI1 faster rate, 115, there appeared to be slightly less delay over the left ventricular pathways. Significant con- tributions to the intraventricular con- duction time due to lesions in the A-V node or common bundle of His seem unlikely because of the normal P-R interval, 0.15 second. Such A-V node localization of the block may be given more consideration in our first case, in which the P-R intervals were increased to 0.24 second or more. These two cases which show evidence of cleln!. of activation over areas which cor- respond to the free walls of the right ancl left ventricles but not in between may be
considered in support of the concept of focal and parietal ventricular blocks re- sponsible for an increase in the duration of QRS with resemblance to ordinary bundle-branch block. The presence in the literature of much evidence for and against the existence of such parietal block leaves the question of its actual existence still unanswered. It should be emphasized, however, that the evidence against its existence is largely experimental and in animals. Therefore, the possibility of its existence in human hearts with diffuse myocardial disease and special focal myo- cardial pathology is not definitely ex- cluded. Such focal parietal block could explain a component of the block in bi- lateral bundle-branch block of TJ-pe Ill.
Summary and conclusion
Three types of bilateral bundle-branch block are described. Type III is charac- terized by a prolonged QRS, and late intrinsicoid deflection over the right and left precordium but not in between. The mean initial 0.04-second frontal QRS vec- tor may be directed from right to left. This type is discussed and two illustrative cases are presented, one with necropsy findings. Simultaneous multilead recordings of limb and right and left precordial poten- tials correlated the intrinsicoid and other deflections. Changes in blocks from single to double and vice versa, bloc d bascule, were noted, with a possible critical heart rate. The mechanism of the intraventricular blocks was considered, and the possibility that a focal block in the flee ventricular wall caused a prolongation of QRS beyond normal was entertained. The literature OH
the subject pro and con was reviewed. Although there is much to support such parietal focal intraventricular block in clinical heart disease, further confirmation is desirahle.
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