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The significance of splintering of the terminal portion of the QRS deflection of the electrocardiogram
THE
SlGNIFIC:AN~!E PORTION
OF OF TIIE
SPrJIs9WmG
oE’ THE
QRS DEFLECTTOS
TERMINAL
OF THE
ELECTROCARDIOGRAM.” LE,ONARD
STETCTEK,
M.D.,
AND
IIAROLD
FEII,,
M.D.
Omo
CLEVELASD.
ONSIDER.ABLE diagnostic importance has been attached to splintering or notching of various portions of the QRS complex. Such notching is usually associated with other electrocardiographic changes which render the records distinctly abnormal. A large bizarre QRS complex, notch,ed, with a duration in excess of 0.1 second and T in the opposite direction completes the picture of a bundle-branch lesion. A notched QRS complex in all leads, low in voltage, is evidence of intraventricular block. Tn this study, however, we wish to limit ourselves to a discussion of splintering of the final deflection of the QR#S complex as an isolated electrocardiographic phenomenon, and to point out the significance of such splintering. A. M. Weddl has already called attention to the significance of notching of the R-wave and states that this is frequently encountered in cases of unquestioned myocarditis. In Wedd’s series of thirty cases, seventeen showed notching of R in Lead III alone ; three showed the notching in all leads ; four in Leads I and III ; three in Leads II and III ; two in Leads I and II ; and one in Lead I alone. Although we agree that notching of the R in one or two leads may be of clinical significance we must admit that similar notching does occur in records of normal individuals. The appearance of such notching in normal individuals has been In a study of fifty normal indipointed out by Lewis and Gilder.’ viduals they found notching of R, in three instances ; of R? in one instance; of R, in six instances in which its identification was not complicated. They likewise found splintering of the S-wave in two instances in Lead II, and noted that apart from eleven cases of splintering in the opening events of ventricular systole, a division of S was never seen in Lead III. Wiggers3 states that humping, notching or splintering of the R.-wave is normal when it occurs on a small wave in a single lead, and when it occurs near the base of the ascending or descending limbs of two clifferent leads. In an effort to check the frequency with which splintering of the terminal part of the QRS deflection occurred in our series of normal records we examined the electrocardiograms of 119 known normal
C
pital
*From the Medical of Cleveland.
Clinic
and
Electrocardiographic 472
Laboratory
of
Mt.
Sinai
Hos-
STEUER
ASI)
FEIIi
:
SI’LINT~RING
TIIE
QKS
DEFLIG’TION
473
individuals. Such notching occurred in one or two leads in twentyone cases of this series. It appeared in Lead I in five instances; in Lead II in eight instances ; in Lead III in two instances; in Leads I and III in two instances; in Leads I and II in one instance; in Leads It is evident, however, that in the total II and III in three instances. of 119 normal individuals studied, in no instance did notching of the final part of the QRS complex occur in all t,hree leads. On the other hand, in a series of 4000 electrocardiograms taken from the files of Mt. Sinai Hospital we found splintering of the final part of the QRS deflection in all leads as the only electrocardioIn all cases where splintering graphic abnormality in 34 instances, occurred in three leads t,here was unquestionable clinical evidence of cardiac abnormality. The types of clinical cardiac abnormalities represented in these cases are as follows: Hypertension Rheumatic heart disease Coronary art,eriosclerosis Hyperthyroidism Developmental defect
14 13 5 1 1
cases cases cases case case
41 38 15 3 3
per per per per per
cent cent cent cent cent
In these records with notching in all leads left preponderance occurred in 22 inst,ances (65 per cent) ; right preponderance in 2 instances (6 per cent) ; no preponderance in 10 inst,ances (29 per cent). The actual cause of this splinterin g is a matter of speculation at present. We know that the QRS group of deflections corresponds to the excitation of the ventricles and that the conus and base of the left ventricle become electrically active at the peak of the R or a little later.” The terminal phase of t,he QRS complex is completed with excitation of both vent,ricles, and it is not unreasonable to assume that the notching is associated with an abnormality in the Purkinje conduction. This may be due t,o myocardial enlargement or endocardial changes-either of which might cause changes in the record of the course of escitation. SUMMARY
A series of 119 electrocardiograms of 119 normal individuals has been studied and notching in the terminal portion of the QRS complex in all three leads has not been found in any of the cases. Thirtyfour cases showing the presence of such notching in all leads have been studied, and it has been found that there is distinct evidence of cardiac abnormality in all instances. It is therefore concluded that an electrocardiogram which shows splintering in the terminal part of the QRS complex in all leads is distinctly abnormal. This finding has been present in various types of cardiac disease. Illustrative cases and records are shown,
ILLUSTRATIVE Cnss
L-E.
Cl.
A
and di&tolic murmurs cardiac margin with Diagnosis: Rheumatic exercise tolerance.
(‘&ES
white malt of 8 years. Rheumatic fever at 3 years. Systolic at apex. Orthodiagram shows straightening of middle left elongation of the shadow of the left ventricle. Clinical heart disease, mitral stenosis and insufficiency with normal
I(. A white female of 19 months. Not a blue baby. Pneumonia CASE 2.-D. at age of 7 months. Musical systolic murmur, best heard along left sternal margin in second and third intercostal spaces. Also heard at apex. Orthodingram shows definite mitral configuration with straightening of the middle left cardiac margin. Considerable bulkiness to right and left suggesting a congenital septal defect. Chest 16 cm. Transverse diameter of heart 8 cm. CIinical Diagnosis: Developmental defect.
/
Casr
i
1.
case
2.
CASE 3.-F. D. White female of 16 years. Attacks of chorea at 7 years and 13 years. Loud systolic murmur at apex. Left border of cardiac dullness 10 cm. from midsternal line in fifth interspace. Orthodiagram shows mitral configuration with bulging of upper left cardiac margin and additional enlargement to right and left. Bulging of left auricle in right lateral position. Chest 33 cm. Aorta 3.5 cm. Transverse 135 cm. Clinical Diagnosis: Mitral insufficiency. CASE 4.-N. G. White female of 62 years. Admitted to hospital in shock two days after severe pectoral pain. Diagnosis of coronary occlusion by one of writers. Notching appeared as first sigu of abnormality in electrocardiogram. Later electrocardiographic signs of coronary occlusion appeared. Clinical Diagnosis: Coronary sclerosis with occlusion of coronary artery. CASE 5.-M. G. White female of 69 years complaining of preeordial pain. I;creased palpable precordial activity. Right border of cardiac dullness 1 cm. to right of sternum. Left border of cardiac dullness 3 cm. to left of midelnvicular line in fift.h interspace. Harsh systolic murmur o~‘er entir<+ prerordium. Blood
STPXTEK
A?C;D
FEII,
:
Sl’IJNTERIE\‘G
TtIE
QRS
I~EFI,E(“l’ION
Case
6
47,i
pressure 210/1%U; 178/86; lYCI/ Ill): ltii)/7li. (‘liuical Diagnosis: Hypertension with cardiac hypertrophy. The following autopsied cases are l)resentkad. These show the splintering of the terminal portion of the QRS deflection iu the presence of other electrocardiographic abnormalities. CASE 6.-L. W. A white female of 60 years admitted to the hospital complain Has ing of shortness of breath and high blood pressure of two years’ duration. taken antiluetic treatment for the past seven years a,nd malaria treatment for genPresented picture of congestive heart failure with eral paresis three years ago. A faint diastolic murmur was heard at the enlargement of the left ventricle. Blood pressure 240/90; 200/90; 190/90. Changed from normal me& aortic area. anism to auricular fibrillation during hospital stay and vvent downhill rapidly. No digitalis had been administered at time of first electrocardiogram. Orthodia-
-
Case
8.
gram shows tremendous enlargement to the left with considerable diffuse diIatation Chest 26 cm. Transverse 16 cm. and marked increased density of the aorta. Hypertension with cardiac hypertrophy, luetic Aorta 9 cm. Clinical Diagnosis: aortitis with insufficiency. Anatomical Diagnosis : Hypertrophy and dilatation of the heart (chiefly left mesaortitis with involvement of ventricle) ; (Heart weight 800 grams) ; luetic the leaflets and slight insufficiency; generalized arterial and arteriolar sclerosis. CASE 7.-M. N. A white male of 56 years admitted complaining of fainting spells of six months’ duration. Patient presented the large head and bowing of Modern enlargement of the left venthe long bones typical of Paget ‘8 disease. tricle with a musical systolic murmur at the apex. Blood pressure 176/80. During fainting spells heart mechanism would change from normal to block. Developed congestive failure and expired. Orthodiagram showed enlargement of heart to left. congestive heart Clinical Diagnosis : Generalized arteriosclerosis ; heart-block; deposits mitral and aortic failure ; Paget’s disease. Anatomical Diagnosis : Calcium
STEUFR 2
ASD
FEII,
:
Sl’LINTlCRING
valves involring conduction system; moderate ; hypertrophy of myocardium,
TIIE
QRS
477
DEFLlX’TION
mitral stenosis, considerable; weight 460 grams.
aortic
stenosis,
CaSE 8.--N. A. White male of 71 years admitted because of fractured skull. Heart enlarged, arrhythmic, no murmurs. Became stuporous, cyanotic and expired. skull, auricular fibrillation. Anatomical Diagnosis: Clinical Diagnosis : Fractured Fractured skull; cardiac hypertrophy and dilatation, weight 350 grams; moderate atherosclerosis of coronary arteries with several areas of scarring in myocardium.
REE’ERENCXS
1. We&l, A. M.: Arch. Int. Med. 25: 515, 1919. 2. Lewis, T., and Gilder, M. D. D.: Phil. Tr. Roy. Xoc. London 3. Wiggers, Carl J.: Principles and Practice of Electrocardiography, 1929, p. 102, The C. V. Mosby Company. 4. Lewis, T.: Mechanism and Graphic Registration of the Heart 9.5, Paul B. Hocber, 9ew York.
202: Beat,
351, 1912. St. Louis, 1925,
p.
SlGNIFIC:AN~!E PORTION
OF OF TIIE
SPrJIs9WmG
oE’ THE
QRS DEFLECTTOS
TERMINAL
OF THE
ELECTROCARDIOGRAM.” LE,ONARD
STETCTEK,
M.D.,
AND
IIAROLD
FEII,,
M.D.
Omo
CLEVELASD.
ONSIDER.ABLE diagnostic importance has been attached to splintering or notching of various portions of the QRS complex. Such notching is usually associated with other electrocardiographic changes which render the records distinctly abnormal. A large bizarre QRS complex, notch,ed, with a duration in excess of 0.1 second and T in the opposite direction completes the picture of a bundle-branch lesion. A notched QRS complex in all leads, low in voltage, is evidence of intraventricular block. Tn this study, however, we wish to limit ourselves to a discussion of splintering of the final deflection of the QR#S complex as an isolated electrocardiographic phenomenon, and to point out the significance of such splintering. A. M. Weddl has already called attention to the significance of notching of the R-wave and states that this is frequently encountered in cases of unquestioned myocarditis. In Wedd’s series of thirty cases, seventeen showed notching of R in Lead III alone ; three showed the notching in all leads ; four in Leads I and III ; three in Leads II and III ; two in Leads I and II ; and one in Lead I alone. Although we agree that notching of the R in one or two leads may be of clinical significance we must admit that similar notching does occur in records of normal individuals. The appearance of such notching in normal individuals has been In a study of fifty normal indipointed out by Lewis and Gilder.’ viduals they found notching of R, in three instances ; of R? in one instance; of R, in six instances in which its identification was not complicated. They likewise found splintering of the S-wave in two instances in Lead II, and noted that apart from eleven cases of splintering in the opening events of ventricular systole, a division of S was never seen in Lead III. Wiggers3 states that humping, notching or splintering of the R.-wave is normal when it occurs on a small wave in a single lead, and when it occurs near the base of the ascending or descending limbs of two clifferent leads. In an effort to check the frequency with which splintering of the terminal part of the QRS deflection occurred in our series of normal records we examined the electrocardiograms of 119 known normal
C
pital
*From the Medical of Cleveland.
Clinic
and
Electrocardiographic 472
Laboratory
of
Mt.
Sinai
Hos-
STEUER
ASI)
FEIIi
:
SI’LINT~RING
TIIE
QKS
DEFLIG’TION
473
individuals. Such notching occurred in one or two leads in twentyone cases of this series. It appeared in Lead I in five instances; in Lead II in eight instances ; in Lead III in two instances; in Leads I and III in two instances; in Leads I and II in one instance; in Leads It is evident, however, that in the total II and III in three instances. of 119 normal individuals studied, in no instance did notching of the final part of the QRS complex occur in all t,hree leads. On the other hand, in a series of 4000 electrocardiograms taken from the files of Mt. Sinai Hospital we found splintering of the final part of the QRS deflection in all leads as the only electrocardioIn all cases where splintering graphic abnormality in 34 instances, occurred in three leads t,here was unquestionable clinical evidence of cardiac abnormality. The types of clinical cardiac abnormalities represented in these cases are as follows: Hypertension Rheumatic heart disease Coronary art,eriosclerosis Hyperthyroidism Developmental defect
14 13 5 1 1
cases cases cases case case
41 38 15 3 3
per per per per per
cent cent cent cent cent
In these records with notching in all leads left preponderance occurred in 22 inst,ances (65 per cent) ; right preponderance in 2 instances (6 per cent) ; no preponderance in 10 inst,ances (29 per cent). The actual cause of this splinterin g is a matter of speculation at present. We know that the QRS group of deflections corresponds to the excitation of the ventricles and that the conus and base of the left ventricle become electrically active at the peak of the R or a little later.” The terminal phase of t,he QRS complex is completed with excitation of both vent,ricles, and it is not unreasonable to assume that the notching is associated with an abnormality in the Purkinje conduction. This may be due t,o myocardial enlargement or endocardial changes-either of which might cause changes in the record of the course of escitation. SUMMARY
A series of 119 electrocardiograms of 119 normal individuals has been studied and notching in the terminal portion of the QRS complex in all three leads has not been found in any of the cases. Thirtyfour cases showing the presence of such notching in all leads have been studied, and it has been found that there is distinct evidence of cardiac abnormality in all instances. It is therefore concluded that an electrocardiogram which shows splintering in the terminal part of the QRS complex in all leads is distinctly abnormal. This finding has been present in various types of cardiac disease. Illustrative cases and records are shown,
ILLUSTRATIVE Cnss
L-E.
Cl.
A
and di&tolic murmurs cardiac margin with Diagnosis: Rheumatic exercise tolerance.
(‘&ES
white malt of 8 years. Rheumatic fever at 3 years. Systolic at apex. Orthodiagram shows straightening of middle left elongation of the shadow of the left ventricle. Clinical heart disease, mitral stenosis and insufficiency with normal
I(. A white female of 19 months. Not a blue baby. Pneumonia CASE 2.-D. at age of 7 months. Musical systolic murmur, best heard along left sternal margin in second and third intercostal spaces. Also heard at apex. Orthodingram shows definite mitral configuration with straightening of the middle left cardiac margin. Considerable bulkiness to right and left suggesting a congenital septal defect. Chest 16 cm. Transverse diameter of heart 8 cm. CIinical Diagnosis: Developmental defect.
/
Casr
i
1.
case
2.
CASE 3.-F. D. White female of 16 years. Attacks of chorea at 7 years and 13 years. Loud systolic murmur at apex. Left border of cardiac dullness 10 cm. from midsternal line in fifth interspace. Orthodiagram shows mitral configuration with bulging of upper left cardiac margin and additional enlargement to right and left. Bulging of left auricle in right lateral position. Chest 33 cm. Aorta 3.5 cm. Transverse 135 cm. Clinical Diagnosis: Mitral insufficiency. CASE 4.-N. G. White female of 62 years. Admitted to hospital in shock two days after severe pectoral pain. Diagnosis of coronary occlusion by one of writers. Notching appeared as first sigu of abnormality in electrocardiogram. Later electrocardiographic signs of coronary occlusion appeared. Clinical Diagnosis: Coronary sclerosis with occlusion of coronary artery. CASE 5.-M. G. White female of 69 years complaining of preeordial pain. I;creased palpable precordial activity. Right border of cardiac dullness 1 cm. to right of sternum. Left border of cardiac dullness 3 cm. to left of midelnvicular line in fift.h interspace. Harsh systolic murmur o~‘er entir<+ prerordium. Blood
STPXTEK
A?C;D
FEII,
:
Sl’IJNTERIE\‘G
TtIE
QRS
I~EFI,E(“l’ION
Case
6
47,i
pressure 210/1%U; 178/86; lYCI/ Ill): ltii)/7li. (‘liuical Diagnosis: Hypertension with cardiac hypertrophy. The following autopsied cases are l)resentkad. These show the splintering of the terminal portion of the QRS deflection iu the presence of other electrocardiographic abnormalities. CASE 6.-L. W. A white female of 60 years admitted to the hospital complain Has ing of shortness of breath and high blood pressure of two years’ duration. taken antiluetic treatment for the past seven years a,nd malaria treatment for genPresented picture of congestive heart failure with eral paresis three years ago. A faint diastolic murmur was heard at the enlargement of the left ventricle. Blood pressure 240/90; 200/90; 190/90. Changed from normal me& aortic area. anism to auricular fibrillation during hospital stay and vvent downhill rapidly. No digitalis had been administered at time of first electrocardiogram. Orthodia-
-
Case
8.
gram shows tremendous enlargement to the left with considerable diffuse diIatation Chest 26 cm. Transverse 16 cm. and marked increased density of the aorta. Hypertension with cardiac hypertrophy, luetic Aorta 9 cm. Clinical Diagnosis: aortitis with insufficiency. Anatomical Diagnosis : Hypertrophy and dilatation of the heart (chiefly left mesaortitis with involvement of ventricle) ; (Heart weight 800 grams) ; luetic the leaflets and slight insufficiency; generalized arterial and arteriolar sclerosis. CASE 7.-M. N. A white male of 56 years admitted complaining of fainting spells of six months’ duration. Patient presented the large head and bowing of Modern enlargement of the left venthe long bones typical of Paget ‘8 disease. tricle with a musical systolic murmur at the apex. Blood pressure 176/80. During fainting spells heart mechanism would change from normal to block. Developed congestive failure and expired. Orthodiagram showed enlargement of heart to left. congestive heart Clinical Diagnosis : Generalized arteriosclerosis ; heart-block; deposits mitral and aortic failure ; Paget’s disease. Anatomical Diagnosis : Calcium
STEUFR 2
ASD
FEII,
:
Sl’LINTlCRING
valves involring conduction system; moderate ; hypertrophy of myocardium,
TIIE
QRS
477
DEFLlX’TION
mitral stenosis, considerable; weight 460 grams.
aortic
stenosis,
CaSE 8.--N. A. White male of 71 years admitted because of fractured skull. Heart enlarged, arrhythmic, no murmurs. Became stuporous, cyanotic and expired. skull, auricular fibrillation. Anatomical Diagnosis: Clinical Diagnosis : Fractured Fractured skull; cardiac hypertrophy and dilatation, weight 350 grams; moderate atherosclerosis of coronary arteries with several areas of scarring in myocardium.
REE’ERENCXS
1. We&l, A. M.: Arch. Int. Med. 25: 515, 1919. 2. Lewis, T., and Gilder, M. D. D.: Phil. Tr. Roy. Xoc. London 3. Wiggers, Carl J.: Principles and Practice of Electrocardiography, 1929, p. 102, The C. V. Mosby Company. 4. Lewis, T.: Mechanism and Graphic Registration of the Heart 9.5, Paul B. Hocber, 9ew York.
202: Beat,
351, 1912. St. Louis, 1925,
p.