clinically nornial.
Doret and Forrero3 studied 32 cases of
"traumatic enieephalopathy" without clinical
evidence of cardiovascular disease. They described various changes but did not find a
characteristic eleetrocardiographic traciilwt.
They divided their cases into six "'sympatheticotonie'" (tachycardia, raised P waves
in leads IT and III, short P-R interval, in-
on
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854
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addition. Within 20 seconds all nine animals without atropine developed bradyeardia,
increased amplitude of the T wave, and a
variety of arrhythmias-nodal rhythm, sinus
arrhythmia, incomplete atrioventricular block,
ventricular extrasystoles, and sinoatrial block;
in addition, seven of them showed decreased
amplitude or inversion of the P wave. In
the atropinized group, on the other hand, no
bradyeardia occurred, one developed T-wave
and P-wave changes, and one showed atrial
extrasystoles. The authors therefore concluded
that the electrocardiographic changes were
due to vagal stimulation. At autopsy all the
animals had subdural and subarachnoid hemorrhages, a few had cortical lacerations and
one had an intracerebral hemorrhage. The
brain stems were normal.
In the present paper the effect of craniocerebral trauma on the electrocardiogram has
been investigated in Bantu subjects.
r--
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Figure 1
Tall peaked P waves of 4 mm. in height in lead
II are seen in A and return to normal 9 months
later. B and C, which were recorded from two
other patients, also show increased voltage of the
P wave in lead II.
Table 1
Changes in Individual Components of Electrocardiogram
P wave 2.5 mm. or
more in 82
P-R interval more
than .22 second
QRS complex
1. Incomplete right
bundle-branch block
2. Complete right
bundle-branch block
3. Voltage S in V2
+ R in Vs*
Q-Te in secondst
S-T segment raised
more than 2.5 mm.
in V leads
Inverted T waves
V4-6
U wave more than
1 mm.
Group A
Group B
Group C
24%
14%
2%
.6%
4%
1%
65% increased
64% increased
48% increased
Average R + S =44 mm. Average R + S =43 mm. Average R +S= 38
All normal
15% increased
1% increased
.24-.54
.29-.44
(normal .24-.43)
(normal .24-.44)
(normal .29-.43)
3%
14%
19%
10%
21%
6%
mm.
21%
.6%
(1.5 mm.)
855
Figure 2
A first shows an increase in the Q-T, interval. Latter the Q-T interval was normal. In
tracings from two other patients (B and C) large U waves are present, best seen in V..
Table 2
Arrhythmias
Group A Group B Group C
Sinus Arrhythmia
(a) fixed pacemaker
3%01
10%
7%
1 3%0
3%01
1%
0%0/
6%
5%cl
2%1
2%
0%
13%
4%01
1%/
Nodal rhythm
Atrioventricular block
0%
0%
0%
Table 3
Heart Rates
Heart rates
between 55
and 70 per minute
Heart rates
between 70
aind 90 per minute
Heart rates
above 90 per minute
Group A
59 Cases
Group B
14 Cases
Group C
18
36
4 Cases
HERSCJI
856
Figure 3
Left. The T waves were inverted in the three
standard leads, aver and V2 to V6. Four days later,
right, T waves became upright except in lead III.
The S-T's were elevated in the standard and precordial leads, more matrked in the later tracing.
(12 cases), group 3 was stuporous (29 cases), and
group 4 was comatose (20 cases). Eleven patients
died, and necropsies were performed in all cases.
The electrocardiographic findings were divided into the two categories of changes in
complexes (table 1) and changes in rhythm
(table 2).
These ehanges occurred with similar frequency in both the groups with trauma (A
and B). At the same time the incidence of
the changes in these groups was greater than
in the healthy control group C. The p values
given below designate the level at which the
difference between the traumatic groups and
the healthy controls was significant.
1. Increased QRS voltage in the precordial
leads (p = 0.02).
2. Raised S-T segments (fig. 5) in preCirculation, Volume XXIII, June 1961
857
Figure 4
A. Ventricular ectopic beats were present (upper) and later (center) the ventricular
ectopic beats constituted trigeminal rhythm. Note also the tall P waves. B. Shows sinus
arrhythmia with a fixed pacemaker and an atrial ectopic beat.
Table 4
Changes in Individual Electrocardiographic Components
Group 1
Type of change
P waves 2.5 mm.
or more
Incomplete right
bundle-branch block
Prolonged Q-T,
S-T segment raised
103 Cases
Group 2
12 Cases
Group 3
29 Cases
23 (22.3%)
3 (256X,)
4.8%T)
16 (15.5%)
5 (
Group 4
20 Cases
(31/o)
( 3%S)
1 ( 5%0)
(21%)
4 (20%)
3 (25%)
4 (14%c,)
4 (25%o)
2 (17%)
1 (17%)
3 (1 0%r)
10 (34%/)
4 (20%o)
13 (65%)
3 (25%)
2 (17%)
5 (21%)
(10%l)
2 (10%)
4 (20%)
1 ( 8%C/.)
2 (17/7)
1 (
1(
3%/)
2 (10%C/)
4 (20%)
1 ( 8%)
0
18
1.50
5 (25%)
3%o)
0
0
44
1.52
4 (2 0%r)
1 (5)
48
2.40
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858
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Figure
A shows
to
the
After
node
uwadering
atrioventricular
the
Valsalva
and
pacemaker
shows
in the
5;Bz
node.
maneuver.,
nodal
Valsalva
D shows
(x) results in
th~e pacemaker to
maneuver
wandering
of
and
show
sinus
r-hythmn (C).
the atrioventricular
wandering
of
the
+w ^-- +
+ * t <
to
therefore only inverted T waves fromn
considered (fig. 3).
4. U waces of increased amplitude (p
<0.03). In normal white subjects U waves
may be seen in precordial leads in 100 per
cent of cases and are usually highest in V3.
Values exceeding 1 mm. are found in only
2 per cent of cases, although values of 2 to
3 mm. may be seen normally. Such waves
(fig. 2B and C) are a well-known feature of
hypokalemia, but this was found in only one
of four cases in which the serum potassium
was estimated.
5. Sinus arrhythmia with fixed pacemaker
(p = 0.01). The criteria22 for this arrhythmia
were (1) P-P interval varying by more thaii
0.16 second, (2) P-R interval of 0.12 second
or more, and (3) P waves not varying in
shape or direction (fig. 4B).
6. Sinus arrhythmia with pacemaker wanV4
V6 were
27/t115e
-- i-h-t
Figure 6
Nodal rhythm reverting to sinus rhythm
sixth day in lead II.
on
the
June
1961
859
deteriorated.
Acknowledgment
My sincerest thanks are due to 'Dr. H. C. Seftel,
for his advice and help with the manuscript, to Mr.
A. M. Shevitz, for the photographs, and to Mr.
W. Lutz, for the statistical analyses.
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HERSCH
860
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1961
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