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The effect of ventricular extrasystoles on the A-V conduction time of the next auricular impulse
THE
EFFECT OF VENTRICULAR EXTRASYSTOLES A-V CONDUCTION TIME OF THE NEXT AUR~ICTJLAR ERNEL~T
IMPULSE*
BLOOMFIELD
THE
t M.D.
ZETSLER,
CI~II(~AGO.
ON
ILL.
I
T IS fairly common for the A-V conduction time of the auricular impulse directly following a ventricular extrasystole t,o be prolonged. A ease is here presented in which this phenomenon was quite prominent. This was analyzed in an essentially quantitative manner, because otherwise the nature of the phenomenon could not be thoroughly understood.
Fig.
l.-Leads
I,
TABLE
II,
II,
I
(FOR
and
III
FIG.
of
_P-R
1.
1) II
R-P
Curve
POST
EXTEASYSTOLJC
~/.94~.92~.91~.88~.88).88~.~4~.82~.82~.78~.76~.72~~.40~.38~.36~.36~.34~.34~.32~.32~.22 //.17/.18~.18(.18~.181.18(.171.17/.181.18~.18~.18~j.30~.26j.31~.32~.30/
- 1- I - I -
Fig. 1 shows port.ions of a curve with frequent right ventricular cxtrasystoles, after which the next auricular impulse is conducted occasionally comeither more slowly or not at all. This partial-and *From iAIded of Diseases
the by
Heart Station, Michael Reese Hospital, the Emil and Fannie K. Wedeles Fund of the Heart and Circulation. 416
Chicago, for the
111. Study
and
Investi+ption
ZEIHLER
:
VENTRI(‘ULAH
ESTRASBSTOLES
AND
A-\‘
U~ND~~(‘TION
41.7
TIME
plete-A-V block is explained as follows: The impulse of the ventricular extrasystole is conducted backward through the common bnndle to the A-V node. It is not conducted past the node to the auricle (this would be a retrogra.de ventricular extrasystole, which has never been proved to occur), but it does renew the refractory period of the node, so that the next auricular impulse finds t.he node either relatively or absolutely refractory and is accordingly either partially or completely blocked. We place the block in the node rather than in the bundle because the refractory period is normally longer in the node and block is more readily produced there.’ The A-V conduction time of every beat depends upon four things: (1) the presence or absence of organic disease of t,he AV node or bundle; (2) the alteration of the A-V nocle or bundle by drugs or other chemical influences; (3) vagus and sympathetic influences at the the uf passage of the impztlsc through the notl~; and (4) the time permit-
Fig.
?.-Leads
I,
II.
am1
III
TABLE
of
Curve II
(FOR
2, taken FIG. II
R-P P-R
two
Aa>-s
after
Curve
1.
2) POST
EXTRASYSTOLIC
~/1.12~1.0"~1.00/.98/.94~.92~.90/.88~.82~.80~~.48/.45/.42~.42~.40~.40~<.36/<.34 // ,181 .181 .18~.18/.18~.18~.18~.19~.20~.22~~.36/.32/ - / - I.341 - /
- 1
-
ted for recovery of the node a.fter the passage of the last preceding impulse. This time interval, which is called the ,*ecovery time, is measured from the beginning of the preceding QRS complex to the beginning of the P-wave, and is designated by R-P. Other things being equal, the conduction time increases monotonically as the recovery time decreases;’ but, as is well known, even with a long recovery time conduction may be slowed by nervous influences. To illustrate these principles I have marked on the electrocardiograms shown in Figs. 1, 2 and 3, the recovery times above the curve and the P-R intervals below. Where the P-wave is partly buried in the T-wave, only an upper limit can be determined for the recovery time; when a beat is completely blocked, the P-R interval is indicated by a
418
TIIE
AMERlCAN
HEART
JOURNAL
dash. The measurements are tabulated in decreasing values of the recovery time as follows : It is seen that in general the P-R interval increases as the recovery time decreases ; the exceptions most, probably indicate temporary changes in tonus of the cardiac efferent nerves. On t,he whole, A-V conduction is slower in Curve 2 than in Curve 1. To find out what part of the delayecl conduction is due to vagus tone we gave the patient !.io gr. of atropine sulphate hypodermically just after Curve 2 was taken; thirty minutes later Curve 3 was taken. The sinus rate was increased only slightly (from 55 to 59). We see again the same general rule for increase of the P-R interval with decrease of the recovery time : Whereas before atropine, complete block occurred with a recovery time as long as 0.42 sec., after atropine, there is no instance of complete block until the recovery time is as short as-O.20 sec. Similarly,
Fig.
3.-Leads
I,
II,
and
III
of
Curve minutes
TABLE
R-P P-R
3. taken on after atropine. 111
(FOR
FIG.
the
smw
day
as
Curve
3.
thirty
3)
POST EXTRASYSTOLIC II 111.08 / .92 1.90 1 .88 1 .86 I .86 / .86 1 .82 I .78 I/ .38 I .38 I .32 1 .28 1 .20 / .16 ) .12 II .18j.18~.18/.16~.16~.16~.18~.18/.18/~.2Oj.21~.22~.32( - I - / -
before atropine we have a P-R of 0.36 sec. with a recovery time as long as 0.48 sec. and after atropine a P-R of only 0.20 sec. with a recovery time as short as 0.38 sec. Thus A-V conduction is greatly improved after atropine. After atropine there is no delay in conduction beyond normal limits (0.22) until the recovery time is reduced to 0.28 sec. or less than half the recovery time (0.65 sec.) at normal sinus rhythm (rate 72, PR = OX), and there is no complete block unt.il the recovery time is reduced to 0.20 sec. or less than one-third the normal. This marked improvement in conduction indicates that the A-V block before atropine was due to vagus influence and not to organic disease. To rule out a possible sympathetic depression adrenalin was injected
ZEISLER
:
VENTRICIJLAR
l!XTKAHYSTOLES
AND
A-V
CONDUCTION
419
TIME
on a subsequent day; this had no effect on the block, so that it appears to have been the vagus which was the controlling factor, though the patient had had no digitalis or other vagus stimulant. These observations indicate that the effect of a ventricular extrasystole on the A-V conduction of the next auricular impulse is no different in nature from the effect of an auricular extrasystole with the same recovery time on its own A-V conduction. It follows that cowpletp
block
eztrasystole
of
th.e
has
azwkzda~r the
sapue
iwpulse
directl!y
sipvificance
following
as a blocked
a late ea.rly
ventricular
a,wicular
cstra-
s!~stole.
his
I wish to express my valuable criticism.
thanks
to Dr.
Louis
N. Katz
for
RE’FERENCE?
1. Lewis, 2. Lewis,
Quart. J. Med., 14: 339, T.: T., and Master, A. M.: Heart,
1921. 12: 209, 1925.
his helpful
discussion
and
EFFECT OF VENTRICULAR EXTRASYSTOLES A-V CONDUCTION TIME OF THE NEXT AUR~ICTJLAR ERNEL~T
IMPULSE*
BLOOMFIELD
THE
t M.D.
ZETSLER,
CI~II(~AGO.
ON
ILL.
I
T IS fairly common for the A-V conduction time of the auricular impulse directly following a ventricular extrasystole t,o be prolonged. A ease is here presented in which this phenomenon was quite prominent. This was analyzed in an essentially quantitative manner, because otherwise the nature of the phenomenon could not be thoroughly understood.
Fig.
l.-Leads
I,
TABLE
II,
II,
I
(FOR
and
III
FIG.
of
_P-R
1.
1) II
R-P
Curve
POST
EXTEASYSTOLJC
~/.94~.92~.91~.88~.88).88~.~4~.82~.82~.78~.76~.72~~.40~.38~.36~.36~.34~.34~.32~.32~.22 //.17/.18~.18(.18~.181.18(.171.17/.181.18~.18~.18~j.30~.26j.31~.32~.30/
- 1- I - I -
Fig. 1 shows port.ions of a curve with frequent right ventricular cxtrasystoles, after which the next auricular impulse is conducted occasionally comeither more slowly or not at all. This partial-and *From iAIded of Diseases
the by
Heart Station, Michael Reese Hospital, the Emil and Fannie K. Wedeles Fund of the Heart and Circulation. 416
Chicago, for the
111. Study
and
Investi+ption
ZEIHLER
:
VENTRI(‘ULAH
ESTRASBSTOLES
AND
A-\‘
U~ND~~(‘TION
41.7
TIME
plete-A-V block is explained as follows: The impulse of the ventricular extrasystole is conducted backward through the common bnndle to the A-V node. It is not conducted past the node to the auricle (this would be a retrogra.de ventricular extrasystole, which has never been proved to occur), but it does renew the refractory period of the node, so that the next auricular impulse finds t.he node either relatively or absolutely refractory and is accordingly either partially or completely blocked. We place the block in the node rather than in the bundle because the refractory period is normally longer in the node and block is more readily produced there.’ The A-V conduction time of every beat depends upon four things: (1) the presence or absence of organic disease of t,he AV node or bundle; (2) the alteration of the A-V nocle or bundle by drugs or other chemical influences; (3) vagus and sympathetic influences at the the uf passage of the impztlsc through the notl~; and (4) the time permit-
Fig.
?.-Leads
I,
II.
am1
III
TABLE
of
Curve II
(FOR
2, taken FIG. II
R-P P-R
two
Aa>-s
after
Curve
1.
2) POST
EXTRASYSTOLIC
~/1.12~1.0"~1.00/.98/.94~.92~.90/.88~.82~.80~~.48/.45/.42~.42~.40~.40~<.36/<.34 // ,181 .181 .18~.18/.18~.18~.18~.19~.20~.22~~.36/.32/ - / - I.341 - /
- 1
-
ted for recovery of the node a.fter the passage of the last preceding impulse. This time interval, which is called the ,*ecovery time, is measured from the beginning of the preceding QRS complex to the beginning of the P-wave, and is designated by R-P. Other things being equal, the conduction time increases monotonically as the recovery time decreases;’ but, as is well known, even with a long recovery time conduction may be slowed by nervous influences. To illustrate these principles I have marked on the electrocardiograms shown in Figs. 1, 2 and 3, the recovery times above the curve and the P-R intervals below. Where the P-wave is partly buried in the T-wave, only an upper limit can be determined for the recovery time; when a beat is completely blocked, the P-R interval is indicated by a
418
TIIE
AMERlCAN
HEART
JOURNAL
dash. The measurements are tabulated in decreasing values of the recovery time as follows : It is seen that in general the P-R interval increases as the recovery time decreases ; the exceptions most, probably indicate temporary changes in tonus of the cardiac efferent nerves. On t,he whole, A-V conduction is slower in Curve 2 than in Curve 1. To find out what part of the delayecl conduction is due to vagus tone we gave the patient !.io gr. of atropine sulphate hypodermically just after Curve 2 was taken; thirty minutes later Curve 3 was taken. The sinus rate was increased only slightly (from 55 to 59). We see again the same general rule for increase of the P-R interval with decrease of the recovery time : Whereas before atropine, complete block occurred with a recovery time as long as 0.42 sec., after atropine, there is no instance of complete block until the recovery time is as short as-O.20 sec. Similarly,
Fig.
3.-Leads
I,
II,
and
III
of
Curve minutes
TABLE
R-P P-R
3. taken on after atropine. 111
(FOR
FIG.
the
smw
day
as
Curve
3.
thirty
3)
POST EXTRASYSTOLIC II 111.08 / .92 1.90 1 .88 1 .86 I .86 / .86 1 .82 I .78 I/ .38 I .38 I .32 1 .28 1 .20 / .16 ) .12 II .18j.18~.18/.16~.16~.16~.18~.18/.18/~.2Oj.21~.22~.32( - I - / -
before atropine we have a P-R of 0.36 sec. with a recovery time as long as 0.48 sec. and after atropine a P-R of only 0.20 sec. with a recovery time as short as 0.38 sec. Thus A-V conduction is greatly improved after atropine. After atropine there is no delay in conduction beyond normal limits (0.22) until the recovery time is reduced to 0.28 sec. or less than half the recovery time (0.65 sec.) at normal sinus rhythm (rate 72, PR = OX), and there is no complete block unt.il the recovery time is reduced to 0.20 sec. or less than one-third the normal. This marked improvement in conduction indicates that the A-V block before atropine was due to vagus influence and not to organic disease. To rule out a possible sympathetic depression adrenalin was injected
ZEISLER
:
VENTRICIJLAR
l!XTKAHYSTOLES
AND
A-V
CONDUCTION
419
TIME
on a subsequent day; this had no effect on the block, so that it appears to have been the vagus which was the controlling factor, though the patient had had no digitalis or other vagus stimulant. These observations indicate that the effect of a ventricular extrasystole on the A-V conduction of the next auricular impulse is no different in nature from the effect of an auricular extrasystole with the same recovery time on its own A-V conduction. It follows that cowpletp
block
eztrasystole
of
th.e
has
azwkzda~r the
sapue
iwpulse
directl!y
sipvificance
following
as a blocked
a late ea.rly
ventricular
a,wicular
cstra-
s!~stole.
his
I wish to express my valuable criticism.
thanks
to Dr.
Louis
N. Katz
for
RE’FERENCE?
1. Lewis, 2. Lewis,
Quart. J. Med., 14: 339, T.: T., and Master, A. M.: Heart,
1921. 12: 209, 1925.
his helpful
discussion
and