Download symptomaticunilateral cannon“a” waves 539

Disseminated
intravascular
coagulation
in
miliary
tuberculosis
is rare. Goldfine
et albo described
an elderly
patient who developed
rectal hemorrhage
in the wake of
respiratory
arrest and died in spite of heparin
treatment.
Unfortunately,
no information
is provided
regarding
the
patient’s
metabolic
status at the time of arrest or subsequently,
and both
shock
and profound
acidosis
are
among
multiple
known
etiologies
of DIC.11
Mavligit
et
all2 reported
a patient
with
miliaiy
tuberculosis
who
developed
gastrointestinal
hemorrhage
and
survived
after
treatment
with heparin,
isoniazid,
ethambutol,
and
streptomycin.
Bleeding
disorders
have been associated
with
miliary
tuberculosis,
and
DIC
has
been
suspected
retrospectively.7’13
Huseby
and Hudson18
have
recently described
three cases of miliary
tuberculosis
and concomitant
adult
respiratory
distress
syndrome.
All three
of their cases and a previously
reported
case by Homan
et al
had evidence
of coagulation abnormalities consistent with DIC. Drug-induced
coagulation
abnormalities
must also remain
a consideration
and the imporance
of
this has recently
been emphasized
by a report
of DIC
occurring
secondary
to isoniazid-induced
hepatitis.15
Sahn
and
Neff
also
noted
drug-induced
marrow
changes
and stressed
the difficulty
of differentiating
the
effect
of the underlying
disease
from that of drug-induced
abnormalities.
In addition,
there
are numerous
reports
of antituberculosis
drug-induced
leulcopenia
and thrombocytopenia.
ACKNOWLEDGMENTS:
The authors
gratefully
acknowledge the thoughtful
review of the manuscript
by Drs. William
Creger,
Roger
Lange and John
Moses,
and the secretarial
assistance
of Mrs. Isabelle
Smith.
REFERENCES
1 Fountain
JR:
tuberculosis.
2 Paulley JW:
tuberculosis.
3
4
5
6
7
8
9
Blood changes
associated
with disseminated
Br Med J 2:76-79,
1954
Blood changes
associated
with disseminated
Br Med J 2:411-412,
1954
Glasser
RM, Walker
RI, Herion
JC: The significance
of
hematologic
abnormalities
in patients
with tuberculosis.
Arch hit Med 125:691-895,
1970
Sahn SA, Neff TA: Miliary
tuberculosis.
Am J Med
54:495-505,
1974
Medd
WE,
Hayhoe
FJG: Tuberculous
miliary
necrosis
with pancytopenia.
Quart J Med 24:351-364,
1955
Coburn
RJ, England
JM, Samson DM, et al: Tuberculosis
and blood disorders.
Br J Hematol 25:793-799,
1973
Cooper
W: Pancytopenia
associated
with
tuberculosis.
Ann Intern Med 50:1497-1501,
1959
Eakins
D, Nelson
MC: Disseminated
tuberculosis
with
associated hematological disorders.
Irish J Med Sci 2:7990,1989
Mangion
PB, Schiller
KFR:
Disseminated
tuberculosis
complicated by pancytopenia.
Proc Roy Soc Med 64:42,
1971
10 Goldfine
ID, Schacter
H, Barclay
WR,
tion coagulopathy
in miliary
tuberculosis.
CHEST, 73: 4, APRIl, 1978
J, Hudson
LD: Miliary
tuberculosis
and adult
syndrome.
Ann Intern Med 85:609-
distress
611, 1976
14 Homan W, Harman
E, Braun MJ, et al: Miliary tuberculosis presenting
as acute respiratory
failure: Treatment
by
membrane
oxygenator
and ventricle
pump.
Chest 67:366369, 1975
15 Stuart JJ, Roberts
HR: Isoniazid
and disseminated
intravascular
coagulation.
Ann
Intern Med 84:490-491,
1976
Symptomatic
Waves
Lawrence
I. Richard
Cannon
in a Patient
Ventricular
Roland
Unilateral
Victor
Werres,
M.D.;#{176}
Gilbert,
M.D.,
Zucker,
M.D.,
A 64-year-old
tent pulsations
that were first
with
“a”
a
Pacemaker*
Parsonnet,
F.C.C.P.;fl
M.D.;ff
and
F.C.C.P.#{176}6
woman
was referred
because
of intermitof the left side of the neck, face, and scalp
noticed after the Insertion
of a ventricular
pacemaker.
The pacemaker
had been Inserted
because
of
2:1 atriovenfrlcular block. Right
cardiac
catherization
showed
cannon “a” waves, and phlebographic
studies
revealed
stenosis
of the right innominate
and Internal
jugular
veins.
The symptoms
were abolished
by conversion
to an afrial synchronous
pacing
system.
Comments
are offered
on the hemodynamic
findings,
the “pacemaking
syndrome,”
and the use of atrial synchronous
pacing.
symptomatIc
G
iant or cannon
“a” waves
of a jugular
pulse can be
observed
when the atria contract
against
the closed
atrioventricular
valves
and the atrial
volume
is discharged
retrogradely
into the peripheral veins.1’2 The
occurrence
of such cannon
“a” waves
is therefore
to be
expected
in various
forms of atrioventricular
dissociation,
particularly
in complete
heart
block
and during
ventricular
pacing
in the presence
of a preserved
sinus
mechanism.3’4
Rarely
are significant
subjective
symjtoms
produced.
The
following
case
report
is of note
of coexistence of ventricular
pacing
(VVI)
and unilateral stenosis
of the right innominate
and
internal jugular
vein, the pulsations in the neck were
unilateral
and of such a degree
that conversion
of the
pacing
system
to an atrial synchronous
mode
(VAT)
was
necessary
(“VVI”
is a code designation
for a ventricular
because
as a result
inhibitory pacemakers).
CASE
et al: ConsumpAnn Intern Med
71:755-757,
1966
Deykin
D: The clinical
challenge
of disseminated
intravascular
coagulation.
N Eng J Med 283:636-644,
1970
12 Mavligit
MD,
Binder
BA, Crosby
WH:
Disseminated
intravascular coagulation
in miliary
tuberculosis.
Arch mt
Med 130:388-389,
1972
11
13 Huseby
respiratory
REPORT
A 60-year-old
white woman
was admitted
for intermittent
pulsations
of the left side of her neck, face, and scalp, which
#{176}FromNewark
Beth
Israel Medical
Department
#{176}#{176}Division
of Cardiology,
fDepartment
Center,
Newark,
of Medicine.
NJ.
of Surgery.
tPacemaker
Division.
Reprint
requests:
Dr.
07112
Werres,
201
Lyons
Avenue,
Newark
SYMPTOMATIC
UNILATERAL CANNON“A” WAVES 539
Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21005/ on 05/15/2017
were particularly prominent
when
she was in the supine
position.
She had had intermittent
second-degree
atrioventricular
block
since
1964 but had been
asymptomatic
until
October 1975. At that time a ventricular inhibitory pace‘maker was inserted at another
hospital,
when the patient had
become
symptomatic from
Ilock.
She had complained
syncope.
persistent
of fatigue,
2:1 atrioventricular
dyspnea,
and near
an alert,
oriented,
cooperain no distress.
The findings
ears,
nose, and throat
were
within
normal
limits.
The thyroid
gland
was normal.
The
veins of the neck were fiat at an elevation
of 45g. Intermittent pulse-synchronous
waves
of varying
and cyclic intensity
were visible
and palpable
in the left side of the neck.
No
similar
pulsations
were observed
on the right.
Carotid
pulses
were equal,
and there were no murmurs.
The pulse generator
was in a well-healed
left infraclavicular
pocket.
The lungs
were
clear.
Examination
of the heart showed
a regular
rhythm
at 72 beats per minute;
the point of maximal
impulse
was not palpable,
and there were no heaves
or thrills. The first
heart
sound was of varying
intensity;
the second
heart sound
was normal.
A soft ejection
murmur
was heard
at the apex.
Third or fourth heart sounds were not audible.
The blood
pressure
was 130/80 mm Hg in both arms. The abdomen
was
soft, and the liver and spleen were not palpable.
There
were
no abdominal
masses,
nor were there
pulsations
similar
to
those in the neck. The liver did not pulsate.
Femoral
pulses
were present
and equal
bilaterally.
There was no peripheral
edema.
Varicose
veins were noted in both
calves.
Findings
from the neurological
examination
were within
normal
limits.
A complete
blood cell count and differential
count,
levels of
electrolytes,
automated
analysis
of blood
chemistry
(SMA12),
clotting
factors,
and urinalysis
revealed no abnormalities.
electrocardiogram
showed
a 1:1 response
to the paceat 70 beats
per minute
and sinus P-waves
at 75
beats per minute.
An x-ray
film of the chest showed
the
cardiac
contour
to be normal;
a unipopular
pacing
electrode
was found to be positioned
properly
in the apex of the right
ventricle.
The pulmonary
fields were clear, without
evidence
of congestive
changes.
The
maker
I u
i
RIGHT
u
Hospitalization
The patient
underwent
selective
phlebographic
by
manual
injection
i-
CAROTID
Ficuax
1. Simultaneous
recording
right carotid
pulse tracing.
200
msec
PULSE TRACING
of left internal
left
internal
(Fig
1).
there
vein
cardiac
catherization
of both internal
jugular
of meglumine
jugular
Stenosis
and
right
of the
diatrizoate
right
was
throughout
massive
its
tracings
of the
were obtained
internal
jugular
vein
demonstrated
(Fig
left internal jugular
was
at the
vein
of the
Pressure
recordings
dilatation
course.
and
veins
(Renografin)
Simultaneous
carotid
pulses
of the right innominate
junction
2);
right
studies
by I.R.Z.).
(study conducted
Physical
examination
showed
tive, middle-aged
white
woman
from examination
of the head,
I
of
Course
obtained
the inferior
vena
cava
failed
to reveal pulses
of similar
nitude.
The mean
pressures
in the inferior
vena cava,
atrium,
and superior
vena
cava were normaL
in
mag-
right
It was believed
that in some way the atrial contraction
had
to be used, either in atrial
synchronous
pacing
(VAT)
or in
bifocal pacing
(DVT)
to relieve the patient’s
symptoms.
In
either event an electrode
would have to be placed
in the
atrium,
as well as a second
electrode
in the ventricle.
This
could be done by removing
the system
on the left and
replacing
new
right,
it with
an entirely
or by a less satisfactory
system and, via thoracotomy,
method of removing
the
attaching
the appropriate
transvenous
system
on the
present
leads
directly
to the atrium
and ventricle. A third alternative was
to utilize
the existing
ventricular
electrode,
and insert
an
atrial electrode
into the atrial appendage
through
an ipsilateral vein.
The last approach
was selected
as being
the most appropriate.
A
bipolar
wire
(American
Optical
J Wire)
was
inserted
through
the subclavian
vein and was positioned
in
the atrial appendix
according
to a previously described
technique.6 Thresholds
were 1.0 v and 1.2 ma in the atrium
and
1.6
v and 1.3 ma in the ventricle. The amplitude of the P
wave
was adequate
to trigger the atrial
input circuit
of a
programmable
atrial synchronous
pacemaker
(Cordis 0mmSystem).
Thereafter,
cannon “a” waves could no longer be observed,
and the patient
experienced
complete
relief from the leftsided pulsations. Intermittent conversion
of the system to the
fixed-rate
mode of pacing with an externally
applied
magnet
Atricor
resulted
in immediate
reappearance
of the
cannon
waves
and
INTERVA
jugular
venous
pressure
540 WERRESET AL
Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21005/ on 05/15/2017
and
external
indirect
CHEST, 73: 4, APRIl,
1978
patient’s
symptoms
of a normal
right
into
the
had
the
innominate
stenosis
patient
would
of the
buffering
have
suggest
two possibilities.
The thrust
atrial contraction
was diverted
solely
and left internal
jugular
veins;
and
on the
right
not
been
present,
the
had
much
milder
symptoms
because
effect of a larger venous
reservoir.
Or is
it possible
that
this patient
has usually
vigorous
atrial
contractions
and would
have experienced
bilateral
pulsations
of a similar
magnitude
even if the right internal
jugular
vein
were
not stenosed?
The
absence
of symptoms
in the left arm was attributed
to the fact that the
veins of the proximal
portion
of the arm are protected
by
valves,
while
the internal
jugular
vein is not similarly
protected.
It is possible
that
a competent
eustachian
valve at the mouth
of the inferior
vena cava prevented
the propagation
of the cannon
waves
into the inferior
vena
cava
and further
accentuated
the jet into the
innominate
and jugular
veins.
Upon
superficial
examination
the symptoms
experienced
by this patient
may resemble
the so-called
“pacemaking
syndrome.”
This
syndrome,
first
described
by
Mitsui
et al”#{176}in 1969, consists
of systemic
symptoms
(such as dyspnea,
weakness,
dizziness,
pain in the chest,
cold sweats,
flushing
of the face, and palpitations)
and is
believed
to be caused
by an inappropriate
rate of pacing,
indicated
by a fast atrial
rate. The symptoms
of this
syndrome
are promptly
relieved
by a change
in the rate
of pacing.
We believe
that our patient
does not fit these
previously mentioned
criteria.Her symptoms
were unrelated to heart
rate
and were
clearly
related
to the
recorded “a” waves in the jugular pulses. Furthermore,
these symptoms
were unilateral,
were limited
to the neck
and head,
and were not associated
with the other sysFicuiu
2. Phlebogram
of right
internal
jugular
vein.
Arrows
indicate areas of stenosis.
the patient’s original symptoms.
She remained
asymptomatic
during
her stay
in the hospital, and the ECG
revealed
consistent
atrioventricular
synchrony.
Six months
later, pacing remained
consistent.
DIscussIoN
Cannon
plete
“a”
heart
ventricular
waves
block.
a common
are
They
pacemaker
also
if
the
occur
sinus
occurrence
in the
presence
mechanism
in com-
of a
is pre-
served;3’4’7
however,
rarely
do cannon
waves
cause
clinically
significant
symptoms,
but in this case,
the
cannon
waves were so severe that a change
of the pacing
system
to an atrial
synchronous
mode was necessary
to
alleviate
the
The
pulse
patient’s
symptoms.
revealed
cyclic
variations
in the
of the jugular
pulsations
and the carotid
pulsations
that were inversely
related
to each other. The
carotid
pulsations
were largest and the jugular
pulsations
were smallest
when P preceded
QRS at an interval
of 80
to 200 msec.14”8
The reverse
was true when
P fell
near
the peak
of a T wave.
The pressure
that
was
recorded
exceeded
20 mm Hg. It was not possible
to
determine
the cause of the stenosis
of the right internal
jugular
vein.
Speculation
as to the effect
of the stenosis
on the
temic symptoms
of the “pacemaking
syndrome.”
Perhaps
worth emphasizing
is the potential
use of the
atrium
in more patients
than has been the custom
in the
United
States.
According
to a recent
survey,
not more
than 2 or 3 percent
of the pacemakers
inserted
transvenously have been
atrial
synchronous
or bifocal
pacing
units,
because
there
is a lack of confidence
in the stability
of the permanent
atrial
electrode
inserted
in this fashion.
Dislodgment
occurs
with about the same frequency
as
for transvenously
placed
ventricular
electrodes,
which
is
about
4 percent
in the first two weeks.
In addition
to
preventing
cannon
“a” waves and the “pacemaking
syndrome,”
the use of the atrium
in pacing
enhances
cardiac
output
from
5 to 35 percent
in our experience,
and it
may be important
in patients
with borderline
left ventricular
function.1”12
tracings
magnitude
CHEST, 73: 4, APRIL, 1978
ACKNOWLEDGMENT:
was performed
by Leonard
Part of the preliminary work-up
Dreifus,
M.D., Philadelphia.
REFERENCES
1 Scully H, Bello
AC, Beierholm
E, et al: The relationship
between
the atrial systole-ventricular
systole
interval
and
left ventricular
function.
J Thorac
Cardiovasc
Surg 85:
684-694,
1973
2 Leinbach
RC, Chamberlain
DA, Kastor JA, et al: A
comparison
of the hemodynamic
effects of ventricular
and
SYMPTOMATIC UNILATERAL CANNON “A” WAVES
Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21005/ on 05/15/2017
541
A-V segmental
pacing
in patients
with heart
block.
Am
Heart J 78:502-508,
1969
3 Sainet P, Jacobs W, Bernstein
WH,
et al: Hemodynamic
sequelae
of idioventricular
pacemaking
in complete
heart
block. Am J Cardiol
31:594-599,
1963
4 Samet P. Bernstein WH,
Castillo
C: Hemodynamic
sequelae of atrial ventricular and A-V sequential
pacing
in
cardiac patients.
Am Heart J 72:725,
1966
5 ISCHD
Report
on Implantable
Cardiac
Pacemakers.
Circulation
50:A-21-A-35,
1974
Zucker IR, Parsonnet
V, Gilbert
L: A method
of permanent transvenous
implantation
of an atrial electrode.
Am
Heart J 85:195-198, 1973
7 Samet
P, Castillo
C, Bernstein
WH:
Hemodynamic
consequences
of atrial
and ventricular
pacing in subjects with
6
normal
hearts.
Am J Cardiol
18:522-525,
N: Cardiac Pacing. New
Stratton,
Inc., 1973, pp 74-100
9 Mitsui T, Mizuno
A, Hasegawa
T, et al:
indicator for optimal
pacing
rate and the
8 Sarnet
1968
P, Segal
York, Grune
Atrial
rate
cardiac
as an
syn-
pacemaking
drome. Ann Cardiol Angeiol 20:371-379,
1971
10 Mitsui T, Hori M, Suma K, et al: Optimal
heart
and
rate
in
pacing
in coronary
sclerosis
and non-sclerosis.
Ann
NYAcad
Sci 167:745,
1969
11 Parsonnet
V: Keynote
address.
Read
before
the Fifth
International
Pacemaker
Conference,
Tokyo, in press
12 Kleinert
M, Beer P, Taylessarn
A: Comparative
studies
of
transmediosternal
dial placement
International
retrocardial
and transvenous
endocarof atrial electrodes.
Read before the Fifth
Symposium
on Cardiac
Pacing,
Tokyo, in
press
Ebstein’s
Disease
Complete
Associated
Atrioventricular
Block*
James E. Price, M.D.;
Ezra A. Amsterdam,
Zakauddin
Vera, M.D.;
Robert
Swenson,
Dean T. Mason, M.D., F.C.C.P.
The
ated
old
first
with
output
complete
who
and
trography
heart
performed
with
with
complete
heart
tervaL
Treatment
maker
implantation.
H-Q
consisted
is reported
in a 49-year-
of low
His
recovery
conduction
of
and
permanent
cardiac
bundle
of
elec-
intermittent
demonstrated
interval
associ-
anomaly
symptoms
block.
during
prolonged
M.D., F.C.C.P.;
B.A.; and
of Ebstein’s
block
presented
atrioventricular
block
case
documented
man
with
infra-His
normal
cardiac
A-H
Inpace-
intra-atrial
a congenital cardiac anomaly
in
which the tricuspid
valve is deformed
and displaced
downward
into the right ventricle,
is characterized clinically
by a constellation
of electrocardiographic
abnormalities
and
dysrhythmias.’4
Most
prominent
among
these
derangements
are supraventricular
tachycardias,2-4
bizarre
forms of right bundle
branch
block,24
542
CalifornIa
95616
and
To
type
our
B Wolffknowledge,
and high
grade
atrioventricular
conblock have not been previously
documented
in
anomaly.
This report
describes
the first case of
anomaly
associated
with complete
heart block.
bradyarrhythmia
duction
Ebstein’s
Ebstein’s
CASE
A 49-year-old
white
man
REPORT
presented
to the
University
of
California, Davis-Sacramento
Medical
Center
emergency
room in October,
1975, complaining
of fatigue, severe dyspnea
and dizziness of six weeks’ duration.
His cardiac history dated
to childhood
when a heart murmur
was noted and decrease
in exercise
tolerance
began. There was no history of rheumatic fever or scarlet fever and family history was negative
for
cardiac disease.
The patient was first hospitalized
for cardiac symptoms
in
1972 at another
institution
because
of exertional
dyspnea.
Physical
examination
and chest roentgenogram
at that time
revealed
cardiomegaly
with particular
enlargement
of the
right atrium.
Electrocardiogram
(Fig
1) demonstrated
normal sinus rhythm
at 78/mm,
complete
right bundle
branch
block and right axis deviation
of + 1650. Cardiac
catheterization was performed
on that admission
and demonstrated
normal right and left heart hemodynainics.
However,
right ventricular
cineangiography
the tricuspid
valve,
revealed
a right
downward
displacement
of
of reduced
volume and
moderate
tricuspid
regurgitation
into a grossly enlarged
right
atrium
with a large saccular
portion
which had a trabeculated endocardium.
An atrial septal
defect was demonstrated
with a small right-to-left
shunt by venae caval dye curves.
Left ventricular cineangiography
revealed a slightly enlarged
chamber
with normal
contractile
pattern
and competent
mitral valve. The saccular,
trabeculated
portion
of the right
atrium
was interpreted as representing
“atrialization
of the
ventricle”
due to an anomalous
attachment
of the tricuspid
valve, which also accounted for its incompetence.
Diagnosis
was Ebstein’s anomaly of the tricuspid
valve. After discharge,
the patient
was lost to follow-up
until he presented
to the
Sacramento
Medical
Center
in October,
1975.
ventricle
Physical
pulse
examination
examination
revealed
blood pressure
130/80
mm
40/mm
and regular,
respirations
14/mm.
Cardiac
revealed
the point of maximum
impulse
in the
fifth intercostal space at the midclavicular
line. 5, varied
in
intensity,
S2 was physiologically
split and there was a grade
2/6,
high-pitched,
early systolic ejection
murmur
along the
left sternal
border
which increased
slightly
in intensity
with
Hg,
inspiration.
Examination
no
There
were
of the chest,
no
gallops
abdomen
or diastolic
and extremities
murmurs.
revealed
abnormalities.
showed
rhythm
advanced
at a rate
atrioventricular
and
intermittent
conduction
of sinus beats. Chest roentgenogram
disclosed prominent
right heart border and normal pulmonary
vascularity.
Routine
hematologic
data, serum chemistries and
urine
studies
were
of 38/min
normal.
The patient was admitted
to the cardiac
care unit where a
temporary
right ventricular
pacemaker
was inserted.
Right
heart catheterization,
performed
with an end hole electrode
catheter,
#{176}From
the Section of Cardiovascular
Medicine,
Departments
of Medicine
and Physiology,
University
of California
School
of Medicine,
Davis and Sacramento.
Reprint
requests:
Dr. Price, Cardiology,
University
of Calif orDavis,
disturbances
syndrome.-6
The electrocardiogram
block with idioventricular
E bstein’s disease,
nia at Davis,
conduction
Parkinson-White
revealed
the
following
data:
right
atrial
mean
pressure
= 2 mm
Hg, right ventricular
pressure
= 2042
mm
Hg, pulmonary
artery.pressure
= 20/7
mm Hg. Simultneous
umpolar
intracardiac
electrogram
and pressure,
obtained
as
the catheter
was withdrawn
from the right ventricle
to right
PRICEEl AL
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CHEST, 73: 4, APRIL, 1978