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Transcript
Complete Heart Block Complicating
Cardiac catheterization*
Prem K . Gupta, M.D., and Jacob I . Haft, M.D.
Complete heart block developed in two patienb during
cardiac catheterization. Left bundle branch block was
present in one patient prior to study and complete heart
bbck developed during catheter nmanipuhtion in tbe
right ventricle. Marked left axis deviation was the only
conduction abnormality in the second patient. Right
bundle branch block developed during right ventricular
catheterization; complete heart block occurred shortly
thereafter. It is suggested that a standby pacer is indicated during catheterization when transient right bundle
branch block occurs in a patient with left axis deviation,
as in patients with left bundle branch block prior to
right heart catheterization.
T
ransient right bundle branch block is seen commonly
during cardiac catheterization but the development
of c o m ~ l e t eA-V block is rare unless the ~ a t i e nhas
t had
evidence of bundle branch block ~ r i o to
r the ~rocedure.
In two large series of patients undergoing cardiac cathet e r i ~ a t i o n ,transient
~~~
A-V block was seen in five and
seven patients respectively. Stein and associatesS reported five patients with stable bundle branch block
prior to the procedure who developed A-V block during
cardiac catheterization. In the series reported by Wood,'
the incidence of transient RBBB was 5 percent, and
LBBB was considered a contraindication to cardiac catheterization.
This report describes two patients who developed
transient complete A-V block during diagnostic cardiac
*From the Cardiac Section, Department of Medicine, Veterans Administration Hospital, Bronx, New York.
Reprint requests: Dr. Haft, V A Hospital, 130 West Kingsbridge Road, Bronx 10468
LI
L2
L3
AVR
catheterization. The first patient had LBBB prior to the
procedure and therefore is similar to those previously
reported by Stein et al.3 In the second case, marked left
axis deviation (LAD) was the only conduction abnormality present prior to catheterization. During the procedure in the second patient, RBBB developed followed
shortly by complete heart block. This presentation draws
attention to the possible complication of complete heart
block that patients with LAD may incur during cardiac
catheterization.
A 38-year-old Negro man with a oneyear history of heart
murmur was admitted because of paroxysmal nocturnal
dyspnea, dyspnea on exertion, and chest pain. Physical examination revealed blood pressure of 150/80 mm Hg, cardiomegaly, and a grade III/VI diastolic decrescendo murmur at
the aortic area that radiated along the left sternal border. The
electrocardiogram showed regular sinus rhythm with 1st
degree A-V block and complete left bundle branch block
(Fig 1).
After treatment with digitalis and diuretics, cardiac catheterization was performed. During passage of the catheter
through the right ventricle, the patient developed runs of
premature ventricular beats, and later complete heart block
(Fig 2 ) . The patient remained symptomfree during the heart
block episode. The catheter was removed and replaced with a
bipolar electrode catheter; and, the heart was paced in the
demand mode at a rate of 75/min. Two hours later the
rhythm reverted to normal sinus rhythm and pacing was
discontinued.
A 62-year-old man with a history of myocardial infarction
two and a half years earlier, was hospitalized with increasing
dyspnea on exertion, and ankle edema. The patient had
received digoxin and diuretics as an outpatient without relief
of symptoms. On physical examination his neck veins were
engorged at 30°, pulse was 98/min and regular, and blood
pressure was 120/80 mm Hg. Examination of the cardiovascular system showed cardiomegaly and the presence of a
grade III/VI holosystolic murmur at the apex with radiation
to the axilla. The electrocardiogram showed regular sinus
rhythm, marked left axis deviation, left ventricular hypertrophy, and a possible old inferior wall myocardial infarction
(Fig 3).
AVL
AVF
FIGURE1. Twelve lead electrocardiogram from patient 1 showing presence of first degree A-V
block and left bundle branch
block.
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GUPTA AND HAFT
186
FIGURE2. Appearance of complete heart block in patient 1.
Strip A shows regular sinus
rhythm with first degree A-V
block and LBBB (time lines =
0.04 sec ). Strip B shows complete A-V block (time lines =
0.1 sec).
* .
After treatment for, cardiac failure, cardiac catheterization
was performed. During manipulation of the catheter in the
right ventricle, the patient developec! right bundle branch
b l o ~ k(Fig 4B). A No. 4F bipolar electrode catheter was
passed into the right ventricle via the right femoral vein as a
precaution gnd the procedure was cqntinued.
During the left-sided cathetedzation, while the catheter
was being passed into the aorta through the right femoral
artery, intermittent noncqnducted P waves were noted on the
monitor. The, catheter was not advanced further. Cardiac
standstill occurred two minutes later. 4 sharp blow to the
anterior chest wall restarted cardiac activity with an idioventricular rate of 40/min. Right ventricular pacing was instih ~ t e dwith a demand rate of 70/min. Shortly thereafter,
Mobih type I1 block yas recorded (Fig 4C); and after an
hor~rof intermittent,.pacing, the right bundle branch block
disappeared and the patient remained in normal sinus
rhythm.
Normally conduction from the atria to the ventiicles
travels through the A-V node and the bundle of His. T h e
bundle of His in turn diirides into the RBB and LBB.
$$R
llli
LI
L2
L3 . AVR AVL AVF
VI
V2
V3' V4
V5
V6
FIGURE
3. Twelve lead electrocardiogram from patient 2 showing regular sinus rhythm, left axis deviation and left ventricular hypertrophy.
'
T h e main left bundle is short and divides immediately
into the left anterior superior and left posterior inferior
divisions. A block in the LAS divisiqn of the left bundle
branch produces left axis deviation while a block in the
LPI division can produce the pattern of right axis deviation on the electrocardiogram. T h e right bundle is long
and thin and lies superficially under the endocardium,
thus making it more vulnerable to the trauma of catheter
manipulation.
T h e development of RBBB was seen in 14 of &I13
cases who underwent right-sided catheterization in the
series described b y Wennevold and associates.2 I n the
same series, seven cases of A-V block were seen. Wennevold e t a1 did not report the ECG patterns prior to
catheterization.
Similarly, in another series of 2958 cases, five incidences of A-V block and 18 incidences'of RBBB were
reported.' Of 1056 cases undergoing left heart catheterization in another s e r i e ~ ,one
~ instance of complete
heart block occumng during a transeptal procedure was
reported.
In five cases of A-V block r e ~ o r t e dbv Stein and
associate^,^ four had previous LBBB, one had RBBB.
Our first case is similar to the four cases of Stein e t a1
with the presence of LBBB prior to the development of
A-V block. T h e patient did not develop any symptom
because of an adequate ventricular rate.
Our second case is somewhat unusual with regard to
FIGURE
4. From patient 2 .
Strip A: Lead I showing R S R (time lines = 1 sec).
Strip B: Appearance of R B B B (lead I, time lines = 0.1 sec).
Strip C : Dropped P wave (hlobitz 11); (ECG during complete heart block was not recorded ) .
CHEST, VOL. 61, NO. 2, FEBRUARY, 1972
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IDIOPATHIC ALVEOLAR HYPOVENTILATION
the occurrence of complete A-V block. This patient had
evidence of left axis deviation prior to the procedure.
This suggested disease of the anterior superior division of
the left bundle. T h e appearance of RBBB in this patient
during right-sided catheterization left him with the left
posterior inferior division of the left bundle as the only
conduction pathway from the common bundle to the
ventricles. Because trauma might occur to this conduction pathway when the left ventricle was entered, a
standby pacing catheter was passed into the right ventricle before going on to left ventricular catheterization.
Subsequently, the patient developed complete A-V
block while a catheter was being passed into the aorta
through the right femoral artery.
I t is d a c u l t to say why conduction failed in the
posterior inferior radiations of the left bundle before the
catheter entered the left ventricular cavity. Bundle
branch block has been reported to occur during passage
of needles or cannulae into blood vessel^.^ This type of
transient block in conduction may b e due to an inappropriate vasovagal type response. Alternatively, passage of
the catheter through the aorta in this patient may have
been coincidental. Clinically, patients with right bundle
branch block and left axis deviation frequently go on to
develop transient or permanent complete heart block7 as
they age or as the disease process effecting the RBB a n d
the anterior radiations of the left bundle extends to
jeopardize the posterior inferior radiations of the left
bundle. I n our patient, the posterior inferior radiations
may already have been compromised, but to a lesser
extent than the anterior superior radiations. Dependence
of all A-V conduction on the posterior radiations, as in
this case, would cause any failure of conduction through
this fascicle to present as complete heart block or as the
dropped beat of Mobitz type I1 second degree heart
block. In our patient both transient complete heart block
and Mobitz 11occurred.
From this experience, w e feel that a standby pacemaker is warranted in patients with previous left axis
deviation who develop right bundle branch block during
right heart catheterization. This indication for a standby
pacer should b e added to those previously accepted; ie,
permanent LBBB before right ventricular catheterization and permanent RBBB before left ventricular catheterization.
1 Bagger M, Biorck G , Bjork VO, et al: On methods and
complications in catheterization of heart and large vessels,
with and without contrast injection. Amer Heart J 54:766,
1957
2 Wennevold A, Christiansen I, Lindeneg 0: Complications
in 4413 catheterizations of the right side of the heart. Amer
Heart J 69: 173, 1965
3 Stein PD, Mathur VS, Herman MV, et al: Complete heart
block induced during cardiac catheterization of patients
with preexistent bundle branch block. Circulation 34:783,
1966
4 Wood P: In Diseases of the Heart and Circulation. (3rd
e d ) , Philadelphia, J. B. Lippincott 1968, p 198
5 Christiansen I, Wennevold A : Complications in 1056 in-
vestigations of the left side of the heart. Amer Heart J 71:
601-610, 1966
6 Report of Committee on Cardiac Catheterization and
Angiocardiography, American Heart hsociation. Circulation 7:769, 1953
7 Lasser RP, Haft JI, Friedberg CK: Relationship of right
bundle branch block and marked left axis deviation (with
left parietal or periinfarction block) to complete heart
block and syncope. Circulation 37:429, 1968
Idiopathic Alveolar Hypoventilation
Related to Head ~ r a u m a *
Wilhert S. Aronow, M.D., F.C.C.P.," a d
Edward A. Stemmer, M.D., F.C.C.P.t
The clinical, laboratory, and postmortem f i n d i i in a
patient with the idiopathic hypoventilation syndrome
probably related to head trauma are described.
T
h e following report illustrates the first case of the
idiopathic hypoventilation syndrome probably related to head trauma.
A 44-year-old white man was first hospitalized at the Long
Beach (California) Veterans Administration Hospital from
June 1, 1965 until September 2, 1965 because of episodes of
unconsciousness for 21 years. At age 23, he became unconscious following multiple blows to his head. Two weeks later,
he developed an episode of unconsciousness which lasted for
two minutes. These episodes gridually increased in freqriency during the next 21 years, occurred from once weekly to
twice daily, and lasted from 1 to 20 minutes. He developed
apnea, cyanosis, loss of muscle tone, and complete loss of
consciousness during these episodes; no ictal phenomena
were associated. He had been hospitalized many times at
different hospitals during this 21-year period with the diagnosis of post-traumatic epilepsy and had been treated unsuccessfully with diphenylhydantoin, phenobarbital, and primidone. There wa5 no family history of any neurologic disorder.
He was 5 feet, 8 inches tall and weighed 177 pounds; his
blood pressure was 140/80 mm Hg and pulse was regular at
a rate of 82 beats per minute; his respiratory rate was 20
respirations per minute. He had a cyanotic appearance;
physical examination was otherwise within normal limits.
His hemoglobin ranged from 16.9 to 19.5 g percent;
'From the Cardiolo y Section, Medical Service and Surgical
Service, Long ~ e a c %Veterans Administration Hospital, and
the University of California College of Medicine, Irvine.
"Cardiologist and Chief of Phonocardiography, Long Beach
Veterans Administration Hospital; Clinical Assistant Professor of Medicine, University of California College of
hledicine, Iwine.
?Chief, Surgical Service, Long Beach Veterans Administration Hospital; Associate Professor of Surgery, University
of California College of Medicine. Iwine.
Reprint requests: D;. Aronow, VA Hospital, Long Beach
90801
CHEST, VOL. 61, NO. 2, FEBRUARY, 1972
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