and change the filters. This may be all that is necessary to
prevent the buildup of M avium complex in hot tubs. M
avium complex is resistant to chlorination and so it is found
in domestic water.32 The high chlorine concentrations
needed for sterilization may be unpleasant for hot tub use.
Superheating the water, if possible, to 70°C for up to an hour
may help.3-5 If our findings prove to occur more frequently in
hot tubs, then a study of how to control the growth of M
avium complex must be done.
ACKNOWLEDGMENT: We acknowledge the consultation
from Dr. A. Pan on the first case, the radiologic assistance of Dr.
B. Maycher for the CT scan, the work of Ms. J. Wolfe in the
Mycobacterial
Laboratory, Winnipeg, and the expertise of Char¬
lotte Smith for serologic testing in the Centers for Disease
Control and Prevention, Atlanta.
1
References
Scully RE, Mark EJ, McNeely WF, et al. Case 6-1996. Case
records of the Massachusetts General Hospital. N Engl J Med
1996; 334:521-26
DS, Peterson DD, Steiner RM,
2 Prince
et
al. Infection with
Mycobacterium avium complex in patients without predispos¬
ing conditions. N Engl J Med 1989; 321:863-68
3 von Reyn CF, Maslow JN, Barber TW, et al. Persistent
colonisation of potable water as a source of Mycobacterium
avium infection in AIDS. Lancet 1994; 343:1137-41
4 Marinkovich VA, Novey HS. Humidifier lung. Clin Rev
Allergy 1983; 1:533-36
5 du Moulin GC, Stottmeier KD, Pelletier PA, et al. Concen¬
tration of Mycobacterium avium by hospital hot water sys¬
tems.
JAMA 1988; 260:1599-1601
6 Yakrus
MA, Reeves MW, Hunter SB. Characterization of
isolates of Mycobacterium avium serotypes 4 and 8 from
patients with AIDS by multilocus enzyme electrophoresis.
J Clin Microbiol 1992; 30:1474-78
7 Gruft H, Katz J, Blanchard DC. Postulated source ot Myco¬
bacterium intracellulare (Battey) infection. Am J Epidemiol
1975; 102:311-18
8 Wendt SL, George
KL, Parker BC, et al. Epidemiology of
by nontuberculous Mycobacteria: III. Isolation of
potentially pathogenic mycobacteria from aerosols. Am Rev
Respir Dis 1980; 122:259-63
9 Parker BC, Ford MA, Gruft H, et al. Epidemiology of
infection by nontuberculous Mycobacteria: IV. Preferential
aerosolization of Mycobacterium intracellulare from natural
waters. Am Rev Respir Dis 1983; 128:652-56
10 Rosenzweig *DY. Pulmonary mycobacterial disease due to My¬
cobacterium intracellulare-avium complex: clinical features and
course in 100 consecutive cases. Chest 1979; 75:115-19
11 Engback HC, Vergmann B, Bentzon MW. Lung disease
caused by Mycobacterium avium/Mycobacterium intracellu¬
lare. An analysis of Danish patients during the period 196276. Eur J Resp Dis 1981; 62:72-83
12 Hawkins CC, Gold JWM, Whimbey E, et al. Mycobacterium
avium complex infection in patients with the acquired immu¬
nodeficiency syndrome. Ann Intern Med 1986; 105:184-88
13 Teirstein AS, Damsker B, Kirschner PA, et al. Pulmonary
infection with Mycobacterium avium-intracellulare: diagnosis,
clinical
treatment. Mt Sinai
infection
patterns,
J Med 1990; 57:209-15
EF, Thiede WH, Fink JN. Hypersensitivity pneu¬
monitis due to contamination of an air conditioner. N Engl
J Med 1970; 283:271-76
15 Hodges GR, Fink JN, Schlueter DP. Hypersensitivity pneu¬
monitis caused by a contaminated cool mist vaporizer. Ann
Intern Med 1974; 80:501-04
14 Banaszak
16 Miller MM, Patterson R, Fink
JN, et al. Chronic hypersen¬
sitivity lung disease with recurrent episodes of hypersensitiv¬
ity pneumonitis due to a contaminated central humidifier.
Clin Allergy 1976; 6:451-62
17 Friend
JAR, Pickering CAC, Palmer KNV, et al. Extrinsic
allergic alveolitis and contaminated cooling-water in a factory
machine. Lancet 1977; 1:297-300
18 Muittari A, Kuusisto P, Virtanen P, et al. An epidemic of
extrinsic allergic alveolitis caused by tap water. Clin Allergy
1980; 10:77-90
19 Lynch DA, Rose CS, Way D, et al. Hypersensitivity pneumo¬
nitis: sensitivity of high-resolution CT in a population-based
study. AJR 1992; 159:469-72
20 Metzger WJ, Patterson R, Fink J, et al. Sauna-takers diseases:
hypersensitivity
pneumonitis due to contaminated water in a
home sauna. JAMA 1976; 236:2209-11
21 Atterholm I, Hallberg T, Ganrot-Norlin K, et al. Unexplained
acute fever after a hot bath. Lancet 1977; 2:684-86
22 Coleman A, Colby TV. Histologic diagnosis of extrinsic
allergic alveolitis. Am J Surg Pathol. 1988; 12:514-18
23 Baur X, Behr J, Dewair M, et al. Humidifier lung and
humidifier fever. Lung 1988; 166:113-24
24 Solley GO, Hyatt RE. Hypersensitivity pneumonitis induced by
Penicillium species. J Allergy Clin Immunol 1980; 65:65-70
25 Edwards
26
JH, Griffiths AJ, Mullins J. Protozoa as sources of
antigen in "humidifier fever." Nature 1976; 264:438-39
Kane GC, Marx JJ, Prince DS. Hypersensitivity pneumonitis
secondary to Klebsiella oxytoca: a new cause of humidifier
lung. Chest 1993; 104:627-29
27 Muittari A, Rylander R, Salkinoja-Salonen M. Endotoxin and
bath water [letter]. Lancet 1980; 2:89
28 Sausker WF, Aeling JL, Fitzpatrick JE, et al. Pseudomonas
folliculitis acquired from a health spa whirlpool JAMA 1978;
239:2362-65
29 Rose
HD, Franson TR, Sheth NK,
pneumonia associated with
use
of
a
et al. Pseudomonas
home whirlpool spa.
JAMA 1983; 250:2027-29
C, Hill JJ, Graham DR. Atypical mycobacterial
infection of soft tissue associated with use of a hot tub. J Bone
Joint Surg 1986; 68A:766-68
Montecalvo MA, Forester G, Tsang AY, et al. Colonisation of
30 Aubuchon
31
potable water with Mycobacterium avium complex in homes
of HIV-infected patients [letter]. Lancet 1994; 343:1639
32 Pelletier PA, du Moulin GC, Stottmeier KD. Mycobacteria in
public water supplies: comparative resistance to chlorine.
Microbiol
Sci 1988; 5:147-48
Another Hot Tub Hazard*
Toxicity Secondary to Bromine and
Hydrobromic Acid Exposure
Michael J. Burns, MD; and
Christopher H. Linden, MD
We describe the clinical
of two patients who
followed by reactive
course
developed acute pneumonitis
*From the Section in Toxicology, Division of Emergency Medi¬
cine, Beth Israel Hospital, Boston (Dr. Burns); and the Depart¬
ment of Emergency Medicine, Division of Toxicology, Univer¬
sity of Massachusetts Medical Center, Worcester (Dr. Linden).
received April 29, 1996; revision accepted Sep¬
Manuscript
tember 19.
Reprint requests: Dr. Michael Burns, 26 Edmunds Way, North-
boro, MA 01532
816
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Selected
Reports
airways dysfunction syndrome after bathing in a hot
tub. Additional findings were present and suggested
that exposure to a corrosive agent was responsible.
Bromine and hydrobromic acid generated from a
implicated as
widely used water disinfectant were
the underlying cause. Physicians should be alert to
the possibility that such exposures may initiate or
exacerbate inflammatory pulmonary disease.
(CHEST 1997; 111:816-19)
Key words: bromine; hot tub; hydrobromic acid; RADS
Abbreviations: Br2=aqueous or gaseous bromine; HBr=hydrobromic acid; HOBr=hypobromous acid; HOCl=hypochlorous
acid; RAD S=reactive airways dysfunction syndrome
a popular recreational activity.
bathing is considered
safe, public facilities
-¦¦"¦-Although generally
hot
tub use by individ¬
have
usually signs warningtakeagainst
or have
certain
TT ot tub
uals who are pregnant,
medicines,
diabetes or cardiovascular disease. A variety of medical
Except
problems have been linked to hotduetubtobathing.13
the fungus, Clafor hypersensitivity pneumonitis
dosporium, however, pulmonary complications have not
been described previously (to our knowledge).4 We de¬
scribe two patients who developed signs and symptoms of
acute bromine toxicity followed by reactive airways dys¬
function syndrome (RADS) after bathing in a hot tub and
discuss the pathogenesis and pathophysiology of their
disease.
Case Reports
Case 1
A 42-year-old woman presented with burning eyes,
chest, and
throat, shortness of breath, and wheezing that began during a
10-min bath in a hot tub 2 h earlier. She reported a strong odor
of "bleach" in the hot tub area, a glass-enclosed room measuring
8X11 feet, located inside a local health club. Black discoloration
of her gold jewelry and green bathing suit was also noted. She had
been in good health previously and did not smoke. Mild inspira¬
tory stridor, expiratory wheezing, and a bleach-like odor to the
breath were noted on examination. Vital signs were normal and
the eyes, nose, throat, and skin were unremarkable. Oxygen
saturation was 98% on room air. Chest radiograph and results of
routine laboratory analyses were unremarkable. She was treated
with humidified oxygen and nebulized albuterol during a 24-h
hospitalization.
She reported
alopecia during
generalized
the following week and month, respectively.
Dyspnea and chest burning continue to occur on exertion and
exposure to cold air and strong odors. Symptoms respond to
inhaled albuterol. Pulmonary function tests performed 3 and 10
months after exposure revealed normal results of spirometry and
challenge.
lung volumes with a strongly positive methacholine
The provocative doses required to produce a 20% fall in FEVX
were 0.008 and 0.007 |jimol, respectively. An c^-antitrypsin level
was normal. Flexible sigmoidoscopy performed 13 months after
her exposure revealed nonspecific proctitis.
intermittent rectal
bleeding
and
Case 2
A 32-year-old woman presented with burning eyes, throat, and
chest; hoarseness; nonproductive cough; and mild dyspnea that
developed during a single 5-min bath in the same hot tub at the
same time as patient 1. She, too, reported a strong acrid odor
while bathing in the hot tub. She was previously healthy and did
not smoke. Results of physical examination were normal. Oxygen
saturation was 99% on room air. Chest radiograph and results of
arterial blood gas analysis were normal. No treatment was
administered. Cough, sore throat, and hoarseness persisted for 7
months. She continues to have chest burning with exertion.
Pulmonary function tests performed 10 months after exposure
revealed normal lung volumes and normal results of spirometry
but a strongly positive methacholine challenge (provocative dose
required to produce a 20% fall in FEVl5 0.447 |jimol).
Discussion
Clinical manifestations and the temporal course of
events suggested exposure to an irritant chemical in the
hot tub water and atmosphere as the etiology of our
patients' signs and symptoms. Bleach (hypochlorous acid,
HOCl) or a chlorine-based disinfectant was initially sus¬
Investigation, however, revealed that a brominepected.
based agent was used in the hot tub in question.
Three brominating compounds are available for recre¬
ational hot tub, spa, and swimming pool sanitation: elemental
bromine, sodium bromide/monopotassium persulfate, and
All three compounds gen¬
bromochlorodimethylhydantoin.
erate aqueous hypobromous acid (HOBr), the primary bac¬
tericidal agent, when dissolved in water.
In the present incident, l-bromo-3-chloro-5,5-dimeth-
("Brom Tabs," "Brominating Tablets") was
ylhydantoin
identified as the brominating agent. When added to pool
water, this compound hydrolyzes to HOBr and HOCl.5
Bromide ions are subsequently generated when HOBr
reacts with microorganisms. In an acidic pH, as occurs at
also exists as hydrobromic
high concentrations, bromide
acid (HBr). Unless the pH is kept relatively neutral (eg, by
adding potassium carbonate), these two compounds
readily react to form aqueous bromine (Br2). The subse¬
quent liberation of Br2 (and possibly HBr) vapors in¬
creases as water temperatures increase. Chlorine gas is not
generated because HOCl reacts with bromide ions result¬
ing in the reformation of HOBr.5
Pool water bromination is achieved similarly with the
sodium bromide/monopotassium persulfate method.
When these compounds are added to water, bromide ions
are oxidized by monopotassium persulfate to HOBr.5
Subsequent reactions are the same. Aqueous Br2 concen¬
are recommended for
between 2 and 4
trations
ppm
residential spas and 4 to 6 ppm for commercial spas.5
Water pH should be between 7.2 and 7.6 optimally.
Br2 and HBr liquids and their vapors are skin and
mucous membrane irritants. The extent of tissue injury is
dependent on their concentration, duration of contact, and
water content of exposed tissue. Pathologic effects include
edema, inflammation, and necrosis. Exposure to atmo¬
considered
spheric concentrations of 10 ppm0.3of Br2 isis the
current
ppm
immediately dangerous to life and
short-term (15-min) exposure limit.6 Human volunteers
could not tolerate a Br2 concentration of 0.9 ppm for
greater than 5 min.7 Br2 is two to three times more
corrosive than HBr. Nasal irritation occurs at HBr vapor
concentrations of 5 to 6 ppm.8
CHEST / 111 / 3 / MARCH, 1997
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817
Like chlorine, the major
to be secondary
presumed
cytotoxic effects of Br2
are
oxidizing effects of
nascent oxygen.9 Br2 reacts rapidly with tissue water to
form HBr and HOBr. HOBr may subsequently break
down into HBr and oxygen free radicals.10 The corrosive
action of the acids generated and reaction of Br2 and these
to
the
acids with cellular proteins to form bromamine and thiol
radicals may contribute to toxicity. Greater water solubil¬
ity, and, thus, tissue permeability may explain why bro¬
mine is more toxic than chlorine.
Clinical manifestations usually begin immediately after
vapor inhalation but may be delayed for up to 10 h.11
Generally, low-concentration exposures will result in eye,
nose, and upper airway injury and higher concentrations
will additionally result in lower airway damage. Sequelae
are infrequent and usually consist of subjective complaints
without objective findings to correlate with symptoms.12
One patient developed chemical pneumonitis and a
restrictive pattern of pulmonary dysfunction following
short-term exposure to a mixture of HBr and phosphorus
tribromide.13 Persistent bronchiolar spasm has been ob¬
served in animals exposed to Br2 vapors but not in
humans.14
Both patients described fulfill the criteria for RADS.15
The abrupt onset of irritant symptoms within minutes of a
single bath suggest high-concentration irritant exposure.
Circumstances strongly implicate exposure to bromine
and HBr as the precipitating event. Allergic asthma (hy¬
persensitivity pneumonitis) was not considered likely be¬
cause it is typically insidious in onset, requiring repetitive
exposures to elicit an inflammatory reaction. Even with
acute hypersensitivity pneumonitis, symptoms do not de¬
velop until 4 to 6 h after exposure. In addition, patients
with hypersensitivity pneumonitis typically have constitu¬
tional symptoms, abnormal chest radiographs, and restric¬
tive pulmonary disease, findings that were not seen in our
patients.
The pathophysiologic state of RADS has not been fully
elucidated. Nonspecific bronchial hyperresponsiveness is
operative and may be mediated by structural airway
abnormalities, immunogenic inflammation, and dysregulation of neurogenic inflammation.16 Bronchial biopsy
specimens from patients with RADS have revealed epi¬
thelial destruction, squamous cell hyperplasia, subepithelial
basement membrane and connective tissue thickening, and
variable nonspecific inflammatory cell response (lymphocytes
and plasma cells).151718 Structural bronchial damage is
closely linked to heightened airway responsiveness.
RADS has been reported following inhalation of chlo¬
rine gas19 and pulmonary toxic reactions have resulted
from the inhalation of vapors generated by swimming pool
tablets.10 Given the widespread use of bro¬
chlorinating
mine compounds as bathing water disinfectants, the lack
of previously reported cases of toxic reactions from bro¬
minating agents is surprising, particularly in the setting of
hot tub use, where high water temperatures would be
expected to promote the liberation of toxic vapors. This
may reflect greater safety of bromine-containing disinfec¬
tants as compared with chlorinated ones. The greater
water solubility of bromine allows for less vapor liberation
from aqueous solutions. Alternatively, similar cases may
have occurred but gone unrecognized or unreported.
We suspect that the bromine concentration and pH of
the hot tub water in which our patients bathed were
higher and lower, respectively, than recommended. The
jewelry and bathing suit discoloration noted by patient 1
supports this contention. We were unable, however, to
obtain any information from the health club management
in regards to these parameters. Although not previously
described, alopecia and proctitis are also consistent with
the known toxicity (ie, corrosive effects) of bromine and its
acid and exposure by way of immersion.
halogen
An abnormally high bromine concentration or abnor¬
mally low pH in the hot tub water would also have resulted
in greater production and liberation of Br2 and HBr
vapors, and, hence, respiratory tract exposure. The fact
that the hot tub was located in a small room rather than
outdoors or in a larger (eg, poolside) indoor area may have
created a situation similar to that of smoke inhalation,
where exposure in an enclosed space is well known to
increase the risk of respiratory tract injury. Since both of
our patients reported that no one else was present in the
hot tub at the same time as they were, we were unable to
determine whether other people used the hot tub in
question and were similarly affected. We suspect that
when our patients reported their symptoms to the health
club management at the time of exposure, the hot tub area
was closed to use until the situation could be investigated
and corrected.
The known chemistry of brominating compounds, their
reported use in the hot tub in question, the temporal
relationship between exposure and toxic effects, clinical
signs and symptoms that were consistent with the known
toxicity of halogen gases and their acids, and the absence
of alternative explanations strongly implicate Br2 and HBr
as the cause of our patients' illnesses. Bromine poisoning
should be added to the list of potential hot tub hazards. As
with chlorine gas exposure, inhalation of Br2 and HBr
vapors may cause RADS. Patients with new-onset RADS
or exacerbation of preexisting pulmonary disease should
be questioned about hot tub use and exposure to halogen
gases or vapors as a precipitating factor. Further study is
necessary to determine the incidence of poisoning result¬
ing from such exposures.
References
1 Press E. The health hazards of saunas and spas and how to
minimize them. Am J Public Health 1991; 81:1034-37
2 Sausker WF, Aeling JL, Fitzpatrick JE, et al. Pseudomonas
folliculitis acquired from a health spa whirlpool. JAMA 1978;
239:2362-65
3
Spitalny KC, Vogt RL, Witherell LE. National survey on
outbreaks associated with whirlpool spas. Am J Public Health
4
Jacobs RL, Thorner RE, Holcomb JR, et al. Hypersensitivity
pneumonitis caused by Cladosporium in an enclosed hot-tub
area. Ann Intern Med 1986; 105:204-06
Mitchell PK. The proper management of pool and spa water:
catalog 88-83735. Decatur, Ga: Hydrotech Chemical Corpo¬
ration, 1988; 17-28
Stokinger HE. The halogens and the nometals boron and
silicon. In: Clayton GD, Clayton FE, eds. Patty's industrial
1984; 74:725-26
5
6
818
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Selected
Reports
7
hygiene and toxicology.
Wiley, 1981; 2965-72
3rd ed (vol IIB). New York:
John
Henschler D. Wirkungen geringer chlor- und
brom-konzentrationen auf den Menschen. Int Arch Gewer-
Rupp H,
bepathologie Gewerbehygiene 1967; 23:79-90
compounds. In: Parmeggiani
8 Alexandrov DD. Bromine and
L, ed. Encyclopedia of occupational health and safety. 3rd ed
(vol 1). Geneva, Switzerland: International Labour Organisa¬
tion, 1983; 326-29
9 Decker WJ, Koch HF. Chlorine poisoning at the swimming
pool: an overlooked hazard. Clin Toxicol 1978; 13:377-81
10 Wood BR, Colombo JL, Benson BE. Chlorine inhalation
toxicity from vapors generated by swimming pool chlorinator
11
tablets. Pediatrics 1987; 79:427-30
Champeix J, Catilina P, Andraud G, et al. Etude clinique et
experimentale de l'intoxication par vapeurs de brome. Pou-
mon Coeur 1970; 26:895-903
12 Carel RS, Belmaker I, Potashnik
G, et al. Delayed health
of accidental exposure to bromine gas. J Toxicol
Environ Health 1992; 36:273-77
13 Kraut A, Lilis R. Chemical pneumonitis due to exposure to
bromine compounds. Chest 1988; 94:208-10
14 Schlagbauer M, Henschler D. Toxicitat von chlor und brom
bei einmaliger und wiederholter Inhalation. Int Arch Gewer-
sequelae
bepathologie Gewerbehygiene 1967; 23:91-8
airways dys¬
function syndrome (RADS): persistent asthma syndrome
after high level irritant exposures. Chest 1985; 88:376-84
15 Brooks SM, Weiss MA, Berstein IL. Reactive
Meggs WJ. RADS and RUDS.the toxic induction of asthma
and rhinitis. Clin Toxicol 1994; 32:487-501
17 Deschamps D, Soler P, Rosenberg N, et al. Persistent asthma
after inhalation of a mixture of sodium hypochlorite and
hydrochloric acid. Chest 1994; 105:1895-96
18 Gautrin D, Boulet LP, Boutet M, et al. Is reactive airways
dysfunction syndrome a variant of occupational asthma?
J Allergy Clin Immunol 1994; 93:12-22
19 Decker WJ. Reactive airway dysfunction syndrome (RADS)
following single acute exposure to chlorine gas [abstract]. Vet
Hum Toxicol 1988; 30:344
16
syndrome is discussed.
'
Neurocardiogenic Syncope and
Prinzmetal's Angina Associated
With Bronchogenic Carcinoma*
Paolo Angelini, MD; and Paul Y.
Holoye, MD
case is presented illustrating a previously
of (1) neurocardiogenic syn¬
unreported association
cope of new onset in a 57-year-old man, (2) Prinz¬
metal's angina, and (3) bronchogenic carcinoma of
the lung. Initiation of aggressive chemotherapy re¬
sulted in immediate suppression of both cardiac
manifestations. This newly described paraneoplastic
A clinical
*From the Departments of Adult Cardiology (Dr. Angelini) and
Medical Oncology (Dr. Holoye), St. Luke's Episcopal Hospital
and the Texas Heart Institute, and the Department of Internal
Medicine, Baylor College of Medicine, Houston.
Manuscript received January 10, 1996; revision accepted
Leachman Cardiology Associates,
Reprint requests: Dr. Angelini,
PO Box
TX 77225-0206
April 24.
20206, Houston,
(CHEST 1997; 111:819-22)
Key words: bronchogenic carcinoma; neurocardiogenic syncope;
Prinzmetal's angina
eurocardiogenic syncope is a well-defined cardiovasT^T^ cular
condition; its cause, however, is still poorly
understood.12 Although several pathophysiologic interpre¬
its cause have been
tations
various
¦**
regarding
mechanisms may contribute
to
the
proposed,
cause
in different
simultaneously in one patient.24 We
present an unusual case of neurocardiogenic syncope,
which was associated with a malignant form of Prinzmet¬
al's angina. In this patient, the causative factor, broncho¬
genic carcinoma, could be substantiated by empirical and
clinical proof. Treatment of carcinoma by chemotherapy
patients
or even
indeed sufficient for prompt elimination of the
diovascular symptoms.
was
car¬
Case Report
A 67-year-old Hispanic man, who was a long-time cigarette
smoker (2 packs per day), was well until February 1995 when he
began to experience episodes of syncope. Initially, he related the
syncope to changing from the supine to the erect position;
eventually, he began to experience these episodes even during
bed rest. On March 30, 1995, he was admitted to a hospital in
Mexico City because of prolonged resting pain, accompanied by
near syncope. After the ECG showed anterior ST-T segment
changes, he was immediately taken to the catheterization labo¬
ratory; a tentative diagnosis was made of acute anterior myocar¬
dial infarction. During the catheterization procedure, the patient
was sedated and the pain disappeared. At that time, coronary
angiography revealed a normal coronary flow pattern, with the
appearance of a left anterior descending coronary artery lesion
that showed about 50% diameter narrowing. While the patient
was being prepared for balloon angioplasty, he again complained
of chest pain and developed severe hypotension and bradycardia.
New coronary angiograms clearly revealed an uneven flow pat¬
tern with slow flow limited to the left anterior descending
coronary artery7 territory, without discrete narrowing. The ECG
showed anterior T-wave changes and mild ST elevation, with
advanced atrioventricular block. Intracoronary nitroglycerin and
temporary ventricular pacing alleviated the bradycardia and
ischemia. The new angiograms revealed no fixed stenosis and
brisk flow in all the coronary branches. The procedure was thus
aborted. Because of recurrent episodes of syncope and atrioven¬
tricular block with long periods of asystole, the patient eventually
received a permanent atrioventricular sequential pacemaker.
Medications were changed to disopyramide (100 mg, 3 times a
day), fludrocortisone (0.1 mg daily), famotidine (40 mg daily), and
sedatives. The patient continued to be bedridden because of
recurrent dizziness and chest pain until his admission to St.
Luke's Episcopal Hospital on May 5, 1995. At that time, physical
examination revealed an anxious, diaphoretic, acutely ill patient.
No significant abnormalities were discovered at the time of
physical examination, which included a detailed neurologic ex¬
amination. BP was 110/70 mm Hg. ECGs obtained over the next
several days (Fig 1) showed sinus or electronic pacemaker atrial
rhythm or intermittent atrial fibrillation, with normally con¬
ducted QRS complex and transient T-wave changes that corre¬
lated with chest pain. A chest x-ray film was read as normal, with
possible linear atelectasis in the left perihilar region.
CHEST/111 /3/MARCH, 1997
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819