(Chest. 2001;120:2098-2100.)
© 2001
American College of Chest Physicians
Hemoptysis Provoked by Voluntary Diaphragmatic Contractions in Breath-Hold Divers*
Esen Kiyan, MD;
Samil Aktas, MD and
Akin Savas Toklu, MD
*
From the Department of Chest Medicine (Dr. Kiyan), and Department of Undersea and Hyperbaric Medicine (Drs. Aktas and Toklu), Istanbul University, Istanbul, Turkey.
Correspondence to: Samil Aktas, MD, Istanbul Universitesi, Istanbul Tip Fakültesi, Deniz ve Sualti Hekimli
i AD, 34390, Capa, Istanbul-Turkiye; e-mail: aktasmil{at}hotmail.com
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Abstract
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Pulmonary barotrauma of descent (lung squeeze) has been described
in breath-hold divers when the lung volume becomes smaller than the
residual volume (RV), with the effect of increased ambient pressure.
However, the ratio between the total lung capacity and the RV is not
the only factor that plays a role in the lung squeeze. Blood shift into
the thorax is another important factor. We report three cases of
hemoptysis in breath-hold divers who dove for spear fishing in
shallower depths than usual. All of the divers performed voluntary
diaphragmatic contractions at the beginning of their ascent, while
their mouths and noses were closed. We suggest that the negative
intrathoracic pressure due to the forced attempt to breathe in with
voluntary diaphragmatic contractions contributes to alveolar
hemorrhage, since it may damage the pulmonary capillaries.
Key Words: alveolar hemorrhage • breath-hold diving • hemoptysis
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Introduction
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Pulmonary
barotrauma of descent (lung squeeze) occurs in breath-hold divers when
the lung volume becomes smaller than the residual volume
(RV).1
As the diver descends deeper, the gas in the lung
will be compressed and the lung volume will be diminished, with the
effect of the increased ambient pressure, according to Boyle’s law.
During descent, total lung capacity (TLC) decreases and reaches the RV
at a certain depth, and further descent may cause alveolar hemorrhage
and pulmonary edema.1
2
The depth at which TLC is reduced
to RV is the theoretical maximal depth for a breath-hold diver. The
rise in water pressure with depth is equivalent to 0.1 atm/m. At
10 m of seawater, 1 atm of air and 1 atm of water will be pressing
on the breath-hold diver, reducing the lung volume to one half of TLC.
Since RV averages one fourth of TLC, a pressure of 4 atm at 30 m
of seawater will reduce the lung volume to RV.
It is known that many breath-hold divers exceed their depth limits
calculated on the basis of the TLC/RV ratio. Additional factors must
therefore be considered. At greater depths, the high negative
transthoracic pressure that develops as the diver passes through
30 m and the chest wall approaches its elastic limit draws about 1
L of blood into the thorax.1
As a result, pulmonary
capillaries bulge prominently into the alveolar spaces, replacing air
and resulting in a decrease of RV and thereby extending the depth
limit.1
2
However, blood shift into the thorax may
predispose to alveolar hemorrhage by causing an increase in the
pulmonary capillary pressure. In this study, we report three cases of
hemoptysis in breath-hold divers following voluntary diaphragmatic
contractions
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Case Reports
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We observed three divers who had experienced hemoptysis while
breath-hold diving. All three divers were nonsmoking healthy men aged
22 to 37 years and had no significant medical histories. They were also
scuba divers, and they had no histories of pulmonary barotrauma of
ascent or decompression sickness. They were free of diseases
predisposing to pulmonary hemorrhage. None of the divers were receiving
medications, including acetylsalicylic acid (aspirin), and none of them
reported aspiration of water. According to the results of an ear, nose,
and throat examination, they had no ear or sinus squeezing as a cause
of hemorrhage. They dove in Mediterranean waters during the summer.
Their characteristics, symptoms, and outcomes are presented in Table 1
.
Case 1
A 37-year-old, healthy, well-trained, male breath-hold diver
performed several dives to the depth of 10 to 12 m. He then dove
to 17 to 18 m and descended to 20 to 22 m for spear fishing. After
30 s at this depth, he developed shortness of breath while he was
making voluntary diaphragmatic contractions. After returning to the
surface, he had a sudden onset of coughing and expectorated bloody
froth. He had no chest pain. Within an hour, he was comfortable and his
symptoms resolved spontaneously. One week after this event, he was
admitted to our clinic. Results of physical examination, lung function
testing, oxygen saturation, and chest radiography were normal, but the
thorax CT obtained 2 h after the diving event revealed
images suggestive of alveolar hemorrhage (Fig 1 ). A diagnosis of alveolar hemorrhage was made based on his history and
CT findings. Because of late hospital admission, we could not perform
BAL to document alveolar hemorrhage. The patient had a history of five
episodes of hemoptysis during breath-hold diving. When we obtained the
detailed history of these episodes, we learned that he had performed
voluntary diaphragmatic contraction during all episodes. Control CT
findings were normal 3 weeks after the event. The follow-up examination
of the diver revealed no evidence of lung, heart, or hematologic
disease.
Case 2
The patient was a 22-year-old, healthy man with 10 years of
breath-hold diving and 3 years of scuba-diving experience. His depth
limit was > 30 m. First, he made a dive to 5 m and ascended to
the surface. Then he dove to 20 m, where he remained for 30
s. During a normal ascent, he experienced voluntary diaphragmatic
contractions at 17 m. After surfacing, he coughed and expectorated
bloody froth. He had no dyspnea and chest pain. His symptoms
disappeared after 5 min, and he did not seek medical attention. Results
of a medical evaluation performed 1 week after the event were normal,
as were physical examination, chest radiography, lung function testing,
and oxygen saturation findings.
Case 3
The patient was a 31-year-old, well-trained man with 9 years of
breath-hold diving and 11 years of scuba-diving experience. His depth
limit was 40 to 45 m. First, he performed 20 dives to a depth of
15 m. For each dive, he spent 2 min at this depth. He had no
diaphragmatic contractions during these dives. Later, he made another
dive to 15 m, where he remained for 2.5 min; however, this time he
had diaphragmatic contractions just before the ascent (because of short
surface interval). After surfacing, he started to cough and
expectorated bloody froth. He had dyspnea but no chest pain. He
recovered after 10 min, and he did not seek medical attention. On
admission to our clinic 2 weeks after the diving event, physical
examination, chest radiography, lung function testing, and oxygen
saturation findings were normal. He had a history of hemoptysis during
breath-hold diving after voluntary diaphragmatic contractions 3 years
previously.
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Discussion
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The pulmonary blood-gas barrier needs to be extremely thin for
efficient gas exchange. However, it also needs to be immensely strong
because the pulmonary capillaries are exposed to very high stresses
when the capillary pressure rises. Abnormally high stress in the walls
of the pulmonary capillaries results in ultrastructural changes,
including disruption of the capillary endothelium and alveolar
epithelium. This condition is referred to as stress failure of
pulmonary capillaries, and it results in pulmonary edema or even
hemorrhage.3
Three factors can affect the pulmonary blood-gas barrier and cause
alveolar hemorrhage or edema. The first is increased blood volume and
BP in the pulmonary capillaries (eg, immersion, exercise,
exposure to cold water, high altitude, and
overhydration).3
4
5
6
7
The second is decreased elasticity and
resistance of the respiratory membrane (eg, Goodpasture’s
syndrome, or the overdistention of the lung by mechanical
ventilation).8
9
The third is negative pressure in the
alveoli (eg, upper-airway obstruction by tumor, foreign
body, spasm, etc).10
11
During diving, immersion causes central blood pooling, thus increasing
cardiac preload.2
Exercise causes an increase in cardiac
output. Cold exposure increases both preload and afterload by
vasoconstriction.12
A combination of these mechanisms, as
occurs during diving, together with an increase in intrathoracic blood
volume could be responsible for an excessive increase in pulmonary
capillary pressure. As a result, increased capillary pressure can
disrupt the blood-gas barrier and causes alveolar edema or hemorrhage.
Boussuges et al13
published a report of three cases
of nonfatal alveolar hemorrhage in breath-hold divers. He speculated
that factors such as immersion, exercise, and exposure to cold, and an
increase in ambient pressure could account for the hemoptysis. In that
study, all of the divers had ingested acetylsalicylic acid (aspirin) a
few hours before diving. The author reported that acetylsalicylic acid
usage might have aggravated the bleeding through its antiplatelet
effect, but it is known that this drug does not cause spontaneous
bleeding from intact vessels.
Most of the factors that can cause alveolar hemorrhage were not obvious
in our patients, who experienced hemoptysis when they dove to a
shallower depth than their limit. They had no known pulmonary or
cardiac diseases, and they were not receiving any medications,
including acetylsalicylic acid. They dove in Mediterranean waters
during the spring, when the water temperature is not very low. They
were not overhydrated and had no water aspiration. However, all of the
divers did the same maneuver: voluntary diaphragmatic contraction at
the depth. This maneuver is used by breath-hold divers to increase the
breath-hold time. Diaphragmatic contractions cause markedly negative
intrapleural pressure generated by a forceful inspiratory effort
against an obstructed extrathoracic airway. Markedly negative
intrapulmonary pressure increases venous return, pulmonary blood
volume, and pulmonary capillary hydrostatic pressure while lowering the
perivascular interstitial hydrostatic pressure.10
11
We suggest that voluntary diaphragmatic contraction could be the main
contributing factor for the alveolar hemorrhage in our divers, in
addition to relatively low water temperature, exercise, and immersion,
which increase the pulmonary capillary pressure. Although hemoptysis in
breath-hold divers has been reported before, this maneuver has not been
cited previously as a contributing factor for hemoptysis in breath-hold
divers.
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Footnotes
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Abbreviations:
RV = residual volume; TLC = total lung capacity
Received for publication January 19, 2001.
Accepted for publication May 16, 2001.
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References
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Abstract
Introduction
