Cardiac Decompression Sickness After Hypobaric Chamber
Training: Case Report of A Coronary Gas Embolism
Alçak Bas›nç Çemberi E¤itimi Sonras›nda Geliflen Kardiyak Dekompresyon Hastal›¤›:
Koroner Gaz Embolismi Olgusu Takdimi
Cengiz Öztürk, MD, Ahmet fien*, MD, Ahmet Ak›n*, MD, Atilla ‹yisoy**MD,
600 Bed Air Force Military Hospital, Eskiflehir, *Department of Aerospace Medicine, Gulhane Military Academy, Eskiflehir
**Department of Cardiology, Gulhane Military Academy, Ankara, Turkey
Air embolism is an uncommon but potentially catastrophic
event, which occurs as a consequence of the entry of air into
the vasculature. Surgery, instrumentation of the central veno-
us system, positive pressure ventilation, trauma and decomp-
ression are the most common causes of air embolism. De-
compression sickness is an illness caused by reduced pressu-
re on the body that results in formation of bubbles of an inert
gas and specific related symptoms. Decompression sickness
is still a risk for both aviators and divers (1). Here we report a
cardiac decompression sickness case due to air embolism.
A 22-year-old male pilot candidate was evaluated for sud-
den dyspnoea and chest pain after hypobaric chamber tra-
ining (Fig. 1). This training is given in order to simulate high al-
titude hypoxia. The pilot candidate had periodic medical exa-
mination, which revealed to be completely normal prior to
hypobaric chamber training. He was exposed to hypobaric en-
vironment for about one hour (total time for ascending and
descending) staying at the maximum 35,000 feet atmospheric
pressure for about 15 min. Two hours after the training he was
transferred to emergency department because of chest pain
at rest typical of myocardial infarction (MI). On admission, he
was anxious with profuse sweating. He was normotensive,
nondiabetic, nonsmoker and had no family history of coronary
artery disease. Blood pressure was 140/90 mmHg, heart rate
was 90 beats per minute. Physical examination was unremar-
kable. His electrocardiogram (ECG) revealed ST segment ele-
vation in the derivations DII, DIII, AVF, V5, V6; ST segment dep-
ression in DI and aVL (Fig. 2). Considered as an acute MI case
due to decompression cardiac sickness (DCS), he was imme-
diately taken into hyperbaric chamber (Fig. 3), because it is a
general rule for decompression sickness that diagnostic pro-
cedures must not cause a delay in the specific treatment. The
patient denied any risk factors known for DCS such as SCUBA
diving, strenuous exercise or Rapid Decompression (cabin
depressurization) in the previous days.
He was given hyperbaric oxygen therapy (HBOT) accor-
ding to US-Navy Treat: Table 6 (2), aggressive hydration and
100% oxygen breathing with a tight fitting mask (3), resulting in
rapid resolution of the symptoms at 15th minute of HBOT. Af-
ter HBOT ECG disclosed changes compatible with an acute in-
ferolateral MI (1 mm ST segment elevations and significant
decrease in R amplitude (poor R wave progression) in DII, DI-
II, aVF, V5, V6; 0.5 mm ST segment depression and increased
T amplitude in V1 and V2 derivations) (Fig. 4). On admission to
coronary care unit, the patient was stabilised and free of
chest discomfort, he was then monitored. He experienced
ventricular extrasystoles and rare couplet forms suggestive of
reperfusion. Chest X-ray, complete blood count and blood
chemistry (including lipid profile) other than cardiac enzymes
were within normal limits. Since he was considered as de-
compression sickness and responded to HBOT dramatically,
no additional medication, including antiaggregant, anticoagu-
lant, thrombolytic or antiischemic drugs were administered.
Creatine phosphokinase, creatine phosphokinase MB fraction
and aspartate aminotransferase enzymes presented early pe-
ak at 24th hour and early wash-out compatible with early re-
perfusion. In serial ECGs, ST segment elevations and decre-
ased R amplitude in lateral derivations regressed and ST seg-
ment elevations in inferior derivations returned to baseline. He
was discharged on the 7th day of hospitalisation having no ot-
her symptoms and complications.
Two months after discharge, transthoracic echocardiog-
raphy revealed inferobasal hypokinesia and mild mitral insuf-
ficiency. Ejection fraction was slightly below normal limits. A
symptom-limited exercise ECG performed up to Bruce stage V,
showed no evidence of myocardial ischaemia and hyperventi-
lation test was also normal. Myocardial perfusion scintigraphy
with Thallium 201 was normal. Coronary angiography disclo-
sed neither lesion nor coronary anomaly. Left ventriculog-
raphy revealed mild hypokinesia in posterobasal segments.
Three months after the episode he was allowed for full flight
Address for Correspondence: Dr. Cengiz Öztürk, 600 Yatakl› Hava Hastanesi 26020, Eskiflehir, Tel: 0 222 2204530/4170, e-mail: email@example.com
Olgu Sunumu Case Report
duties. The rationale for this decision was the intact structure
of coronary arteries. He has been in active duty as a fighter pi-
lot for 3 years without any cardiac event.
Decompression sickness may cause potentially fatal out-
comes by means of gas embolism. Although it is mainly obser-
ved in divers after rapid ascent, it may also occur in aviators
during high altitude flights or simulated training conditions.
Decompression sickness, also known as “bends”, was origi-
nally described as "caisson disease" when it was first recog-
nised in 1843 among tunnel workers following return from the
compressed environment of the caissons to the normal at-
mospheric pressure (2).
Under higher atmospheric pressures the tissues become
loaded with increased quantities of oxygen and nitrogen. As
atmospheric pressure decreases, ie. while divers ascend to
surface or aviators climb up to higher altitudes, the sum of the
gas tensions in the tissue may exceed the ambient partial
pressure of the gas and lead to the liberation of free gas from
the tissues in the form of bubbles. The liberated gas bubbles
can alter organ function by blocking vessels, rupturing or
compressing tissue, or activating clotting and inflammatory
Overall incidence of DCS occurring after hypobaric cham-
ber training was found about 0.19-0.32 (4). Among these cases
incidence of cardiac DCS cases, which are characterized with
coronary gas embolus or cardiovascular collapse is 0.2% (5).
However a detailed description of such a case was not ava-
ilable in the medical literature.
Approximately 75% of patients with decompression sick-
ness develop symptoms within 1 hour and 90 percent within 12
hours of exposure; only a small number of the cases become
symptomatic after 24 hours. Symptoms differ according to or-
gan systems involved (6). Although it is suspected that there is
a tendency for a person who develops DCS under given con-
ditions to again develop DCS under similar circumstances, it
has not been proven yet. It is also interesting that bubble for-
mation may not always result in symptoms or embolus (7).
Since sudden loss of cabin pressure is a major risk for
DCS, pilots and candidates who take this type of training in
Figure 1. Hypobaric chamber
Figure 3. Hyperbaric oxygen chamber
Figure 4. Patient’s electrocardiogram after hyperbaric oxygen therapy
Figure 2. Patient’s initial electrocardiogram on admission.
Anadolu Kardiyol Derg
Öztürk et al.
Cardiac Decompression Sickness257
hypobaric chamber must adequately be informed of these Download full-text
dangers. Sudden cabin explosion of airline transport planes at
high altitudes generally would not pose a serious risk because
of the rapid descent, however signs or symptoms of MI occur-
ring after such an event must be evaluated carefully.
Atherosclerosis of coronary arteries resulting in MI is still
one of the most important causes of morbidity and mortality.
Besides atherosclerosis, gas and air emboli are among rare
causes of MI. As little as 0.5 ml of air in the coronary circula-
tion can lead to dysrhythmias, myocardial infarction, and/or
cardiac arrest. Gas emboli are encountered in divers and avi-
ators due to decompression sickness; whereas the most com-
mon causes of air emboli in daily clinical practice are surgery
(especially open heart surgery), trauma, central venous cat-
heterisation, barotrauma due to positive pressure ventilation,
cardiac catheterisation and ruptured angioplasty balloon (8).
Therapeutic approach in management of MI differs greatly
in case of gas or air emboli; therefore it must be kept in mind
to prevent potentially fatal outcomes in patients with compa-
The primary aims of the treatment are identification of the
source of air or gas, prevention of further embolisation, remo-
val of embolised gas and restoration of circulation. Nitrogen
washout by means of high flow supplemental oxygen with a
tight fitting mask, supine positioning, supportive measures in
addition to HBOT are the main therapeutic strategies. Hyper-
baric oxygen therapy reduces air bubble size, accelerates nit-
rogen resorption, and increases the oxygen content of arteri-
al blood, potentially ameliorating ischaemia. Although prompt
initiation of HBOT is preferred, it may improve outcome even if
delayed up to 30 hours (9).
Acute MI in our patient was considered to be due to gas
embolus. Being evaluated medically normal prior to hypobaric
chamber training, absence of cardiac risk factors and underl-
ying systemic disease, development of symptoms two hours
after decompression and dramatic response to recompressi-
on were the key factors in diagnosis. Time-gap between de-
compression and onset of the symptoms is due to circulating
silent bubbles before lodging.
Clinical causes of air/gas emboli such as open heart sur-
gery, trauma, pulmonary barotrauma, cardiac catheterisation
and ruptured angioplasty balloon can be seen in daily practi-
ce. In such cases HBOT will be helpful as well. In order to bet-
ter understand the mechanisms acting in the pathological pro-
cess of Cardiac Decompression Sickness, controlled experi-
mental studies should be planned.
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Balldin UI, Borgström P. Intracardiac bubbles during decompres-
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20. YY’da Birecik’ten bir enstantane.
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Öztürk et al.
Cardiac Decompression Sickness