ECG Changes in Tension Pneumothorax : A

Hypothesis
Mitsuhiro Kamimura, Koichiro Kudo, Tatsuya Kubota and Jichi Medical
School
Chest 2000;117;1527
DOI 10.1378/chest.117.5.1527
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2000 American College of Chest Physicians

appear higher with inhaled rather than IV corticosteroids, the

studies by Lin et al2 and by Rodrigo and Rodrigo5 are not directly
comparable, since only the first study evaluated steroids in
second-line treatment.
I submit that, contrary to the view by Rodrigo and Rodrigo, the
evidence favors the use of IV rather than inhaled corticosteroids
in the supplementary treatment of patients with acute severe
asthma in the emergency department.
T. K. Lim, MD
National University Hospital
Singapore
Correspondence to: T. K. Lim, MD, Department of Medicine,
National University Hospital, Lower Kent Ridge Rd, Singapore
119074; e-mail: mdclimtk@nus.edu.sg

References
1 Rodrigo G, Rodrigo C. Corticosteroids in the emergency
department therapy of acute adult asthma: an evidence-based
evaluation. Chest 1999; 116:285295
2 Lin RY, Pesola GR, Bakalchuk L, et al. Rapid improvement of
peak flow in asthmatic patients treated with parentral methylprednisolone in the emergency department: a randomized
controlled study. Ann Emerg Med 1999; 33:487 494
3 Gallagher EJ. Reconciliation of conflicting evidence [editorial].
Ann Emerg Med 1999; 33:561564
4 Chew FT, Goh DYT, Lee BW. The economic cost of asthma
in Singapore. Aust NZ J 1999; 29:228 233
5 Rodrigo G, Rodrigo C. Inhaled flunisolide for acute severe
asthma. Am J Respir Crit Care Med 1998; 157:698 703

ECG Changes in Tension

Pneumothorax
A Hypothesis
To the Editor:
We read with great interest the article by Strizik and Forman
(June 1999)1 reporting ECG changes associated with a tension
pneumothorax. The authors predicted that the PR-segment elevation was due to atrial ischemia. Usually, ECG changes associated
with atrial ischemia may be absent or minimal because the voltage
generated by thin-walled atria is low.2 PR-segment elevation in their
case was quite high, and it does not seem appropriate to explain it as
arising from an ischemic origin only. We would like to propose our
interpretation of the ECG changes in their case.
Previously, we reported marked ST-T changes on ECG after
retrosternal reconstruction of the esophagus,3 and the prediction
of the mechanism in our case can explain their ECG changes. In
our report, the patient showed significant elevation of the ST-T
segment from leads V1 to V4, which abruptly disappeared after
expulsion of the air in the reconstructed esophagus. The distinct
feature of retrosternal reconstruction is the existence of an
air-containing structure between the heart and the anterior chest
wall. Under such circumstances, pendular motion is generated as
the heart contracts, which alters the distance between the heart
and the chest wall. When the heart enters systole, the heart
moves toward the sternum because a recoil force produced by
the ejection of blood into the aorta thrusts the left ventriculum in
the anterior direction4 and away from the sternum during
diastole. Therefore, in the precordial leads, the ECG baseline
changed in accordance with the cardiac cycle. The positive wave
was generated during the systole, which corresponded to the
ST-T elevation and return to the baseline during diastole.

The common features shared between Dr. Striziks case and

ours is the dislocation of the heart from its original point, and we
hypothesize the mechanism of their ECG changes as a baseline
fluctuation in accordance with the cardiac systole and diastole.
When the heart entered diastole, the inferior wall, which was
pushed up by the air within the thoracic cavity, moved toward the
caudal side by the force of influx of the blood stream into the left
ventriculum, with the accentuation of the atrial kick. Therefore,
the positive wave was generated during the diastolic phase in the
inferior leads and negative wave in aVR and aVL, which reflects
the component of the force toward the cranial side. As the patient
had a first degree atrioventricular block, the diastolic phase was
almost started from the P wave, resembling PR-segment alteration. When the heart entered systole, the inferior wall moved
away from the caudal side, which resulted in the negative wave or
the return to the baseline in the ST-T phase.
Moreover, continuous recording of lead II in Figure 2 (the
lowest in the Figure) seems to show alteration of the PR-segment
voltage according to the respiratory cycle. The sixth to the ninth
beats are quite different from the others in the respect of
diminished PR elevation and normalization of the ST-T depression. Altered intrathoracic pressure according to the respiratory
cycle might have influenced the amplitude of cardiac shift in
accordance with systole and diastole. Increased intrathoracic
pressure during the inspiratory phase if the patient was on a
respirator, or during the expiratory phase if the patient breathed
spontaneously, restricted the downward shift of the heart, which
resulted in the diminished PR elevation.
We have not encountered any reports or patients whose findings
suggest the pendular motion of the heart in the air within the
thoracic cavity as the etiology of the ECG baseline fluctuation in the
period since we published our experience,3 and we believe the case
presented by Strizik and Forman1 might be one of such cases.
Mitsuhiro Kamimura, MD
Koichiro Kudo, MD
International Medical Center of Japan
Tokyo, Japan
Tatsuya Kubota, MD
Jichi Medical School
Tochigi, Japan
Correspondence to: Mitsuhiro Kamimura, MD, Pulmonology
Department, International Medical Center of Japan, 1-21-1
Toyama-Cho Shinjuku, Tokyo 162-8655, Japan; e-mail:
mkamimur@imcj.hosp.go.jp

References
1 Strizik B, Forman R. New ECG changes associated with a
tension pneumothorax. Chest 1999; 115:17421744
2 Lazar EJ, Goldberger J, Peled H, et al. Atrial infarction:
diagnosis and management. Am Heart J 1988; 116:1058 1063
3 Kamimura M, Murata K, Ohtake K, et al. Marked ST-T
electrocardiographic changes after retrosternal reconstruction of the esophagus. Anesth Analg 1995; 81:411 413
4 Constant J. Essential of bedside cardiology. Boston, MA:
Little Brown, 1989; 82 83

Erratum
On the cover of the April 2000 issue, the Basic
Science entry should have read:
Anti-inflammatory Cytokines(p1162)
Opal and DePalo
Editorial comment by Alan Fein and Edward Abraham
Our apologies to these authors.
CHEST / 117 / 5 / MAY, 2000

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2000 American College of Chest Physicians

1527

ECG Changes in Tension Pneumothorax : A Hypothesis

Mitsuhiro Kamimura, Koichiro Kudo, Tatsuya Kubota and Jichi Medical
School
Chest 2000;117; 1527
DOI 10.1378/chest.117.5.1527
This information is current as of April 18, 2012
Updated Information & Services
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2000 American College of Chest Physicians