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Communications to the Editor |

ECG Changes in Tension Pneumothorax : A Hypothesis FREE TO VIEW

Mitsuhiro Kamimura, MD; Koichiro Kudo, MD; Tatsuya Kubota, MD; Jichi Medical School
Author and Funding Information

International Medical Center of Japan Tokyo, Japan 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



Chest. 2000;117(5):1527. doi:10.1378/chest.117.5.1527
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To the Editor:

We read with great interest the article by Strizik and Forman (June 1999)1reporting 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,3and 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. Strizik’s 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.

Strizik, B, Forman, R (1999) New ECG changes associated with a tension pneumothorax.Chest115,1742-1744. [CrossRef] [PubMed]
 
Lazar, EJ, Goldberger, J, Peled, H, et al Atrial infarction: diagnosis and management.Am Heart J1988;116,1058-1063. [CrossRef] [PubMed]
 
Kamimura, M, Murata, K, Ohtake, K, et al Marked ST-T electrocardiographic changes after retrosternal reconstruction of the esophagus.Anesth Analg1995;81,411-413. [PubMed]
 
Constant, J Essential of bedside cardiology.1989,82-83 Little Brown. Boston, MA:
 

Figures

Tables

References

Strizik, B, Forman, R (1999) New ECG changes associated with a tension pneumothorax.Chest115,1742-1744. [CrossRef] [PubMed]
 
Lazar, EJ, Goldberger, J, Peled, H, et al Atrial infarction: diagnosis and management.Am Heart J1988;116,1058-1063. [CrossRef] [PubMed]
 
Kamimura, M, Murata, K, Ohtake, K, et al Marked ST-T electrocardiographic changes after retrosternal reconstruction of the esophagus.Anesth Analg1995;81,411-413. [PubMed]
 
Constant, J Essential of bedside cardiology.1989,82-83 Little Brown. Boston, MA:
 
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