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(Chest. 1999;115:1742-1744.)
© 1999 American College of Chest Physicians

New ECG Changes Associated With a Tension Pneumothorax*

A Case Report

Brian Strizik , MD and Robert Forman , MD

* From the Division of Cardiology, Department of Medicine, Albert Einstein College of Medicine, Jack D. Weiler Hospital, Bronx, NY.


   Abstract
TOP
 Abstract
Introduction
 Case Report
 Discussion
 References
 
This case report reveals new ECG changes associated with a left tension pneumothorax, specifically, PR-segment elevation in the inferior leads and reciprocal PR-segment depression in the aVR lead. A mechanism of atrial injury and/or ischemia is proposed as the cause, and the ECG changes associated with a left tension pneumothorax are briefly reviewed.

Key Words: atrial injury • atrial ischemia • ECG • PR segment • tension pneumothorax


   Introduction
TOP
 Abstract
 Introduction
Case Report
 Discussion
 References
 
The ECG manifestations of a tension pneumothorax have been well described. For a left tension pneumothorax, these include a rightward shift of the mean frontal QRS axis, reduced precordial R-wave voltage, decreased and/or alternating QRS amplitude (electrical alternans), or precordial T-wave inversions.1 Commonly, two or three of the above are present, and less often, all four are present. We present a case of ECG manifestations that have not been reported before (to our knowledge), such as PR-segment elevation and depression associated with a left tension pneumothorax. These ECG changes were transient, and they promptly reverted to the baseline on relief of the tension.


   Case Report
TOP
 Abstract
 Introduction
 Case Report
Discussion
 References
 
An 82-year-old woman presented with acute onset of shortness of breath and left-sided chest pain. Her medical history was significant for > 80 pack-years of smoking and GI bleeding from diverticulosis. On presentation to the emergency department, her BP was 140/80 mm Hg, with a pulse rate of 148 beats/min and a respiratory rate of 34 breaths/min. Her oxygen saturation, as measured by pulse oximetry, was 94%. On physical examination, she was in mild respiratory distress, she was without jugular venous distention, and she had diminished breath sounds in both lung fields. An ECG revealed atrial fibrillation with a ventricular response of 150 beats/min. She was placed on a regimen of 100% oxygen with the use of a face mask and was given IV diltiazem, which slowed her heart rate to 80 beats/min. Her mental status and oxygen saturation then progressively declined. On emergent intubation, her symptoms and oxygenation improved. However, she suddenly became hypotensive, and her oxygenation saturation dropped once again. Results of her physical examination at this time were remarkable for absent breath sounds over the left lung and distended neck veins. The chest radiograph (Fig 1 ) showed a 100% left tension pneumothorax. The ECG (Fig 2 ) showed a bizarre pattern of sinus tachycardia at 100 beats/min with a first-degree atrioventricular block, <= 8 mm of PR-segment elevation, which particularly occurred in the inferior leads (II, III, and aVF) and was accompanied by PR-segment depression in the aVR lead, very low-amplitude r waves in the precordial QRS complexes, and an isoelectric QRS complex in V6. A chest tube was immediately placed in the patient, and the pneumothorax and bizarre ECG manifestations (Fig 3 ) were resolved. In addition, there was a marked increase in the R-wave amplitude in the precordial leads, a shift in the horizontal axis toward normal, and resolution of the PR segments to the baseline. The patient subsequently died from pneumonia and sepsis 4 weeks later.



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  		Figure 1. Chest radiograph showing a 100% left tension pneumothorax.

 


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  		Figure 2. ECG revealing marked PR-segment elevation in the inferior leads and PR-segment depression in the aVR lead in a patient with a 100% left tension pneumothorax.

 


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  		Figure 3. ECG demonstrating resolution of the PR-segment changes following relief of the left tension pneumothorax.

 

   Discussion
TOP
 Abstract
 Introduction
 Case Report
 Discussion
References
 
Numerous mechanisms have been proposed whereby a tension pneumothorax may cause ECG changes. Simple displacement of the heart has been reported to cause only minor changes.2 ,3 Others have proposed that rotation around the posteroanterior or longitudinal axis causes shifts in the heart's axis as well as loss of anterior forces and precordial R waves.4 ,5 Air within the thoracic cavity has also been suggested as a cause of the ECG changes.6 Although both Lewis2 and Dieuaide et al3 have shown that changes caused by air in the thoracic cavity are minimal, others have said that it is the combination of retrosternal air and rotation around the longitudinal axis of the heart that causes the ECG changes.5

Our case represents the unique finding of the PR-segment elevation in inferior leads with reciprocal PR-segment depression in the aVR lead. After an exhaustive search of the literature, we found that this has never been reported (to our knowledge) in conjunction with a pneumothorax, with or without tension. We propose that the mechanism behind the PR-segment changes is atrial ischemia or injury.

Some ECG changes that have been reported to occur in a left tension pneumothorax have been attributed to a "cor pulmonale theory," which says that a sudden rise in intrathoracic pressure increases pulmonary vascular resistance, which, in turn, leads to a decrease in coronary blood flow and an increase in inward pericardial force.1 The ECG changes attributed to this theory were ventricular in origin, and they included loss of R-wave7 and T-wave inversions1 ; however, no P-wave changes were noted. We propose that a combination of inward pericardial force and atrial injury was the mechanism behind the very marked PR-segment elevations in the inferior leads and the PR-segment depression in the aVR lead in our patient. With the sudden rise in intrathoracic pressure in a left tension pneumothorax, the heart rotates clockwise and rightward, leaving the inferior surface and the left atrium in close proximity to the collapsed lung. With air under tension, force is placed on the collapsed lung, which translates into force also being placed on the heart; consequently, the blood flow of the left atrial branch of the circumflex artery may be jeopardized, or the direct pressure that is placed on the left atrium could lead to atrial injury. This would persist only if the tension remained unrelieved. Although our patient's cardiac enzyme levels were normal, the "ischemic" period only lasted for 15 to 20 min, and at least 45 min is necessary to elicit permanent myocardial damage. In support of our theory that the heart was displaced rightwardly and rotated clockwise are the ECG manifestations of electrical neutrality seen in lead 1 and the positive ECG forces seen in the inferior leads. This phenomenon is transient, and it is reversed by releasing the tension. As this happens, the affected left lung expands, the compressive or injurious forces on the epicardial surface are released, blood flow is restored, and the ECG changes revert to the baseline.

The mechanism we have proposed is highly speculative and theoretical, and it has not been verified scientifically. We encourage readers to communicate with us about their own interpretation via the correspondence column or e-mail.


   Footnotes
 
Correspondence to: Brian Strizik, MD, Division of Cardiology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Forchheimer G46, Bronx, NY 10461; e-mail: Strizik@Yahoo.com

Received for publication July 24, 1998. Accepted for publication December 7, 1998.


   References
TOP
 Abstract
 Introduction
 Case Report
 Discussion
 References
 

  1. Walston, A, Brewer, D, Kitchens, C, et al (1974) The electrocardiographic manifestations of spontaneous left pneumothorax. Ann Intern Med 80,375-379
  2. Lewis Sir T. The mechanism and graphic registration of the heart beat. London, UK: Shaw and Sons, 1925
  3. Dieuaide, FR (1921) The determination and significance of the electrical axis of the human heart. Arch Intern Med 27,558-570[CrossRef][ISI]
  4. Feldman, D, Silverberg, C (1928) Electrocardiographic changes in pulmonary collapse therapy: artificial pneumothorax. Am Heart J 35,800-812
  5. Master, AM (1928) The electrocardiographic changes of pneumothorax in which the heart has been rotated. Am Heart J 3,472-483[CrossRef][ISI]
  6. Feldman, T, January, CT (1984) ECG changes in pneumothorax: a unique finding and proposed mechanism. Chest 86,143-145[Abstract/Free Full Text]
  7. Botz, G, Brock-Utne, JG (1992) Are electrocardiogram changes the first sign of impending peri-operative pneumothorax? Anesthesia 47,1057-1059[CrossRef][ISI][Medline]



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This Article
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Right arrow Articles by Forman, R.

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