Case Report

Electrocardiogram manifestation of Spontaneous pneumothorax

Abstract

A 64-year-old man with severe emphysema presented to our institution with sudden onset of shortness of breath due to Tension pneumothorax. His electrocardiogram revealed new extreme Right axis deviation, which resolved after treatment of the pneumothorax. This case highlights one of several previously described manifestations of tension pneumothorax on an electrocardiogram. Although these changes are not specific, pneumothorax should be in the differential of patients presenting with shortness of breath and new right axis deviation on electrocardiogram. Review of the literature for other electrocardiographic manifestations of pneumothorax and their proposed mechanisms is provided.

Spontaneous pneumothorax can result in tension pneu- mothorax, which is considered a life-threatening condition. Patients with pneumothorax commonly present with sudden shortness of breath and chest pain that mimic myocardial infarction. An electrocardiogram (ECG) is often ordered as the first test to evaluate patients with chest pain and shortness of breath before obtaining chest x-ray. Although ECG is not at all considered a primary test for pneumothorax, it can be a useful tool to help recognize pneumothorax when the diagnosis is not certain from history and physical examina- tion. Several changes on an ECG may suggest the possibility of tension pneumothorax, hereby facilitating the diagnosis. We report a case of tension pneumothorax and transient right axis deviation on an ECG, which resolved after emergent chest tube placement. We discuss other electro- cardiographic manifestations of tension pneumothorax and their proposed mechanism.

A 64-year-old man with 25 pack-year smoking history presented to our institution’s emergency department (ED) with sudden onset of left-sided chest pain and shortness of breath. His past medical history included severe emphysema with evidence of large left lower lobe blebs on prior chest x- rays. He also has hypertension and gastroesophageal reflux disease and has been treated for renal cancer with interferon and right nephrectomy 15 years ago. He has been on chronic prednisone 10 mg daily.

The patient was attending church and was in standing position when he suddenly developed sharp, left-sided chest pain radiating to his left lateral torso and back along with moderate dyspnea. He presented to the ED 11 hours later. On physical examination, he appeared to be a thin male in moderate respiratory distress. He was tachypneic but was able to speak full sentences. His respiratory rate was 24 breath/min; pulse oximetry revealed 91% oxygen saturation on room air, which improved to greater than 95% on 2 L nasal canula. His blood pressure was 184/139 mm Hg, with regular heart rate of 117 beat/min. Auscultation of his chest revealed decreased breath sound over the left lung field. There was no evidence of jugular venous distension. His trachea appeared slightly shifted to the right side. The remainder of his physical examination was unremarkable.

His initial ECG demonstrated sinus tachycardia at 114 beat/min with right axis deviation, initially interpreted as left posterior fascicular block, and late transition consistent with his prior chronic pulmonary disease (Fig. 1).

Initial chest x-ray (Fig. 2) showed a left-sided pneu- mothorax encompassing greater than 50% of the left lung, with deviation of the trachea to the right side. There was a bleb in the left lung base, which was still intact and was seen on the prior studies.

Computed tomography (CT) scan of the chest was ordered to confirm the diagnosis of pneumothorax and rule out giant emphysematous bleb suggesting spontaneous pneumothorax, given the patient’s prior history of emphysematous bleb and his sufficiently stable clinical condition. The chest CT axial images and topogram (Figs. 3 and 4) confirmed the large left pneumothorax and revealed slight mediastinal shift to the right. A 7.8 x 6.2-cm air-filled sac within the left lower lobe was seen, consistent with a bleb. There was near complete collapse of the left lower lobe. Increased attenuation, primarily within the right lung base, was noted likely representing interstitial pulmonary fibrosis or bronchiectasis. His labora- tory tests including complete blood count and chemistry were all within normal limits.

The patient underwent emergent chest tube placement. Later, he underwent Left thoracotomy for wedge resection of the bleb and pleurodesis with doxycycline. A tissue sample sent for pathological analysis revealed histological changes consistent with interstitial chronic inflammation. A repeat chest x-ray (Fig. 5) revealed resolution of the left pneumothorax.

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Fig. 1 Electrocardiogram on presentation.

A repeat ECG (Fig. 6) demonstrated resolution of the right axis deviation.

The remainder of his hospitalization was free of complications. His chest tube was successfully removed after few days.

Several electrocardiographic changes associated with spontaneous or experimental pneumothorax have been described in the literature. Walston et al [1] found at least 4 relatively consistent changes including (1) right axis deviation in the mean frontal QRS axis, (2) decrease in the precordial lead R voltage, (3) decrease and/or alternation in the QRS amplitude, and (4) inversion of precordial T wave. They explained these ECG changes are secondary to a “cor pulmonale theory,” a state where sudden increase in the intrathoracic pressure leads to an

increase in the Pulmonary vascular resistance, thereby decreasing blood flow to the left ventricle, causing decrease in Coronary blood flow. This ultimately leads to an increase in inward pericardial forces.

Several case reports described phasic voltage alternation on the ECG after pneumothorax that resolved after reexpansion of the lung [2-5]. This phenomenon has been found to be similar to the phasic voltage variation in electrical alternans seen in pericardial effusion where the heart swings in pericardial fluid resulting in changes in the electrical axis. Other explanations for phasic voltage alternation of pneumothorax have been suggested. In large pneumothorax, the heart is shifted to the opposite side, and the position of its normal anatomy is altered. Compared to the expiratory phase, during the inspiratory phase the

Fig. 2 Initial chest x-ray. Fig. 3 Chest CT axial image.

Fig. 4 Chest CT topogram.

displacement is more exaggerated resulting in further changes in heart position and axis, which ultimately results in voltage alternation on ECG. Others have also explained this phasic voltage phenomenon by a respiratory-dependent change in cardiac anatomy and a change in the volume conductor with respiration as the air within the thoracic cavity acts as a conductor insulating the heart from the chest wall [6,7].

It has been proposed that the loss of anterior forces and precordial R waves are the result of the rotation of the heart around the posterior-anterior longitudinal axis and displace- ment of the mediastinum [8,9]. Feldman and Silverberg [8] reported a case of bilateral pneumothorax after anterior myocardial infarction. Left pneumothorax was associated with reappearance of precordial R waves, whereas right pneumothorax caused no ECG change. They suggested that the mechanism explaining left pneumothorax ECG changes was an insulating effect of air in the chest rather than cardiac rotation, dilatation, or displacement.

Other ECG findings in patients with left pneumothorax have been described. Strizik and Forman [10] demon- strated that PR-segment elevation in the inferior leads and reciprocal PR-segment depression in aVR can occur in tension pneumothorax. They proposed that the mechanism behind the PR-segment changes is atrial ischemia or injury. They postulated that sudden rise in intrathoracic pressure results in clockwise and rightward rotation of the heart, bringing the left atrium and inferior surface of the heart in close proximity to the collapsed lung. The air trapped between the collapsed lung and left atrium compromises blood flow to the left atrial branch of the Circumflex artery causing transient atrial ischemia and PR- segment depression.

Kamimura et al [11] hypothesized a different mechanism for the PR-segment changes associated with pneumothorax.

They suggested that such ECG changes are baseline fluctuations in accordance with the cardiac cycle. During diastole, the inferior wall, which is already pushed up by air trapped within the thoracic cavity, moves caudally upon the influx of blood into the left ventricle; this gets further accentuated by the atrial kick. Such movement generates a positive wave of the PR-segment during diastole in the inferior leads and a negative wave in the opposite leads (aVR and aVL). In systole, the inferior wall moves away from the caudal side, resulting in a negative wave or return to baseline in the ST-T phase.

Right pneumothorax usually causes no ECG changes. However, Maheshwari and Mittal [12] showed p-pulmonale with ST-segment elevation and T wave inversion in leads V₁- V₃ in right pneumothorax. They postulated that the changes were secondary to (a) transient shift of heart to left side, exposing more of right atrial and right ventricular cavity under leads V₁-V₃, and (b) transient increase in pulmonary Arterial hypertension with increase in right ventricular overload causing transient right ventricular ischemia. God- dard and Scofield [13] presented a patient with a spontaneous right pneumothorax who had an S1Q3T3 pattern on initial ECG; a pattern that has been most often associated with pulmonary embolus. This pattern resolved, and the ECG returned to normal after reexpansion of the lung. Moreover, although rare, right-sided tension pneumothorax has been shown to present with ECG changes mimicking acute myocardial infarction such as anterior [14] or inferolateral

[15] ST-segment elevation.

Intraoperative ECG has been shown [16,17] to help detect new or recurrent pneumothorax, which is a rare complication of laparoscopic abdominal surgery and considered to be a difficult diagnosis in the anesthetized patient. In a sheEP model study conducted by Ludemann et al [18], ECG

Fig. 5 Repeat chest x-ray after chest tube placement.

Fig. 6 Repeat ECG after chest tube placement.

changes were evaluated as a potential indicator of intrao- perative pneumothorax. They demonstrated that induced pneumothorax with minimal air volume of 20 mL produced consistent ECG changes. The amplitude of the precordial QRS complex was seen to diminish, and this lowering of the QRS amplitude continued as pneumothorax volume increased up to 100 mL. The ECG changes resolved after aspiration of air from the left chest. Based on this observation, they recommended intraoperative use of pre- cordial ECG leads to rapidly identify pneumothorax during laparoscopic surgery.

In conclusion, although ECG is a readily available bedside test used for evaluation of patients with chest pain and shortness of breath prior to acquiring chest x-ray, it is not considered the major test for diagnosis of pneu- mothorax. However, it can be a useful tool to help recognize pneumothorax in the appropriate clinical setting where the Initial diagnosis is not apparent from history and physical examination. It may be particularly useful in the intraoperative setting and in other patients on ventilator support because pneumothorax in these situations could develop anteriorly to the lung, causing it to be unrecog- nized on a supine chest X-ray. Furthermore, an ECG with little or no progression of the R waves or extremely low voltage in the precordial leads should raise the suspicion of pneumothorax in a patient with acute chest pain and dyspnea. Pneumothorax should remain as part of the differential diagnosis in patients with acute chest pain and dyspnea who have electrocardiographic signs of infarction of the anterior wall, dextrocardia, pulmonary embolism,

and right axis deviation, especially if the initial workup does not corroborate these diagnoses.

Peyman Soltani MD

cardiology department, University of South Alabama

Mobile, Alabama, AL, USA E-mail address: [email protected]

Christopher M. Malozzi DO

Cardiology Department, University of South Alabama

Mobile, Alabama, AL, USA

Bernard Abi Saleh MD

Cardiology Department, University of South Alabama

Mobile, Alabama, AL, USA

Bassam Omar MD, PhD

Cardiology Department, University of South Alabama

Mobile, Alabama, AL, USA

doi:10.1016/j.ajem.2008.09.037

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