International Journal of Cardiology 117 (2007) e73 – e75 www.elsevier.com/locate/ijcard
Letter to the Editor
Pneumomediastinum mimicking acute ST-segment elevation myocardial infarction William D. Brearley Jr., Lee Taylor III, Michael W. Haley, Laszlo Littmann ⁎ Department of Internal Medicine, Carolinas Medical Center, Charlotte, North Carolina, USA Received 29 September 2006; accepted 18 November 2006 Available online 22 February 2007
Abstract Pneumomediastinum is characterized by dissecting air within the connective tissues supporting the mediastinum. This condition has been associated with multiple electrocardiographic abnormalities including T-wave inversion, electrical alternans, loss of R wave progression, and low voltage QRS. We describe a case of pneumomediastinum with electrocardiographic changes mimicking acute ST-segment elevation myocardial infarction. Laboratory studies and echocardiography demonstrated no evidence of myocardial injury, and the electrocardiographic abnormality promptly resolved with resolution of the pneumomediastinum. The apparent ST-segment elevation appeared to be the result of electrocardiographic artifact, possibly related to epidermal stretch synchronous with the cardiac cycles. © 2007 Elsevier Ireland Ltd. All rights reserved. Keywords: Pneumomediastinum; Myocardial infarction; Electrocardiographic artifact
1. Introduction Pneumomediastinum is a rare occurrence characterized by free air within the supporting connective tissue of the mediastinum [1]. This condition has been associated with a variety of electrocardiographic (ECG) abnormalities including electrical alternans, T-wave inversion, loss of R wave progression, and low voltage QRS [2–6]. The following report describes a case of pneumomediastinum with apparent ST-segment elevation noted in the electrocardiogram that suggested acute myocardial infarction. To our knowledge, this ECG manifestation of pneumomediastinum has not been reported previously. 2. Case report A 46-year-old male with a recent diagnosis of HIV was transferred to our institution from an outside facility with ⁎ Corresponding author. Tel.: +1 704 355 3165; fax: +1 704 355 7626. E-mail address:
[email protected] (L. Littmann). 0167-5273/$ - see front matter © 2007 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2006.11.156
refractory pneumonia and worsening hypoxemia. The patient had been previously healthy until two months prior when he reported increasing cough, dyspnea, subjective fever and weight loss of approximately 30 lb. Initial chest radiograph demonstrated a pattern consistent with atypical pneumonia. An initial ECG was recorded with a GEMarquette system using the 12SL interpretation software and was found to be normal. The patient's respiratory status continued to decline despite treatment for both community acquired pneumonia and pneumocystis carinii pneumonia. He eventually required endotracheal intubation and mechanical ventilatory support. On hospital day seventeen a chest X-ray revealed the presence of pneumomediastinum (Fig. 1). Subcutaneous crepitus was not observed. An ECG performed on the same day (Fig. 2A) demonstrated sinus tachycardia with up to 3 mm (0.3 mV) ST-segment elevation in the inferior leads and a somewhat unusual ST-segment elevation in precordial leads V3–V5. An ECG 4 h later (Fig. 2B) continued to show ST-segment elevation. The interpretation software indicated septal infarct, inferior injury pattern, and acute MI. The pneumomediastinum resolved spontaneously within 2–
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3. Discussion
Fig. 1. Chest radiograph (anteroposterior and lateral views) of a 46-year-old male with refractory pneumonia demonstrating pneumomediastinum (arrows).
3 days. Subsequent ECGs showed complete normalization without the development of T wave inversion or abnormal Q waves typically observed with evolving myocardial infarction. Cardiac troponin-I and CK-MB were also normal. A transesophageal echocardiogram revealed preserved systolic function without any evidence of regional wall motion abnormality or pericardial effusion. The estimated left ventricular ejection fraction was 55–60%.
Several case reports have described electrocardiographic changes associated with pneumomediastinum, none of which appeared to be the result of myocardial ischemia or injury. Pneumomediastinum can present with T-wave inversion [3–5], electrical alternans [2], and low voltage [6]. These findings have been attributed to several mechanisms including cardiac rotation or displacement, right ventricular enlargement, and the insulation of the heart by mediastinal air [1–6]. In this patient with a critical respiratory illness, it was not unreasonable to suspect myocardial infarction or injury [7]. Lack of laboratory or echocardiographic abnormality, however, effectively excluded this diagnosis. With resolution of the pneumomediastinum, the apparent ST-segment elevation noted in two consecutive ECGs resolved spontaneously without the development of T wave inversion or Q waves typical for myocardial infarction. A meticulous analysis of the ECGs revealed several characteristics that strongly suggested artifact. The precordial ST-segment elevation noted in Fig. 2A was followed in each cardiac cycle by a second tall deflection in front of the QRS complexes (curved arrows); these large, broad deflections did not appear to be physiologic. In the ECG recorded 4 h
Fig. 2. A, Electrocardiogram demonstrating sinus tachycardia with inferior and precordial ST-segment elevation. Note a broad second “hump” preceding each QRS complex in leads V2–V5 (curved arrows). B, Electrocardiogram 4 h later demonstrating persistent inferior and precordial ST-segment elevation with an unusual double peaked appearance (straight arrows).
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later (Fig. 2B) a “double peaking” within each cardiac cycle became visible (straight arrows). The apparent ST-segment elevation initially noted in the inferior leads was also replaced 4 h later by a double-peaked deflection (Fig. 2B). These findings appeared to be inconsistent with a true injury pattern. Electrocardiographic artifact is a common finding in the intensive care setting. Artifact can simulate a broad range of cardiac abnormalities including ischemia [8], ventricular tachycardia [8–10], and rarely, acute myocardial infarction [8,11–13]. The most common type is motion artifact. These are epidermal signals manifesting as large swings in the ECG baseline in association with skeletal muscle tension or motion [8,14]. When the motion artifact is random, recognition is typically straightforward [13]. Artifact occurring consistently within each cardiac cycle, on the other hand, is more likely to mimic a true ECG abnormality [12]. In many cases the exact cause of artifact cannot be ascertained [11,12]. In our case too the mechanism of artifact mimicking acute ST-elevation myocardial infarction was uncertain. A possible explanation is that with the initially tense pneumomediastinum, each cardiac systole and diastole resulted in epidermal stretch which caused the cyclic swings in the electrocardiographic baseline. This case should serve as a reminder of the importance of clinical correlation combined with both imaging and laboratory evaluation in patients with pneumomediastinum and apparent ischemic changes in the electrocardiogram. It adds yet another peculiar ECG abnormality associated with pneumomediastinum, namely electrocardiographic artifact mimicking ST-elevation myocardial infarction. References [1] Munsell WP. Pneumomediastinum: a report of 28 cases and review of the literature. JAMA 1967;202:689–93.
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[2] Kounis NG, Zavras GM, Papadaki PJ, et al. Pneumomediastinum and cervical emphysema associated with unusual clinical and electrocardiographic manifestations. Angiology 2003;54:631–5. [3] Martinez CM, Gaspar ML, Ribes EA, Amenos AM, Prevosti EF, Robert LP. Pneumomediastinum following a surgical renal biopsy. J Urol 1976;116:94–5. [4] Sakabe K, Fukuda N, Wakayama K, Nada T, Shinohara H, Tamura Y. Spontaneous pneumomediastinum: a cause of T-wave inversion in electrocardiogram. Int J Cardiol 2004;94:123–6. [5] Tse TS, Tsui KL, Yam LYC, et al. Occult pneumomediastinum in a SARS patient presenting as recurrent chest pain and acute ECG changes mimicking acute coronary syndrome. Respirology 2004;9:271–3. [6] Zimmermann A, Rafii SE, Strom JA. Subcutaneous emphysema and pneumomediastinum: a cause of low-voltage electrocardiogram. Heart Dis 2001;3:85–6. [7] Myrianthefs MM, Zambartas CM. Acute, reversible myocardial ischemia in a patient with an asthmatic attack. J Electrocardiol 1996;29:337–9. [8] Chase C, Brady WJ. Artifactual electrocardiographic change mimicking clinical abnormality on the ECG. Am J Emerg Med 2000;18:312–6. [9] Knight BP, Pelosi F, Michaud GF, Strickberger SA, Morady F. Clinical consequences of electrocardiographic artifact mimicking ventricular tachycardia. N Engl J Med 1999;341:1270–4. [10] Littmann L, Monroe MH. Electrocardiographic artifact [letter]. N Engl J Med 2000;342:590–1. [11] Hung SC, Chiang CE, Chen JD, Ding PYA. Pseudo-myocardial infarction. Circulation 2000;101:2989–90. [12] Hall BW, Knight BP. An abnormal electrocardiogram in a young man: what is the etiology? Pacing Clin Electrophysiol 2002;25:1510–2. [13] Siddiqui MA, Munugoti S, Khan IA. Electrocardiographic artifact mimicking acute myocardial infarction. Int J Cardiol 2003;87:99–101. [14] Surawicz B, Knilans TK. Chou's electrocardiography in clinical practice. Fifth edition. Philadelphia: W.B. Saunders; 2001. p. 580–2.