Reversible ST-segment elevation associated with atelectasis of the left lung.

Abstract: A 22-year-old male with cerebral palsy and respiratory failure had acute reversible ST-segment elevation in the inferior leads during acute collapse of the left lung, which resolved with re-expansion of the left lung several hours later. This suggests that major lung actelectasis needs to be added to the group of noncardiac conditions considered when evaluating ST elevation in the critically ill patient.

Key Words: atelectasis, electrocardiogram, lung collapse, ST-segment elevation

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Recognition of acute cardiac ischemic events in the intensive care unit is highly important, since rapid treatment reduces morbidity and mortality rates. Nevertheless, a number of nonischemic myocardial and nonmyocardial problems in the critically ill patient may lead to ST-segment elevation, including left ventricular hypertrophy, left bundle branch block, acute pericarditis, acute pulmonary embolism, hyperkalemia, and intrathoracic processes such as pneumothorax. (1-6) This report describes a patient with development of significant ST-segment elevation concomitant with major atelectasis of the left lung that resolved with re-expansion of the left lung. To our knowledge, this association has not been reported previously.

Case Report

A 22-year-old male with cerebral palsy, mental retardation, and seizures was brought to the emergency department for altered level of consciousness. Physical examination at admission included vital signs of blood pressure of 74/38 mm Hg, heart rate of 120 per minute, respiratory rateof 14 per minute, and temperature of 40.8[degrees]C. Chest auscultation revealed equal breath sounds with bilateral rhonchi. The remainder of the examination was unremarkable except for multiple abdominal scars, a subcutaneous baclofen pump, and flexion contractures of the extremities. Arterial oxygen saturation (Sa[O.sub.2]) was 66% on room air. The patient was intubated and mechanically ventilated and transferred to the medical intensive care unit, where he subsequently underwent tracheostomy. At 12 AM on the 22nd hospital day, there was sudden decrease in Sa[O.sub.2] to 80%, and the patient was placed back on a mechanical ventilator on Fi[O.sub.2] of 1.0. A chest radiograph obtained at 12:57 AM showed volume loss and complete opacification of the entire left hemithorax consistent with total atelectasis of the left lung (Fig. 3). An electrocardiogram (ECG) at 2:52 AM showed new ST elevation in the inferior (II, III, and aVF) leads (Fig. 2). The patient was placed in the right lateral decubitus position, and he was administered salicylates, 5 mg IV metoprolol, 25 [micro]g IV fentanyl, 4,000 U IV heparin, and nebulized albuterol and N-acetylcysteine. A follow-up ECG at 5:26 AM revealed complete resolution of ST-segment elevation in the inferior leads (Fig. 2) and a chest radiograph at 7:23 AM showed resolution of the left lung collapse (Fig. 4), with concomitant improvement in oxygenation with Sa[O.sub.2] of 96% on Fi[O.sub.2] of 0.60 and pressure support ventilation. Serial serum troponin levels obtained at 3:00 AM, 6:43 AM, and 10:24 AM were below 0.08 ng/mL. The patient was transferred to the general medicine ward 3 days later (Fig. 1).

Discussion

Possible mechanisms for ST elevation in atelectasis include those postulated by Slay et al (4) for pneumothorax and include clockwise rotation of the heart, right ventricular dilation, and myocardial ischemia. The ECG with ST-segment elevation also revealed development of a deep S in lead I and a new Q wave in lead III, but the T-wave was unchanged, thereby not fulfilling the classic "SIQ3T3 pattern" observed in a small number of patients with pulmonary embolism and pneumothorax. (3) Nevertheless, it is possible that atelectasis led to hypoxemic vasoconstriction of the pulmonary circulation, which, combined with diversion of the cardiac output to the right lung, led to increase in pulmonary hypertension sufficient to pressure overload the right ventricle, resulting in the inferior ST-segment changes. Because we did not assess pulmonary arterial pressure or the right ventricle before or during the episode of atelectasis, we have no direct evidence on this possibility. There was no evidence that ST-segment elevation in this patient was related to myocardial infarction. Negative serum troponins and the age of the patient are against this possibility. There was no evidence for left bundle branch block, and the rapid and complete resolution of ECG changes make pericarditis unlikely. There was no evidence for hyperkalemia during the ECG abnormalities. Acute pulmonary embolism is well known to be associated with focal ST-segment changes that suggest acute myocardial infarction. However, the rapid resolution of the ST-segment abnormalities and hypoxemia with re-expansion of the left lung and the progressive improvement of the patient during the remainder of his hospital course make pulmonary embolism unlikely.

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Conclusion

We report a 22-year-old patient with cerebral palsy who had acute ST-segment elevation concomitant with major atelectasis of the left lung, probably secondary to mucous plug. Although myocardial ischemia must be considered first and foremost with ST-segment elevation in the critically ill patient, a growing number of nonmyocardial conditions, such as pneumothorax or pulmonary thromboembolism, must also be entertained because they may be equally threatening to the patient. Clinicians should be aware of the possibility that major atelectasis of the left lung may also result in ST-segment elevation.

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ST-segment elevation is an important sign of acute myocardial ischemia, but noncardiac conditions in critically ill patients may also cause ST-segment elevation. We report a 22-year-old patient with cerebral palsy who developed acute, reversible, inferior limb lead ST-segment elevation concomitant with complete left lung atelectasis.

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References

1. Wang K, Asinger RW, Marriott HJ. ST-segment elevation in conditions other than acute myocardial infarction. N Engl J Med 2003;349:2128-2135.

2. Kounis NG, Zavras GM, Kitrou MP, et al. Unusual electrocardiographic manifestations in conditions with increased intrathoracic pressure. Acta Cardiol 1988;43:653-661.

3. Goddard R, Scofield RH. Right pneumothorax with the SIQ3T3 electrocardiogram pattern usually associated with pulmonary embolus. Am J Emerg Med 1997;15:310-312.

4. Slay RD, Slay LE, Luehrs JG. Transient ST elevation associated with tension pneumothorax. JACEP 1979;8:16-18.

5. Kuritzky P, Goldfarb AL. Unusual electrocardiographic changes in spontaneous pneumothorax. Chest 1976;70:535-537.

6. Janssens U, Koch KC, Graf J, et al. Severe transmyocardial ischemia in a patient with tension pneumothorax. Crit Care Med 2000;28:1638-1641.

For a successful technology, reality must take precedence over public
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--Richard Feynman

Matt Sampson, BS, and C. Edward Rose, Jr, MD

From the Department of Internal Medicine, University of Virginia Health System, Charlottesville, VA.

The authors have no commercial or proprietary interest in any drug, device, or equipment mentioned in this article. The authors have no financial interest in any item mentioned in this article.

Reprint requests to C. Edward Rose, Jr, MD, Division of Pulmonary and Critical Care Medicine, Box 800546, University of Virginia Health System, Charlottesville, VA 22908. Email: [e-mail]

Accepted February 17, 2005.

RELATED ARTICLE: Key Points

* ST-segment elevation is an important finding that can lead to the early detection of myocardial ischemia and infarction.

* A number of nonischemic cardiac and noncardiac problems can be associated with ST-segment elevation.

* Complete atelectasis of the left lung is an additional problem that can lead to ST-segment elevation.