International Journal of Cardiology 149 (2011) e47 – e49 www.elsevier.com/locate/ijcard
Letter to the Editor
Hyperventilation-induced ST segment elevation mimicking acute myocardial infarction in a comatose patient with tracheostomy Cesare de Gregorio ⁎, Francesco Saporito, Giuseppe Andò, Gaetano Morabito, Marco Cerrito, Giuseppe Oreto Department of Medicine and Pharmacology, Messina University Medical School, Messina, Italy Received 18 March 2009; accepted 22 March 2009 Available online 23 April 2009
Abstract Controlled hyperventilation leading to respiratory alkalosis may induce coronary artery spasm. This manoeuvre is currently used in the diagnosis of Prinzmetal's angina. We describe the case of a comatose patient with tracheostomy in whom hyperventilation, caused by excessive bronchial secretion resulting in partial obstruction of the tracheal cannula, was followed by ST segment elevation mimicking acute myocardial infarction. © 2009 Elsevier Ireland Ltd. All rights reserved. Keywords: Hyperventilation; Respiratory alkalosis; Acute coronary syndrome; Coronary artery spasm
Dear Editor, Vasospastic angina may occur in patients with or without coronary artery disease, but it still debated whether this phenomenon can occur in the complete absence of coronary atherosclerosis or not. Hyperventilation and/or cold-pressor test have been proposed as valuable methods for reproducing the spasm, even during stress-echocardiography [1–4]. This report deals with a comatose Caucasian patient with tracheostomy in whom hyperventilation, due to excessive bronchial secretion, induced ST segment elevation mimicking acute myocardial infarction. 1. Case report A long-term comatose 46-year-old male was referred to our Coronary Care Unit (CCU) from the local Neurology Rehabilitation Hospital (NRH), because of sudden tachy⁎ Corresponding author. Dipartimento Clinico-sperimentale di Medicina e Farmacologia, Unità Operativa di Cardiologia, Azienda Ospedaliera Universitaria di Messina, Via Consolare Valeria, 98125, Messina, Italy. Tel./fax: +39 090 221 3531. E-mail address:
[email protected] (C. de Gregorio). 0167-5273/$ - see front matter © 2009 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2009.03.095
cardia and tachypnea following acute bronchopneumonia, successfully treated with antibiotics. The patient was in a vegetative state since 2007, when he had a cranial trauma leading to multiple and severe brain injuries. His clinical history was negative for heart disease and hypertension. During tachycardia and tachypnea, a 12-lead ECG recorded at the NRH (Fig. 1, panel A, time 10:41) showed sinus tachycardia (126 bpm), normal PR interval (168 ms), normal QRS duration (90 ms), and ST segment elevation in leads II, III, aVF and V6, associated with ST segment depression in leads aVL and V1–V3, a pattern suggestive for acute infero-postero-lateral myocardial infarction. Due to these findings, the patient was immediately transferred to our CCU. However, the admission ECG showed complete normalization of the previously observed abnormalities (Fig. 1, panel B, time 12:41). Serial blood samples did not reveal an increase in Troponin-I and CK-MB serum levels. On the subsequent morning, the ECG again demonstrated mild ST segment elevation in the inferior leads, and the echocardiogram showed hypokinesis of the basal segment of the inferior wall.
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Coronary angiography demonstrated normal coronary arteries (Fig. 2). On the following day, the patient manifested progressively worsening dyspnea (breath rate N 25 per minute) associated with acute hypoxic syndrome (partial O2 pressure 56 mmHg and CO2 pressure 30 mmHg) and new evidence of ST segment elevation at ECG monitoring. A partial obstruction of the tracheal device, likely caused by excessive bronchial secretion, was then disclosed. Cleaning of tracheal cannula resulted in disappearance of both symptoms and ECG abnormalities.
2. Discussion Although not directly demonstrated during coronary angiography, it is very likely that this patient had hyperventilation-induced coronary vasospasms. Respiratory alkalosis by hyperventilation is an effective stimulus for coronary artery spasm, and has been proposed as a part of the diagnostic workup for Prinzmetal's angina [1–4]. In our patient, hyperventilation was due to excessive bronchial secretion resulting in a partial obstruction of the tracheostomy cannula. As a consequence, a transient ST
Fig. 1. Electrocardiograms recorded during tachypnea and hyperventilation (panel A) and on admission to coronary care unit (panel B).
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Fig. 2. Coronary angiograms of the right (panel A) and the left coronary artery (panel B).
segment elevation, mimicking acute myocardial infarction, ensued. On the basis of ECG and echocardiographic findings, the spasm was thought to involve the right coronary artery. Long-term clinical management of patients with irreversible brain injury raises several problems. In particular, tracheostomy reduces unnecessary resource utilization [5], but needs special care, especially when exacerbation of chronic respiratory disease occurs. Conflict of interest Not declared. Acknowledgement The authors of this manuscript also certify that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [6].
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