Case Report

Coronary Artery Air Embolism Causing Pulmonary Edema Secondary to Acute Coronary Syndrome in a Diver

Mark Adrian Sammut, MD, MRCP(UK), Andrew Cassar, MD, MRCP(UK), Herbert Felice, MD
Mark Adrian Sammut, MD, MRCP(UK), Andrew Cassar, MD, MRCP(UK), Herbert Felice, MD
Author Affiliations: From the Cardiology Department, Mater Dei Hospital, Tal-Qroqq, Malta. The authors report no conflicts of interest regarding the content herein. Manuscript submitted April 25, 2008, provisional acceptance given May 8, 2008, and final version accepted May 19, 2008. Address for correspondence: Andrew Cassar, MD, MRCP, Cardiology Department, Mater Dei Hospital, Tal-Qroqq, Malta. E-mail: andrew.a.cassar@gov.mt

_______________________________________________ ABSTRACT: Air embolism in the coronary arteries is a known complication of coronary angiography. Diving is a noniatrogenic cause of arterial air embolism, commonly presenting with neurological and musculoskeletal symptoms. This is the first known case of coronary air embolism confirmed on coronary angiography in a diver presenting with pulmonary edema secondary to acute coronary syndrome. The possible mechanisms of coronary air embolism during a dive are reviewed in this article.

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J INVASIVE CARDIOL 2008;20:E331–E333 Case Report. A 48-year-old male Russian tourist was brought by ambulance to the Accident and Emergency Department (A&E), complaining of sudden onset of shortness of breath while scuba diving. The patient, a fairly experienced diver, had descended to a depth of about 18 meters of seawater when he suddenly experienced shortness of breath and weakness of his lower limbs. Over the next few minutes, the dyspnea worsened and the patient had to slowly ascend to the surface where he swallowed a small quantity of water. Shortly afterwards, he noted some epistaxis from the right nostril, but there was no hemoptysis and he denied any chest pain. The dive time amounted to about 20 minutes in total. The patient gave no previous history of heart disease, hypertension, diabetes mellitus, asthma or hypercholesteremia, and was on no regular medications. He smoked about 15 cigarettes daily and denied alcohol or drug abuse. There was no family history of coronary artery disease. On examination, the patient was tachypneic, with a heart rate of 120 beats/minute and a blood pressure of 130 /70 mmHg. His heart sounds were normal, and chest auscultation revealed good air entry and bilateral crepitations up to the apices. There was no lower limb edema and no signs of deep venous thrombosis. Neurological examination revealed no abnormality. Arterial blood gasses on O2 showed a PO2 of 111 mmHg, a PCO2 of 41 mmHg, an O2 saturation of 97%, a pH of 7.27 and a base excess of -8 mmol/l. Electrocardiography (ECG) showed a left bundle-branch block and a chest X-ray showed bilateral alveolar congestion and no evidence of pneumothorax. The total blood count revealed a leucocytosis of 27.4 x 109/L, 95% of which were neutrophils. The patient’s serum electrolytes, renal, liver and thyroid function tests were normal. Serial creatine kinase (CPK) levels did not rise significantly during the first 48 hours (233, 262, 183 U/L), but subsequently increased over the next few days (868, 1768, 1777, 1169, 794 U/L). His MB fraction, however, remained consistently outside the cardiac range. Urgent echocardiography was performed, revealing akinesia of the anteroseptal wall and hypokinesia of the inferior wall. An urgent coronary angiogram was subsequently arranged with a view to possible primary percutaneous coronary intervention. This showed the presence of air bubbles in the mid-right coronary artery (RCA) with slow distal filling, which disappeared after three contrast injections (Figure 1). The air bubbles were not seen originating from the catheter and were clearly obstructing flow. There was mild insignificant narrowing of the proximal RCA. The left coronary system was normal. Ventriculography confirmed the findings on echocardiography (Figures 2 and 3). The patient’s global left ventricular (LV) contractility was moderately impaired. The patient was given oxygen, intravenous (IV) diuretics, IV nitrates and aspirin in the A&E, with some effect. Significant improvement in symptoms occurred following reperfusion of the RCA. Angiotensin-converting enzyme (ACE) inhibitors were subsequently added and antibiotics were given to cover for any possible aspiration. Over the following few days, the patient made a steady recovery. A multiple gated acquisition (MUGA) scan, performed on day 4 after admission, showed a normal ejection fraction and LV wall contractility. A transthoracic echocardiogram with contrast showed no right-to-left shunting during the Valsalva maneuver. The patient was discharged on day 7 in good clinical condition on ACE inhibitors. Discussion. We have described here the case of a previously healthy middle-aged male who developed acute pulmonary edema while diving. Echocardiography and ventriculography showed that the pulmonary edema was caused by acute LV failure secondary to regional wall motion dysfunction. This, in turn, was due to myocardial ischemia caused by subocclusion of the coronary arteries from arterial gas emboli, as demonstrated by the presence of gas bubbles in the RCA on coronary arteriography. The absence of a significant rise in the CPK-MB fraction, and the almost complete recovery in cardiac wall motion revealed by follow-up echocardiography and MUGA scanning, suggest that myocardial dysfunction was the result of ischemia with stunning, rather than infarction. Since this myocardial dysfunction involved the anterior and inferior regions, there must have also been transient occlusion from air embolism of the left coronary system. Moreover, the patient had complained of lower limb weakness during the dive, which had resolved by the time of admission and which could have been caused by transient cerebral arterial gas embolism. The release of air bubbles entering the circulation during diving can occur via two broad mechanisms: 1) pulmonary overinflation; and 2) liberation of a gas phase in tissues due to decompression.1 Pulmonary overinflation most commonly manifests itself by features of lung injury such as hemoptysis or pneumothorax. However, overexpanding gas may rupture alveoli and may be released into the pulmonary vasculature,2 causing arterial gas embolism (AGE) when distributed systemically. Classically, AGE presents with features secondary to gas embolization to the brain, such as loss of consciousness, hemiparesis, confusion and loss of coordination. These are often transient and tend to resolve spontaneously. However, in its most severe form, AGE may present catastrophically with collapse and cardiac arrest (

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