Intracoronary air embolism detected by transoesophageal echocardiography for aortic valve replacement

Abstract

Editor—Intracoronary air embolism is a rare complication of open heart surgery which is characterized by the appearance of hypotension, ST elevation, and ventricular fibrillation after aortic clamping removal or in the last minutes of cardiopulmonary bypass (CPB).1Tingleff J Joyce FS Petterson G Intraoperative echocardiographic study of air embolism during cardiac operations.Ann Thorac Surg. 1995; 60: 673-677Abstract Full Text PDF PubMed Scopus (77) Google Scholar Several authors have demonstrated the effectiveness of monitoring transoesophageal echocardiography (TOE) during cardiac surgery for diagnosis of intracoronary air embolism as it detects the presence of air in the coronary arteries and intraoperative myocardial ischaemia due to alterations in segmentary ventricular contractility.2Cabrera Schulmeyer MC Santelices E Vega R Allamand F De la Maza JC Detección de embolia aérea intracoronaria con ecocardiografía transesofágica intraoperatoria.Rev Esp Anestesiol Reanim. 2005; 52: 367-370PubMed Google Scholar, 3Smith JS Cahalan MK Benefiel DJ et al.Intraoperative detection of myocardial ischemia in high-risk patients: electrocardiography versus two-dimensional echocardiography.Circulation. 1985; 72: 1015-1021Crossref PubMed Scopus (354) Google Scholar, 4Lamm G Auer J Punzengruber C Ng CK Eber B Intracoronary air embolism in open heart surgery—an uncommon source of myocardial ischaemia.Int J Cardiol. 2006; 112: e85-e86Abstract Full Text Full Text PDF PubMed Scopus (10) Google Scholar We report a case of intracoronary air embolism detected by TOE in a patient undergoing aortic valve replacement for severe stenosis. Intraoperative TOE showed a marked depression in ventricular myocardial activity with severe hypokinesia and areas with hyper-refringency due to intracoronary air (Fig. 1). A 43-yr-old, 91 kg man, with a history of hypertension and hypercholesterolemia who was treated with captopril, propranolol, and statins underwent general anaesthesia for valve replacement surgery for severe aortic stenosis secondary to bicuspid valve calcification. He had dyspnoea at rest for 8 weeks and episodes of upper retrosternal chest pain pressing in character. Transthoracic echocardiography study showed a transvalvular gradient of 76 mm Hg and left ventricular hypertrophy with preserved systolic function. The patient was premedicated with oral diazepam 10 mg 1 h before surgery. In the operating theatre, arterial pressure was monitored at the left radial artery, with five-lead electrocardiography, pulmonary artery pressure by Swan Ganz catheter, regional cerebral oxygen saturation, bispectral index (BIS), pulse oximetry, partial pressure of end-tidal carbon dioxide, oesophageal temperature, and neuromuscular function monitoring. Intraoperative haemodynamic status was assessed by TOE, using 5 MHz frequency Philips Sonos multiplanar transducer. Induction was achieved with etomidate 0.3 mg kg−1, cisatracurium 0.2 mg kg−1, and fentanyl 4 μg kg−1. Anaesthesia was maintained with sevoflurane 1–2%, remifentanil 0.3 μg kg−1 min−1 in the 40–60 BIS range. During surgery, haemodynamic stability was maintained with CBP uneventfully at 80 min with 60 min of aortic clamping, and sinus rhythm with adequate segmentary contractility in TOE. Fifteen minutes later, hypotension with a systolic pressure of 60 developed, despite apparent good function of the prosthetic valve with a transvalvular gradient of 23 mm Hg. There was a severely hypokinetic area on the anterior wall with hyper-refringency areas attributable to intracoronary air, with calculated left ventricular ejection fraction of 20% and ST elevation in leads V1 and V2. This progressed to ventricular fibrillation in spite of internal defibrillation, and it was necessary to restore the CBP. With the diagnosis of intracoronary embolism, it was decided to increase arterial pressure by the infusion of levosimendan 0.1–0.2 μg kg−1 min−1 and also the flow speed of CBP, improving coronary perfusion, anterior wall segmentary contractility, and haemodynamic function, with subsequent disappearance of hyper-refringency area. CBP and the inotrope were later withdrawn and normal arterial pressure maintained. The postoperative period in ICU was uneventful with extubation 5 h after admission and return to the ward in 48 h. Intracoronary air embolism during extracorporeal surgery is characterized by the presence of hyper-refringency areas in the ventricular myocardium and left ventricular hypokinesia resulting from ischaemia. The right coronary artery is most frequently affected due to the anterior position of the right Valsalva sinus. In our patient, the hyper-refringency area and myocardial hypokinesia was in the left ventricular anterior wall due to embolism of the anterior descending branch of the left coronary artery. TOE excluded early prosthetic dysfunction and the possibility of inadequate blood. The hyper-refringency area and ventricular hypokinesia and immediate recovery after treatment with inotropic drugs facilitated the diagnosis of intracoronary air embolism as the cause of myocardial ischaemia, and excluded thrombosis and spasm. In intracoronary air embolism, symptomatic treatment with increase in coronary perfusion pressure and the use of inotropic agents is recommended.4Lamm G Auer J Punzengruber C Ng CK Eber B Intracoronary air embolism in open heart surgery—an uncommon source of myocardial ischaemia.Int J Cardiol. 2006; 112: e85-e86Abstract Full Text Full Text PDF PubMed Scopus (10) Google Scholar In our case, reconnection to CBP and levosimendan to increase myocardial contractility and coronary perfusion pressure returned left ventricular contractility to normal.