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From the Department of Anesthesiology, Pennsylvania State University College of Medicine and Pennsylvania State Heart and Vascular Institute, Hershey, Pennsylvania.
Address correspondence and reprint requests to Mikhail R. Sukernik, MD, PhD, Department of Anesthesiology, Pennsylvania State Milton S. Hershey Medical Center, P.O. Box 850, Mailcode H-187, 500 University Drive, Hershey, PA 17033. Address e-mail to mrs21{at}columbia.edu.
A 66-yr-old woman was admitted for video-assisted thoracoscopic surgery for a left upper lobe pulmonary nodule. The patient's medical history was significant for rheumatic mitral stenosis. She underwent mitral valve replacement with a St. Jude mitral valve prosthesis and maze procedure 2 yr ago. A transthoracic echocardiogram performed 10 mo before admission demonstrated a left ventricular (LV) ejection fraction of 55%, a normal right ventricle, a dilated left atrium (LA), a right atrium of normal size, and a normally functioning bileaflet mechanical mitral prosthesis.
After induction of anesthesia, systemic arterial hypotension with a mean arterial blood pressure of 40 mm Hg resistant to administration of phenylephrine in divided doses (0.7 mg total) developed. To exclude valvular pathology or ventricular dysfunction as a cause of systemic hypotension, transesophageal echocardiography (TEE) was performed. TEE revealed normal LV size and function, no regional wall motion abnormalities, normal right ventricular size and function, mild to moderate LA dilation, normal right atrial size, normal aortic dimensions, and a trileaflet aortic valve with systolic doming and mildly restricted motion but no significant pressure gradient. The bileaflet mechanical prosthetic mitral valve had no significant stenosis or regurgitation; the tricuspid valve was structurally normal. TEE also identified a separate chamber adjacent to the anterolateral wall of the LA with bidirectional turbulent flow between the chamber and the LA (Figs. 1–3, Video clip 1; please see video clip available at www.anesthesia-analgesia.org). This flow, discovered during the time of systemic hypotension, initially raised a concern of serious structural and functional pathology, such as paravalvular regurgitation or LA dissection. With careful examination, however, these possibilities were excluded. Incomplete surgical ligation of the left atrial appendage (LAA) was suspected and subsequently confirmed by referring to the intraoperative TEE records performed after weaning from cardiopulmonary bypass at the time of prior heart surgery. In the meantime, the patient's arterial blood pressure was stabilized with adjustment of anesthesia depth and hypovolemia correction. Surgery was completed without further complications.
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TEE is the "gold standard" of LAA evaluation. LAA can be easily identified in the standard esophageal two-chamber view. Rotation of the omniplane angle from 0 degrees to 180 degrees at or slightly above the midesophageal window allows detailed LAA assessment in the majority of cases (Video clips 2–4; please see video clips available at www.anesthesia-analgesia.org).
A bidirectional turbulent jet from an incompletely ligated LAA in the presence of a prosthetic mitral valve can be mistaken for, and should be distinguished from, a paravalvular leak, a prosthetic valve washing jet, LA dissection, as well as aorta to LA and coronary artery to LA fistulas. Washing regurgitant jets are normal findings in mechanical prosthetic valves intentionally engineered to decrease thrombogenicity of the prosthetic valve.5 These jets are small, located inside of the sewing ring, and are short in duration. A washing jet can be seen on Figure 2 (arrow). The flow we identified was relatively large and located outside of the sewing ring, making either physiologic or pathologic transvalvular regurgitation unlikely. Paravalvular regurgitation is located outside of the sewing ring and, unless of insignificant size, is a pathologic finding. Systolic para- or intravalvular mitral regurgitation assessed from the midesophageal window will present as flow directed towards the transducer. In our case, the systolic component of bidirectional flow was directed away from the transducer, excluding the possibility of mitral regurgitation or other pathologic communications between the LV and LA, such as fistula or LA dissection.6 Aorta to LA fistulas are likely to be associated with continuous systolic-diastolic flow. Coronary arteries to LA fistulas usually drain in the right chambers of the heart.7 The key elements that are helpful in the successful identification of incomplete LAA ligation include: 1) being alert to the possibility in patients with a history of mitral valve surgery, 2) visualization of an additional chamber in the vicinity of the LAA, 3) a shape and trabeculation of this chamber consistent with the LAA as demonstrated in Figure 1, and 4) an additional chamber emptying during atrial systole (Fig. 3).
Although the clinical impact of incomplete LAA ligation is unknown, it is not associated with hemodynamic instability and does not require immediate intervention.
Footnotes
Accepted for publication November 5, 2007.
REFERENCES
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