|
|
||||||||
Department of Thoracic and Cardiovascular Surgery, AHEPA University Hospital, 1 Stilponos Kyriakidi St, Thessaloniki, 54636 Greece
(Email: cforoulis{at}otenet.gr).
Patients at high risk for the development of supraventricular tachyarrhythmia (SVT) after thoracic surgery are those who undergo pneumonectomy (especially right or intrapericardial), whereas lobectomies and lesser resections are associated with considerably lower rates of postoperative SVTs. The cause of SVTs after thoracic surgery is multifactorial and the main predisposing factors are impaired oxygenation, right ventricle (RV) dysfunction, pre-existing heart disease, low postoperative forced expiratory value in 1 second, and mechanical factors, such as mediastinal shifting or deviation, pericarditis, or pericardial effusions after intrapericardial dissections [1]. Echocardiographic studies have demonstrated that an increase of postoperative right ventricular systolic pressure to abnormal levels after major lung resection is well connected with the development of postoperative SVT [1, 2]. Histologic studies have also demonstrated that degenerative changes of the right atrial appendage are associated with the development of a new onset of atrial fibrillation after either on-pump or off-pump coronary artery bypass grafting. These atrial degenerative changes correlated well with left atrium dilation and advanced age [3].
The right ventricle myocardial performance index (MPI) is echocardiographically derived, reliable, reproducible, and validated in previous studies index of stress induced RV dysfunction. In their well-designed pilot study, Matyal and colleagues [4] detected that left atrium dilation and significant RV MPI changes after lung isolation in patients with normal baseline RV MPI are independent predictors of postoperative SVT. However, lateral decubitus position and one-lung ventilation induce a complex physiologic response that is reversed at the end of the operation when the patient returns back to the supine position and both lungs are ventilated [5]. On the other hand, major lung parenchyma resection permanently reduces pulmonary vascular bed and increases RV afterload [1, 2]. Future studies correlating RV MPI changes during one-lung ventilation and after its discontinuation with the extent of pulmonary parenchyma resection, will confirm the value of RV MPI as a strong predictor index of development postoperative SVTs after thoracic surgery.
| References |
|---|
|
|
|---|
Related Article
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |