The observation that thoracotomy performed for non cardiac reasons is often complicated by postoperative supraventricular arrhythmias, dates back more than 50 years. The etiology remains unclear and is almost certainly multifactorial, with the postoperative hyperadrenergic condition and atrial distention as probably most important pathophysiologic factors.
The majority of reports in the literature are retrospective with the incidence of dysrhythmias determined by chart review with its inherent lack of sensitivity. The reported incidence of dysrhythmias after thoracotomy also varies (10–28% in the international literature) [5, 6] in part because of definition of dysrhythmias and methods of detection. In this study we purposefully excluded sinus tachycardia often related to presence of pain or intravascular volume depletion. In our material 43 (21.6%) out of 199 patients developed supraventricular arrhythmia with atrial fibrillation being by far the most common (88.3%). This is in agreement with all recently published studies.
Numerous authors [7, 8] have suggested that the time of peak onset of development of postoperative dysrhythmias is during the 2nd postoperative day and this also confirmed by our study (65.7% of the patients had the onset of the arrhythmia on the 2nd postoperative day). In contrast Richie and colleagues  reported that the most common time for onset of supraventricular arrhythmia is during the first postoperative day.
According to the literature, previously stated risk factors for the development of supraventricular arrhythmias after pulmonary resection include increasing age, sex, side of procedure, extent of resection, history of diabetes mellitus, hypertension, beta-blockers ingestion and previous cardiopulmonary disease, anesthetic agents and preoperative pulmonary functional status. Many authors experienced opposite opinions to these factors [10–12]. In our study increasing age (>65 years) and the extent of pulmonary resection were the only statistically significant factors as we excluded patients with previous history of cardiopulmonary disease.
The extent of pulmonary resection as a risk factor for supraventricular arrhythmias has been a standard for many studies [13, 14]. Surgical factors are related to the destruction of cardiac nervous structures. Both sympathetic and parasympathetic cardiac nerves innervate the heart. The vagal and sympathetic fibres emerge, from left to right sides, to form cardiac plexus located between the aortic arch and the tracheal bifurcation. Their filaments accompany the coronary arteries and their branches. The extent of pulmonary resection could determine direct damage to the above mentioned anatomic structures by the dissection of pulmonary hilum during lung resection or hilar and mediastinal node sampling. The significance of these structures was also confirmed by Haissaguerre and colleagues  who studied a population of non-surgical patients affected by frequent paroxysms of atrial fibrillation. Electrophysiological study proved that pulmonary veins, especially in their proximal tract, are covered by myocardial tissue, with electrical properties which can generate ectopic beats with consequent atrial fibrillation. So, surgical knots to the wall of pulmonary veins or other surgical manipulations could probably cause mechanical or ischaemic damage to the zone which is often covered by myocardial excitable tissue. This could generate ectopic beats and atrial fibrillation. No mortality was directly attributed to dysrhythmia. Others have shown mortality associated with dysrhythmia after thoracotomy. Recently, Amar and colleagues  have approved that early supraventricular dysrhythmias after resection of non- small cell lung cancer is associated with poor long-term survival, although this finding has to be confirmed by more studies.
Treatment of postoperative supraventricular arrhythmias after pulmonary resection remains a controversial topic. Supraventricular tachyarrhythmias respond well to rate control drugs such as beta-blockers (esmolol, metoprolol) or calcium channel antagonists (diltiazem, verapamil). Class III antiarrhythmic drugs (amiodarone, ibutilide) have been used recently with satisfactory results although there are different opinions [4, 16].
Beta-blockers are preferred in patients with ischemic heart disease but may be relatively contraindicated in patients with proven bronchospastic potential, in those with congestive heart failure, severe sinus bradycardia or high degree AV-block . Calcium channel blockers are contraindicated in patients with Wolff-Parkinson-White syndrome since they can accelerate the ventricular rate with atrial fibrillation . Of the class III antiarrhythmic drugs, ibutilide has been used currently with moderate success to convert acute atrial fibrillation in 57% of patients after cardiac surgery, however polymorhic ventricular tachycardia was reported in 1.8% of patients and was attributed primarily to electrolyte imbalance .
Amiodarone has been used in recent studies in the management of patients with supraventricular arrhythmia with great success. Ciriaco and colleagues  report 90.9% success in establishing sinus rhythm with no side effects. This is in agreement with our study, where amiodarone established sinus rhythm in 86% of the patients with most common side effect bradycardia (<50 beats per minute) in 13.5% of the patients. Only 6 patients required electrical cardioversion due to the fact that they were hemodynamically unstable. In contrast Van Mieghem and colleagues  report that amiodarone may be implicated in the development of adult respiratory distress syndrome after lung surgery and especially pneumonectomy.
Because of the greater incidence of supraventricular tachyarrhythmias in the postoperative period most efforts have focused on prevention. A recent review  summarized the results of numerous studies examining the efficacy of a variety of drugs to prevent this complication in cardiac surgery patients. It is unclear whether prophylactic treatment against postoperative atrial arrhythmias improves clinical outcomes or shortens hospital stay and whether to employ rate control or rhythm control drugs. But these studies demonstrated also the effectiveness of beta-blockers and class III antiarrhythmics (amiodarone, ibutilide) in reducing the atrial fibrillation incidence after cardiac operations (valvular surgery, coronary artery by pass grafting) [19, 20]. Amar and colleagues  published the first large, randomized control trial to demonstrate that diltiazem clearly prevents occurence of atrial fibrillation after major thoracic operations. Lanza and colleagues  demonstrated that low dose oral amiodarone prophylaxis significantly reduces the incidence of atrial fibrillation after pulmonary resection. Other randomized control trials to test prophylactic effects of the drugs are mandatory to confirm these results in patients after major thoracic non-cardiac operations.