Forde-Thielen and Konia Journal of Medical Case Reports 2011, 5:257 http://www.jmedicalcasereports.com/content/5/1/257 positive-pressure respiration (PEEP) 4, FiO2 1.0). Incisions were made soon after initiation of one-lung ventilation, and ports were inserted. Vitals signs at the time of incision included saturated oxygen 99-100%, noninvasive blood pressure 150/75 mmHg and pulse 80/min. Her right hemi- thorax was insufflated with carbon dioxide to a pressure of 10 mmHg at a rate of 25 L/min. At this point in the proce- dure we noted changes in our patient’s hemodynamic sta- tus. Her blood pressure dropped to 112/63 and her heart rate precipitously dropped to 35/min for a few seconds. This was followed by asystole. The surgeon was notified, insufflation was stopped and glycopyrrolate 0.4 mg and atropine 0.4 mg were administered. Within 10 seconds of pleural deflation our patient resumed a normal sinus rhythm. Her next blood pressure reading was 125/75. In the absence of further rhythm or hemodynamic abnormal- ities the surgery was continued. The pleural cavity was slowly insufflated to a pressure of 8 mmHg and the case progressed without any further complications. Our patient had an uncomplicated post-operative course. Discussion Insufflation of the pleural cavity with carbon dioxide is believed by some to facilitate lung deflation during one- lung ventilation and improve surgical exposure. Insuffla- tion also enlarges the intrapleural space by pushing the mediastinum away from the operative field [1]. The tech- nique is often used in thoracoscopic harvesting of the internal mammary artery. The practice of insufflation has further been used successfully in collapsing emphysema- tous lung [1]. It has, however, been suggested that insuffla- tion is unnecessary for adequate exposure in the majority of thoracoscopic surgeries and may increase the risk of hemodynamic compromise [2-4]. It has also been sug- gested that opening a port to air is safer than and just as effective as insufflations [5]. The initial reports of significant hemodynamic compro- mise during positive pressure insufflation of the pleural cavity came from pig studies [6]. The anatomy and phy- siology of a pig, however, is significantly different from that of a human [7]. Based on human studies, most authors agree that insufflation of the hemithorax up to a pressure of 10 mmHg with one-lung ventilation causes some hemodynamic change. Right-sided insufflation causes more pronounced hemodynamic effect compared to left-sided insufflation because the right heart is a low- pressure system [1,5,6]. Human studies have demonstrated that positive pressure insufflation of the right or left pleural cavity increases central venous pressure (CVP) by 4-10 mmHg [1,7,8] and pulmonary artery (PA) pressure by 2-7 mmHg [1,7], which ultimately results in a decrease in preload. The effects of positive pressure insufflation of the pleural cavity have less significant effects on systemic pressures and cardiac function [3,4,7-9]. Page 2 of 3 There are several theories that explain the mechanisms of hemodynamic changes. Positive pressure insufflation of the thoracic cavity creates physiologic effects similar to a tension pneumothorax [6]. This effect can explain the increase in CVP and decrease in venous return. More pronounced effects in certain reports could be explained by higher than intended intrathoracic pressures caused by incomplete lung collapse at initiation of pleural cavity insufflation. In this situation the pleural pressure may increase enough to close off the small airways. Respira- tory gases get trapped in the lung and further insufflation induces a rapid increase in intrathoracic pressure instead of collapsing the lung. The high intrathoracic pressure further reduces venous return and lowers the cardiac output [5]. Increases in mean PA pressure and pulmonary capillary wedge pressure may be caused by positive intrapleural pressure together with hypoxic pulmonary vasoconstric- tion in the collapsed pulmonary parenchyma [1,7]. There are no prior reports of asystole on commence- ment of pleural insufflation during one-lung ventilation in the human literature. However, Harris et al. reported a case of severe bradycardia following hypotension during right-sided thoracoscopic dorsal sympathectomy with insufflation up to a pressure of 15 mmHg [5]. Our case began with mild hypotension and bradycardia which pro- gressed to asystole, suggesting that these hemodynamic changes are all part of a spectrum of derangements caused by the same inciting mechanism. The incidence and mechanisms of bradycardia and asys- tole are poorly defined. Besides the hemodynamic effects described above, increased intrathoracic pressure could cause direct vagal stimulation and thereby induce brady- cardia or asystole. Some authors have proposed a Bezold- Jarisch reflex as an underlying mechanism [5]. The Bezold-Jarisch reflex occurs when a patient with an intact autonomic nervous system experiences hypotension. This is sensed by baroreceptors in the aortic arch and carotid sinuses, which compensate with greatly increased cardiac contractility. The cardiac baroreceptors then sense this high intramural tension and induce significant parasympa- thetic discharge resulting in bradycardia or asystole. To explain asystole in our patient, we turn to the sequence of events to help elucidate the pathophysiology. After positioning of our patient and preparation of the surgical field we initiated one-lung ventilation. Ports were immediately inserted and positive pressure insuffla- tion of her right pleural cavity with high flows (25 L/min) to a pressure of 10 mmHg was started. Full deflation of the lung was not carefully assessed prior to positive pres- sure insufflation. As demonstrated by Jacobs et al., the actual pressure in an insufflated cavity may briefly be much higher than the insufflator pressure presetting [10]. Temporary deviations of up to 78.8% from the displayed