Haemodynamic and ventilatory effects of laparoscopic surgery
Abstract: Background: It has been shown repeatedly that the establishment of pneumoperitoneum (PP) is associated with increased cardiac filling pressures, as well as increased blood pressure and systemic vascular resistance. Patients without heart or lung disease can compensate for these effects of PP, but cardiopulmonary compromised patients may develop cardiac failure during PP. Mechanisms involved could be an increased filling of the central circulation, a mere transmission of the intra-abdominal pressure to the thorax, and a regional sympathetic activation, respectively. Further, previous studies have shown that PP transiently reduces the shunt and increases the arterial oxygen tension. Aim: The aim of the present study was to explore the mechanisms behind the haemodynamic and ventilatory responses caused by C02 pneumoperitoneum. Therefore, the influence of PP on central blood volume and cardiac output, the vascular resistance in leg skeletal muscle and the arterio-venous difference of the catecholamines in the leg was studied. It was postulated that PP reduces atelectasis formation and/or ameliorates ventilation- perfusion relationships. Another aim was to compare the effects of two different laparoscopic techniques (pneumoperitoneum and abdominal wall lift) on central haemodynamics and intrathoracic pressure. Methods: 56 patients without heart or lung disease (ASA I) were studied. They were all scheduled for laparoscopic cholecystectomy. The measurements were performed during stable anaesthesia before and after pneumoperitoneum, with an intra-abdominal pressure between 11-13 mmHg. The central blood volume and cardiac output (CO) were determined by the indicatordilution technique, using in-line densitometric measurements of indocyanine green (study I). CO was also measured by thermodilution technique (study II, IV). Abdominal wall lift was performed by using a Laparolift (study II). The intrathoracic pressure was monitored by using an intraesophageal balloon (study II). The arterial blood flow in the legs was determined by mercury- in-Silastic strain gauge venous occlusion plethysmography and the plasma levels of noradrenaline and adrenaline were analyzed by high performance liquid chromatography (study III). Ventilation-perfusion relationships were evaluated by the multiple inert gas technique (study IV). Atelectasis, total lung volume and regions of aeration were measured by spiral computed tomography (study V). Results: PP significantly increased mean arterial and cardiac filling pressures as well as systemic and leg vascular resistance, but did not affect cardiac output, central blood volume, calf blood volume or the catecholamines response in skeletal muscle. PP resulted in a small transient reduction of the pulmonary shunt and increased the arterial oxygen tension. Further, PP increased the volume of atelectasis, decreased the total lung volume and shifted the diaphragm cranially. Abdominal wall lift increased cardiac index and did not affect cardiac filling pressures or systemic vascular resistance. Conclusions: It is suggested, that the increased cardiac filling pressures during PP are secondary to a transmission of the intra-abdominal pressure to the thorax. Further, the increase in systemic vascular resistance during PP is not a result of an increased central blood volume or of a catecholamine response in the resistance vasculature in skeletal muscle. A abdominal wall lift does not increase systemic vascular resistance and improves CO, it is suggested that it is a safer alternative than pneumoperitoneum. The fact that PP increases arterial oxygen tension and decreases the pulmonary shunt despite an increase of the atelectatic area suggests that PP improves the ventilation-perfusion matching.
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