HEMODYNAMIC-CHANGES DURING PROLONGED LAPAROSCOPIC SURGERY

Citation
U. Windberger et al., HEMODYNAMIC-CHANGES DURING PROLONGED LAPAROSCOPIC SURGERY, European surgical research, 26(1), 1994, pp. 1-9
Citations number
17
Categorie Soggetti
Surgery
Journal title
ISSN journal
0014312X
Volume
26
Issue
1
Year of publication
1994
Pages
1 - 9
Database
ISI
SICI code
0014-312X(1994)26:1<1:HDPLS>2.0.ZU;2-4
Abstract
7 healthy pigs, anesthetized with ketamine/azaperon/thiopentone and ve ntilated with O-2/N2O by volume control, underwent anterior resection of the descending colon by laparoscopic view. During operation a pneum operitoneum by inflating CO2 to an abdominal pressure of 14 mm Hg was installed. Immediately (+2 min) after the onset of insufflation, both systemic and pulmonary arterial pressure increased. However, pulmonary artery pressure started to decrease after 10 min, whereas systemic ar terial pressure remained elevated until the end of the experimental pr otocol. Left ventricular (LV) pressure and LV dp/dt increased in paral lel with the systemic arterial pressure. Peak inspiratory pressure and central venous pressure increased in parallel with the abdominal pres sure. Blood gas analysis of arterial and pulmonary blood demonstrated increased pCO(2) associated with mild acidosis. Arterial pO(2) did not change significantly indicating that the decreased pulmonal distensib ility did not endanger the oxygenation. Pulmonary pO(2) and pulmonary O-2 saturation increased early (+10 min) after start of insufflation a nd were stable during the 2 h of observation indicating either increas ed cardiac output or decreased O-2 extraction. We conclude that the sh arp initial rise of both arterial pressures could be the effect of a m echanical action, whereas sustained hemodynamic alterations would invo lve complex regulatory mechanisms like an increase of sympathetic acti vity, baroreceptor control, or a response to acidosis. The acute and, in the systemic circulation, stable increase of ventricular afterload should be considered in patients with underlying cardiac diseases such as ischemic heart disease or valvular dysfunction or in patients taki ng drugs which interfere with normal compensatory processes.