Effects of pneumoperitoneum on hemodynamics evaluated by continuous noninvasive arterial pressure monitoring. A single-center observational study
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Abstract
BACKGROUND AND OBJECTIVES: The induction of pneumoperitoneum (PP) during laparoscopy may cause hemodynamic alterations, especially in patients with unknown cardiovascular diseases. While invasive arterial monitoring could be considered excessive, continuous noninvasive arterial pressure (CNAP) monitoring may allow careful evaluation of hemodynamic variations during laparoscopy.
MATERIALS AND METHODS: The objective of this single center observational study was to evaluate hemodynamic changes after insufflation and after deflation of PP with CNAP monitoring. Patients included where adults undergoing elective laparoscopic cholecystectomy (American Society of Anesthesiologists physical status classification II and III). The Hemodynamic data (blood-pressure, cardiac-index, heart-rate, stroke-volume index, stoke-volume variation and arterialelastance) were collected 30 seconds before pneumoperitoneum (t1), and compared to values at 2 (t2), 10 (t3) and 20 (t4) minutes after pneumoperitoneum insufflation. We also compared data 30 seconds before and 2 minutes after release of pneumoperitoneum.
RESULTS: 65 patients were included. Compared with reference values at t1, blood-pressure values increased at all timepoints (t2-t 3-t4); cardiac-index augmented at t3 and t4 (p<0.05); heart-rate increased at t3 (p<0.005); stroke-volume index decreased at t2 (p<0.005) and was higher at t4 (p<0.005). While stoke-volume variation remained always stable after pneumoperitoneum induction, arterial-elastance increased significantly at all time-points (t2-t 3-t4). The only difference at pneumoperitoneum deflation was a reduction in stoke-volume variation (p<0.05).
CONCLUSIONS: In patients undergoing elective cholecystectomy, CNAP monitoring showed significant hemodynamic changes that would have been underappreciated with standard non-invasive monitoring with increase in arterial elastance under stable preload conditions. Whether this effect is due to unknown cardiovascular diseases facilitating ventriculo-arterial decoupling remains to be determined.