Anesthesia-induced atelectasis is more pronounced in morbidly obese patients.1–5 The alveolar recruitment strategy (ARS) eliminates such atelectasis, reinstating normal lung function without collapse.6 However, the level of positive end-expiratory pressure (PEEP) needed to keep the lungs open is expected to be higher than in patients of normal weight.7–9 The high intrathoracic pressures reached during the maneuver could potentially compromise hemodynamics, especially in morbidly obese patients, because of their predisposition for cardiovascular diseases.10–13
The objective of this prospective study was to analyze the hemodynamic consequences of ARS and PEEP before and during capnoperitoneum in anesthetized morbidly obese patients.
After obtaining ethics committee approval and written informed consent from patients, we examined 20 patients with a body mass index (BMI) above 40 kg/m2 undergoing laparoscopic gastric banding. Patients with known cardiopulmonary diseases were excluded. Selected data from 11 of these 20 patients appear in this issue of the Journal.8
Anesthesia was induced with etomidate 0.15–0.3 mg/kg, sufentanyl 0.1–0.5 μg/kg, and succinylcholine 1 mg/kg of lean body weight and maintained with sevoflurane and boluses of 0.1–0.5 μg/kg sufentanyl. After tracheal intubation, lungs were ventilated using a Cicero EM (Dräger, Lübeck, Germany) with a tidal volume of 10 mL/kg of lean body weight, a respiratory rate of 10–12 bpm, an I:E ratio of 1:1, and an Fio2 of 0.4.
One liter of colloidal solution RheoHAES 70/0.4 6% (Braun, Melsungen, Germany) was administered IV for intravascular volume expansion before induction of anesthesia, whereas the preload status was assessed by measuring the end-diastolic area (EDA), with values between 16.0 and 31.2 cm2 defining “euvolemia.”14 A continuous infusion of saline solution was run at 5 mL per kg lean body weight and hour during anesthesia.
Electrocardiogram, pulse oximetry, and invasive arterial blood pressure measurement in a radial artery were monitored. A pulmonary artery catheter (Swan-Ganz, Baxter, Irvine, CA) was placed through the right internal jugular vein and cardiac output (CO) was measured using triplicate thermodilutions. Systemic vascular resistance (SVR) was calculated using a standard formula with the mean systemic arterial blood pressure (MAP), the central venous pressure (CVP), and the CO values as follows:
Pulmonary vascular resistance (PVR) was calculated using a standard formula with the mean pulmonary arterial pressure (MPAP), the pulmonary capillary wedge pressure (PCWP), and the CO values as follows:
Transesophageal echocardiography (TEE) was conducted using the Sonos 5500® (Phillips Medical Systems, Böbligen, Germany). The echocardiographic probe was initially inserted into the stomach to examine the morphology and function of the heart. Thereafter, the probe was withdrawn into the esophagus and had to remain there during the study to facilitate the surgery in the upper gastric region. We measured EDA of the left ventricle by planimetry using the leading edge method.14
Protocol: Patients were placed in a reverse Trendelenburg position (approximately 30°). ARS and PEEP titrations were sequentially performed before (without capnoperitoneum) and after (with capnoperitoneum) the start of surgery. The ARS was performed by increasing PEEP in increments of 5 cm H2O from 0 to 15 (without capnoperitoneum) and to 20 cm H2O (with capnoperitoneum). The patients’ lungs’ opening pressures were assumed to be around 50 cm H2O of airway pressure without capnoperitoneum and 60 cm H2O with capnoperitoneum. Therefore, plateau pressures of 50 and 60 cm H2O were applied for about 10 breaths to actively recruit collapsed lung tissue before and during capnoperitoneum, respectively. After approximately 1 min at maximal airway pressures, PEEP was decreased in steps of 5 cm H2O down to 0 cm H2O. Each level of PEEP before and after ARS was maintained for 3 min. Hemodynamic measurements and arterial blood samples were taken during the 3rd min of each PEEP period. Intraabdominal pressure was around 20 mm Hg as measured by the insufflator UHI-2 (Olympus, Tokyo, Japan).
Statistical analysis was performed using SPSS version 13.0 (SPSS, Chicago, IL). Descriptive analysis and the Wilcoxon’s test were applied. Variables are presented as mean ± sd, and a value of P < 0.05 was considered significant.
Morbidly obese patients aged 39 ± 6 yr with a BMI of 50 ± 9 kg/m2 were enrolled in the study. All patients finished the protocol without complications.
At the highest airway pressures, CO decreased from 6.3 ± 1.3 to 5.5 ± 1.4 L/min before capnoperitoneum and from 6.5 ± 1.3 to 5.6 ± 1.3 L/min during capnoperitoneum, returning to baseline values within the next PEEP step. The absolute values of SVR and PVR did not show significant differences during the protocol. However, PVR values were slightly lower immediately after ARS than before ARS (Fig. 1).15,16 The remaining variables were stable during the entire protocol (Table 1).
TEE did not reveal previous heart disease, evidence of segmental wall motion abnormalities, or significant differences in EDA during ARS (Table 1).
The ARS and high levels of PEEP were hemodynamically well tolerated in intravascular volume-loaded morbidly obese patients undergoing laparoscopic surgery. This hemodynamic stability was observed both before and during capnoperitoneum.
The potential hemodynamic repercussions of a reverse Trendelenburg position, capnoperitoneum, and mechanical ventilation depend mainly on their negative effect on venous return.17–21 Thus, the intravascular volume status plays a crucial role in any patient undergoing bariatric surgery, regardless of BMI. Jellinek et al.22 demonstrated the absence of any hemodynamic compromise at high levels of PEEP if CVPs were kept higher than 10 mm Hg. Our data confirm these results: no hemodynamic consequences were observed at higher airway pressures, provided that preload was kept within a normal range, as documented by the unremarkable EDAs and filling pressures. This is not too surprising, because the significantly elevated intraabdominal pressures of morbidly obese patients, particularly during the surgery, reduced the transmural pressure acting on the hemodynamics. The intravascular volume loading with colloid (15 mL/kg of lean body weight) before anesthesia obviously prevented any hemodynamic disturbances in these fasted morbidly obese patients. Our results are also in agreement with those of Erlandsson et al.,17 who found that infusion of 1 L of intravascular volume expanders before applying high levels of PEEP avoided any negative effects in hemodynamics in morbidly obese patients.
Limitations: Because of the particular surgical procedure, we could not assume the intragastric TEE position typically needed for optimal CO measurement. Therefore, we decided to report only values for EDA and the presence or absence of segmental wall motion abnormalities.
After optimization of preload, lung recruitment and high positive airway pressures were hemodynamically well tolerated in morbidly obese patients with or without capnoperitoneum.
The authors thank Stefan Maisch, Clinic of Anesthesiology, University Hospital Hamburg-Eppendorf, Germany, for his help during the conduct of this study and for valuable input during the revision process.
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© 2009 International Anesthesia Research Society
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