Relation of the Static Compliance Curve and Positive End-expiratory Pressure to Oxygenation during One-lung Ventilation

Background : Positive end-expiratory pressure (PEEP) is commonly applied to the ventilated lung to try to improve oxygenation during one-lung ventilation but is an unreliable therapy and occasionally causes arterial oxygen partial pressure (Pao2) to decrease further. The current study examined whether the effects of PEEP on oxygenation depend on the static compliance curve of the lung to which it is applied.

Methods : Forty-two adults undergoing thoracic surgery were studied during stable, open-chest, one-lung ventilation. Arterial blood gasses were measured during two-lung ventilation and one-lung ventilation before, during, and after the application of 5 cm H2O PEEP to the ventilated lung. The plateau end-expiratory pressure and static compliance curve of the ventilated lung were measured with and without applied PEEP, and the lower inflection point was determined from the compliance curve.

Results : Mean (+/- SD) Pao2 values, with a fraction of inspired oxygen of 1.0, were not different during one-lung ventilation before (192 +/- 91 mmHg), during (190 +/- 90), or after ( 205 +/- 79) the addition of 5 cm H2O PEEP. The mean plateau end-expiratory pressure increased from 4.2 to 6.8 cm H2O with the application of 5 cm H2O PEEP and decreased to 4.5 cm H2O when 5 cm H2O PEEP was removed. Six patients showed a clinically useful (> 20%) increase in Pao2 with 5 cm H2O PEEP, and nine patients had a greater than 20% decrease in Pao2. The change in Pao2 with the application of 5 cm H2O PEEP correlated in an inverse fashion with the change in the gradient between the end-expiratory pressure and the pressure at the lower inflection point (r = 0.76). The subgroup of patients with a Pao2 during two-lung ventilation that was less than the mean (365 mmHg) and an end-expiratory pressure during one-lung ventilation without applied PEEP less than the mean were more likely to have an increase in Pao2 when 5 cm H2O PEEP was applied.     

Relation of the static compliance curve and positive end-expiratory pressure to oxygenation during one-lung ventilation.

BACKGROUND: Positive end-expiratory pressure (PEEP) is commonly applied to the ventilated lung to try to improve oxygenation during one-lung ventilation but is an unreliable therapy and occasionally causes arterial oxygen partial pressure (PaO(2)) to decrease further. The current study examined whether the effects of PEEP on oxygenation depend on the static compliance curve of the lung to which it is applied. METHODS: Forty-two adults undergoing thoracic surgery were studied during stable, open-chest, one-lung ventilation. Arterial blood gases were measured during two-lung ventilation and one-lung ventilation before, during, and after the application of 5 cm H(2)O PEEP to the ventilated lung. The plateau end-expiratory pressure and static compliance curve of the ventilated lung were measured with and without applied PEEP, and the lower inflection point was determined from the compliance curve. RESULTS: Mean (+/- SD) PaO(2) values, with a fraction of inspired oxygen of 1.0, were not different during one-lung ventilation before (192 +/- 91 mmHg), during (190 +/- 90), or after ( 205 +/- 79) the addition of 5 cm H(2)O PEEP. The mean plateau end-expiratory pressure increased from 4.2 to 6.8 cm H(2)O with the application of 5 cm H(2)O PEEP and decreased to 4.5 cm H(2)O when 5 cm H(2)O PEEP was removed. Six patients showed a clinically useful (> 20%) increase in PaO(2) with 5 cm H(2)O PEEP, and nine patients had a greater than 20% decrease in PaO(2). The change in PaO(2) with the application of 5 cm H(2)O PEEP correlated in an inverse fashion with the change in the gradient between the end-expiratory pressure and the pressure at the lower inflection point (r = 0.76). The subgroup of patients with a PaO(2) during two-lung ventilation that was less than the mean (365 mmHg) and an end-expiratory pressure during one-lung ventilation without applied PEEP less than the mean were more likely to have an increase in PaO(2) when 5 cm H(2)O PEEP was applied. CONCLUSIONS: The effects of the application of external 5 cm H(2)O PEEP on oxygenation during one-lung ventilation correspond to individual changes in the relation between the plateau end-expiratory pressure and the inflection point of the static compliance curve. When the application of PEEP causes the end-expiratory pressure to increase from a low level toward the inflection point, oxygenation is likely to improve. Conversely, if the addition of PEEP causes an increased inflation of the ventilated lung that raises the equilibrium end-expiratory pressure beyond the inflection point, oxygenation is likely to deteriorate.     

Airway pressure settings during general anaesthesia

In volume-controlled mechanical ventilation with constant inspiratory gas flow, which is most often used during general anesthesia, only the end-expiratory airway pressure (PEEP) has to be set by the user. Inspiratory airway pressures result from the combination of tidal volume and respiratory compliance as well as instantaneous gas flow and respiratory resistance. Given a normal respiratory compliance of 50-60 ml/mbar in mechanically ventilated patients, a driving pressure of 7-10 mbar is necessary for a tidal volume of about 6 ml/kg predicted body weight. The profile of airway pressure over time offers valuable information about respiratory mechanics. However, since the respiratory settings have a tremendous influence on the airway pressure-time profile, its interpretation has to be performed knowing the specific ventilator settings like inspiratory gas flow, presence or absence of an inspiratory pause and respiratory rate. Surprisingly, PEEP does not improve gas exchange in an unselected group of patients, although PEEP decreases the size of atelectasis and atelectasis can be detected after induction of anesthesia in 90% of adult patients. However, in obese patients gas exchange improves significantly when PEEP is applied. Furthermore, PEEP increases the apnoea interval tolerated without desaturation and thereby increases the safety margin during induction of anesthesia. If atelectasis shall be completely recruited, an airway pressure of 40 cm H2O is needed for 40 seconds. In order to avoid a severe drop in arterial blood pressure which may be accompanied by cardiac arrhythmia, such a recruitment manoeuvre should only be performed in normovolemic patients.     

The effects of the alveolar recruitment maneuver and positive end-expiratory pressure on arterial oxygenation during laparoscopic bariatric surgery

Abnormalities in gas exchange that occur during anesthesia are mostly caused by atelectasis, and these alterations are more pronounced in morbidly obese than in normal weight subjects. Sustained lung insufflation is capable of recruiting the collapsed areas and improving oxygenation in healthy patients of normal weight. We tested the effect of this ventilatory strategy on arterial oxygenation (Pao2) in patients undergoing laparoscopic bariatric surgery. After pneumoperitoneum was accomplished, the recruitment group received up to 4 sustained lung inflations with peak inspiratory pressures up to 50 cm H2O, which was followed by ventilation with 12 cm H2O positive end-expiratory pressure (PEEP). The patient's lungs in the control group were ventilated in a standard fashion with PEEP of 4 cm H2O. Variables related to gas exchange, respiratory mechanics, and hemodynamics were compared between recruitment and control groups. We found that alveolar recruitment effectively increased intraoperative Pao2 and temporarily increased respiratory system dynamic compliance (both P < 0.01). The effects of alveolar recruitment on oxygenation lasted as long as the trachea was intubated, and lungs were ventilated with high PEEP, but soon after tracheal extubation, all the beneficial effects on oxygenation disappeared. The mean number of vasopressor treatments given during surgery was larger in the recruitment group compared with the control group (3.0 versus 0.8; P = 0.04). In conclusion, our data suggest that the use of alveolar recruitment may be an effective mode of improving intraoperative oxygenation in morbidly obese patients. Our results showed the effect to be short lived and associated with more frequent intraoperative use of vasopressors.     

Pressure controlled-inverse ratio ventilation and pulmonary gas exchange during lower abdominal surgery

Although pressure controlled-inverse ratio ventilation (PC-IRV) has been used successfully in the treatment of respiratory failure, it has not been applied to the treatment of respiratory dysfunction during anaesthesia. With PC-IRV the inspiratory wave form is fundamentally altered so that inspiratory time is prolonged (inverse I:E), inspiratory flow rate is low, and the peak inspiratory pressure is limited. Positive end-expiratory pressure (PEEP) can be applied and the mean airway pressure is higher than with conventional ventilation. To assess the clinical efficacy of this new mode of ventilation we studied ten patients having lower abdominal gynaecologic surgery in the Trendelenburg position under general anaesthesia. Pulmonary O2 exchange was determined during four steady states: awake control (AC), after 30 and 60 min of PC-IRV during surgery, and at the end of surgery. Patients' lungs were ventilated with air/O2 by a Siemens 900C servo ventilator in the PC-IRV mode with an I:E ratio of 2:1 and 5 cm H2O of PEEP. The FIO2 was controlled at 0.5 and arterial blood gases were used to calculate the oxygen tension-based indices of gas exchange. There were significant increases of (A-a) DO2 at 30 and 60 min (41 and 43%). These changes were less than those reported in a previous study using conventional tidal volume ventilation (7.5 ml.kg-1) and were similar to those in patients whose lungs were ventilated with high tidal volumes (12.7 ml.kg-1). Thus, in this clinical model of compromised gas exchange, arterial oxygenation was better with PC-IRV than with conventional ventilation, but not better than with large tidal volume ventilation.     

利用动态肺顺应性设定呼气末正压在胸腔镜肺叶切除术中的运用

目的 探讨单肺通气利用动态肺顺应性设定呼气末正压通气(positive end-expiratory pressure,PEEP)的优势及可行性. 方法 选择预行右侧肺叶切除患者80例,完全随机分为A组和B组,每组40例:A组,单肺通气实施肺膨胀(sustained inflation,SI)复张后加用20 cmH2O(1 cmH2O=0.098 kPa)的PEEP并递减滴定,随后以得到最大肺顺应性的PEEP值通气,直到恢复双肺通气;B组,通气PEEP值固定为5 cmH2O,其他通气方法同A组.记录患者血气、呼吸等参数. 结果 两组设定的PEEP值[A组(9.2±1.2) cmH2O,B组5 cmH2O]差异有统计学意义(P＜0.05);在单肺通气1 h(T3)、手术结束(T4)时,两组动脉血氧分压(partial pressure of oxygen,PaO2)比较,差异有统计学意义(P＜0.05);B组的PaO2在T3～T4逐步降低,差异有统计学意义(P＜0.05),而A组则维持较好(P＞0.05);T3、T4时刻A组的动态肺顺应性[(30.8±5.9)、(30.7±6.4) ml/cmH2O]与B组[(26.6±5.5)、(26.4±5.2) ml/cmH2O]比较,差异有统计学意义(P＜0.05). 结论 胸腔镜肺叶切除术中的单肺通气,利用动态肺顺应性设定的PEEP值通气能够得到更好的氧合及呼吸参数,并且维持较好.     

Optimal positive end-expiratory pressure during pumpless extracorporeal lung membrane support

The aim of this study was to determine the optimal positive end-expiratory pressure (PEEP) required during extracorporeal lung membrane support (interventional lung assist [iLA]; Novalung GmbH, Hechingen, Germany). Twenty healthy pigs were initially (4 h) mechanically ventilated with a tidal volume (V(T)) of 10 mL/Kg, respiratory rate (RR) of 20 breaths/min, PEEP of 5 cm H(2)O, and fraction of inspired O(2) (FiO(2)) of 1.0. Thereafter, the iLAs were placed arteriovenously transfemorally and settings reduced to reach near static ventilation (V(T) < or = 2 mL/Kg, RR 4 breaths/min, PEEP of 5, FiO(2) 1.0). Then, animals were assigned to four study groups evaluating 5 cm H(2)O increasing levels of PEEP for 8 h. Gas exchanges with PEEP < or = 10 cm H(2)O were significantly worse than those with PEEP > 12 cm H(2)O, and this without hemodynamical imbalance. This study suggests that the iLA may provide adequate gas exchange during static ventilation only with PEEP levels > 10 cm H(2)O, and this without pulmonary or systemic hemodynamic imbalance.     

根据静态压力-容量曲线指导开胸手术病人保护性单肺通气的效果

目的 评价根据静态压力.容积曲线(P-V曲线)设置开胸手术病人的呼气末正压(PEEP)行单肺通气(OLV)的效果.方法 择期行肺叶切除术病人120例,性别不限,年龄20～60岁,体重40～ 80 kg,ASA分级Ⅱ或Ⅲ级.双肺通气(TLV)3 min后,描绘准静态P-V曲线,确定P-V曲线低位拐点对应的压力(PLIP).采用随机数字表法,将病人随机分为5组(n＝24):对照组(C组)和不同保护性OLV方式组(P1～4组).C组PEEP为0,vT为10 ml/kg;P1组PEEP为0,vT为6ml/kg; P2组PEEP为PLIP,-2 cm H2O,VT为6ml/kg;P3组PEEP为PLIP,VT为6 ml/kg;P4组PEEP为PLIP+2 cmH2O,VT为6 ml/kg.分别于TLV和OLV呼吸力学指标平稳后,记录气道峰压、气道平台压、气道阻力和肺顺应性.分别于麻醉诱导前、TLV 20 min和OLV 20 min时,取动脉血样,进行血气分析,计算肺内分流率.分别于OLV开始时和OLV结束时采集动脉血样,采用酶联免疫吸附法测定血浆II-6和TNF-α的浓度.结果 与C组比较,P4组TLV和OLV呼吸力学指标平稳后气道峰压和气道平台压升高,气道阻力降低,OLV结束时血浆IL-6浓度降低,P1组、P2组、P3组和P4组PaC02升高(P<0.05或0.01);P1组、P2组和P3组各呼吸力学指标、血气分析指标和血浆IL-6和TNF-α的浓度比较差异无统计学意义(P＞0.05).与P1组、P2组和P3组比较,P4组气道峰压和气道平台压升高,OLV结束时血浆IL-6浓度降低(P<0.05或0.01).结论 VT为6 ml/kg,根据PLIP+2 cm H2O确定PEEP,有助于改善开胸手术病人的氧合,抑制炎性反应,是保护性OLV的有效手段.     

Surfactant impairment after mechanical ventilation with large alveolar surface area changes and effects of positive end-expiratory pressure

We have assessed the effects of overinflation on surfactant function and composition in rats undergoing ventilation for 20 min with 100% oxygen at a peak inspiratory pressure of 45 cm H2O, with or without PEEP 10 cm H2O (groups 45/10 and 45/0, respectively). Mean tidal volumes were 48.4 (SEM 0.3) ml kg-1 in group 45/0 and 18.3 (0.1) ml kg- 1 in group 45/10. Arterial oxygenation in group 45/0 was reduced after 20 min compared with group 45/10 (305 (71) vs 564 (10) mm Hg); maximal compliance of the P-V curve was decreased (2.09 (0.13) vs 4.16 (0.35) ml cm H2O-1 kg-1); total lung volume at a transpulmonary pressure of 5 cm H2O was reduced (6.5 (1.0) vs 18.8 (1.4) ml kg-1) and the Gruenwald index was less (0.22 (0.02) vs 0.40 (0.05)). Bronchoalveolar lavage fluid from the group of animals who underwent ventilation without PEEP had a greater protein concentration (2.18 (0.11) vs 0.76 (0.22) mg ml- 1) and a greater minimal surface tension (37.2 (6.3) vs 24.5 (2.8) mN m- 1) than in those who underwent ventilation with PEEP. Group 45/0 had an increase in non-active to active total phosphorus compared with nonventilated controls (0.90 (0.16) vs 0.30 (0.07)). We conclude that ventilation in healthy rats with peak inspiratory pressures of 45 cm H2O without PEEP for 20 min caused severe impairment of pulmonary surfactant composition and function which can be prevented by the use of PEEP 10 cm H2O.      

Mechanical ventilation with positive end-expiratory pressure preserves arterial oxygenation during prolonged pneumoperitoneum

BACKGROUND: Laparoscopic surgery usually requires a pneumoperitoneum by insufflating the abdominal cavity with carbon dioxide (CO2). Increased intraabdominal pressure causes diaphragmatic displacement resulting in compressed lung areas, which leads to formation of atelectasis, especially during mechanical ventilation. Application of positive end-expiratory pressure (PEEP) can maintain pulmonary gas exchange. The objective of this study was to investigate the effect of abdominal gas insufflation on arterial oxygenation during mechanical ventilation with and without PEEP in rats. METHODS: In experiment 1, two groups of six rats were continuously insufflated with CO2 at 12 mmHg for 180 min. Group 1 was ventilated with 8 cm H2O PEEP and group 2 had 0 cm H2O PEEP. Group 3 served as a control. This group had abdominal wall lifting and was ventilated with 0 cmH2O PEEP. In experiment 2, two groups of six rats had abdominal CO2 insufflation and were ventilated with or without PEEP during 180 min (group 4 and 5). In this experiment, abdomens were desufflated in both groups for 5 min at 60 and 120 min. Blood pressure monitoring and measurement of arterial pO2 was performed by placement of an indwelling carotid artery catheter in both experiments. RESULTS: In both experiments, paO2 values decreased significantly in insufflation groups that were ventilated with 0 cmH2O PEEP (groups 2 and 5). Insufflation groups ventilated with 8 cmH2O PEEP had paO2 values comparable to these of control group. There were no significant differences in mean arterial pressure between insufflation groups ventilated with or without PEEP. CONCLUSION: PEEP preserves arterial oxygenation during prolonged pneumoperitoneum in rats with minimal adverse hemodynamic effects.     

Effect of mechanical ventilation on cytokine response to intratracheal lipopolysaccharide

BACKGROUND: Mechanical ventilation may cause lung injury through the excitation of an inflammatory response and the release of mediators, such as cytokines. The authors tested the hypothesis that intratracheal lipopolysaccharide amplifies the cytokine response to mechanical ventilation. METHODS: Rat lungs were intratracheally instilled with lipopolysaccharide followed by ex vivo mechanical ventilation for 2 h with low tidal volume of 7 ml/kg with 3 cm H2O positive end-expiratory pressure (PEEP), high tidal volume of 40 ml/kg with zero PEEP, medium tidal volume of 15 ml/kg with 3 cm H2O PEEP, or medium tidal volume and zero PEEP. RESULTS: In the absence of lipopolysaccharide, lung lavage concentrations of tumor necrosis factor and interleukin 1 beta but not macrophage inflammatory protein 2 were significantly higher in lungs ventilated at high tidal volume/zero PEEP than at low tidal volume. There was a marked increase in lavage tumor necrosis factor and macrophage inflammatory protein 2 concentrations in lungs ventilated at low tidal volume after exposure to intratracheal lipopolysaccharide at doses of 100 ng/ml or greater. However, in lungs ventilated at high tidal volume, this response to lipopolysaccharide was markedly reduced. In addition, the number of alveolar macrophages recovered in the lavage was significantly lower in lungs ventilated at high tidal volume. CONCLUSION: Ventilation strategy can modify lung cytokine responses to lipopolysaccharide, likely through an effect on the alveolar macrophage population.     

Effect of Mechanical Ventilation on Cytokine Response to Intratracheal Lipopolysaccharide

Background: Mechanical ventilation may cause lung injury through the excitation of an inflammatory response and the release of mediators, such as cytokines. The authors tested the hypothesis that intratracheal lipopolysaccharide amplifies the cytokine response to mechanical ventilation.

Methods: Rat lungs were intratracheally instilled with lipopolysaccharide followed by ex vivo mechanical ventilation for 2 h with low tidal volume of 7 ml/kg with 3 cm H2O positive end-expiratory pressure (PEEP), high tidal volume of 40 ml/kg with zero PEEP, medium tidal volume of 15 ml/kg with 3 cm H2O PEEP, or medium tidal volume and zero PEEP.

Results: In the absence of lipopolysaccharide, lung lavage concentrations of tumor necrosis factor and interleukin 1[beta] but not macrophage inflammatory protein 2 were significantly higher in lungs ventilated at high tidal volume/zero PEEP than at low tidal volume. There was a marked increase in lavage tumor necrosis factor and macrophage inflammatory protein 2 concentrations in lungs ventilated at low tidal volume after exposure to intratracheal lipopolysaccharide at doses of 100 ng/ml or greater. However, in lungs ventilated at high tidal volume, this response to lipopolysaccharide was markedly reduced. In addition, the number of alveolar macrophages recovered in the lavage was significantly lower in lungs ventilated at high tidal volume.     

Different Ventilation Strategies Affect Lung Function but Do Not Increase Tumor Necrosis Factor-α and Prostacyclin Production in Lavaged Rat Lungs In Vivo

Background: Using an in vivo animal model of surfactant deficiency, the authors compared the effect of different ventilation strategies on oxygenation and inflammatory mediator release from the lung parenchyma.

Methods: In adult rats that were mechanically ventilated with 100% oxygen, acute lung injury was induced by repeated lung lavage to obtain an arterial oxygen partial pressure < 85 mmHg (peak pressure/positive end-expiratory pressure [PEEP] = 26/6 cm H2O). Animals were then randomly assigned to receive either exogenous surfactant therapy, partial liquid ventilation, ventilation with high PEEP (16 cm H2O), ventilation with low PEEP (8 cm H2O), or ventilation with an increase in peak inspiratory pressure (to 32 cm H2O; PEEP = 6 cm H2O). Two groups of healthy nonlavaged rats were ventilated at a peak pressure/PEEP of 32/6 and 32/0 cm H2O, respectively. Blood gases were measured. Prostacyclin (PGI2) and tumor necrosis factor-[alpha] (TNF-[alpha]) concentrations in serum and bronchoalveolar lavage fluid (BALF) as well as protein concentration in BALF were determined after 90 and 240 min and compared with mechanically ventilated and spontaneously breathing controls.

Results: Surfactant, partial liquid ventilation, and high PEEP improved oxygenation and reduced BALF protein levels. Ventilation with high PEEP at high mean airway pressure levels increased BALF PGI2 levels, whereas there was no difference in BALF TNF-[alpha] levels between groups. Serum PGI2 and TNF-[alpha] levels did not increase as a result of mechanical ventilation when compared with those of spontaneously breathing controls.     

Partial liquid ventilation with perfluorocarbons for treatment of ARDS in burns

Pulmonary failure remains the major determinant of mortality and morbidity following burn injury. We hypothesized that intratracheal instillation of perfluorocarbon liquids could be a therapeutic measure in combination with conventional mechanical ventilation to improve pulmonary gas exchange in acute respiratory distress syndrome with thermal injury. Forty-five New Zealand rabbits were used for this prospective and randomized experimental study. The animals were burned by scald to reach full-thickness 40% burn surface area. After inducing respiratory distress by repeated lung lavage with saline, animals were divided randomly into three groups of 15 rabbits each. First group (control group) received conventional treatment (continuous positive-pressure ventilation) using a FiO(2) of 1.0, tidal volume of 12 ml/kg, respiratory frequency of 30 cycles/min and PEEP of 6 cm H(2)O. Second group was treated with 9 ml/kg of intratracheal perfluorocarbon. Third group was treated with 15 ml/kg of intratracheal perfluorocarbon. All groups were ventilated for 6 h. In the perfluorocarbon groups, PaO(2) increased significantly (P<0.05) from 46+/-4 to 439+/-10 mmHg compared to the control group in a dose-related manner. In pulmonary parameters we observed significant (P<0.05) decrease in mean airway pressures from the pre-treatment value of 11.44+/-0.15 cm H(2)O to the post treatment 10.22+/-0.12 cm H(2)O and increase (P<0.05) in respiratory system compliance from 1.8+/-0.02 to 2.46+/-0.07 ml/cm H(2)O with the perfluorocarbon. Perfluorocarbon instillation did not result in statistically significant changes in arterial pressure, heart rate and central venous pressure. In conclusion, partial liquid ventilation with perfluorocarbon is a new technique leading to a marked and sustained improvement in oxygenation and pulmonary function in an experimental model of ARDS in burns.     

Comparison of exogenous surfactant therapy, mechanical ventilation with high end-expiratory pressure and partial liquid ventilation in a model of acute lung injury

We have compared three treatment strategies, that aim to prevent repetitive alveolar collapse, for their effect on gas exchange, lung mechanics, lung injury, protein transfer into the alveoli and surfactant system, in a model of acute lung injury. In adult rats, the lungs were ventilated mechanically with 100% oxygen and a PEEP of 6 cm H2O, and acute lung injury was induced by repeated lung lavage to obtain a PaO2 value < 13 kPa. Animals were then allocated randomly (n = 12 in each group) to receive exogenous surfactant therapy, ventilation with high PEEP (18 cm H2O), partial liquid ventilation or ventilation with low PEEP (8 cm H2O) (ventilated controls). Blood-gas values were measured hourly. At the end of the 4-h study, in six animals per group, pressure-volume curves were constructed and bronchoalveolar lavage (BAL) was performed, whereas in the remaining animals lung injury was assessed. In the ventilated control group, arterial oxygenation did not improve and protein concentration of BAL and conversion of active to non-active surfactant components increased significantly. In the three treatment groups, PaO2 increased rapidly to > 50 kPa and remained stable over the next 4 h. The protein concentration of BAL fluid increased significantly only in the partial liquid ventilation group. Conversion of active to non-active surfactant components increased significantly in the partial liquid ventilation group and in the group ventilated with high PEEP. In the surfactant group and partial liquid ventilation groups, less lung injury was found compared with the ventilated control group and the group ventilated with high PEEP. We conclude that although all three strategies improved PaO2 to > 50 kPa, the impact on protein transfer into the alveoli, surfactant system and lung injury differed markedly.      

Different ventilation strategies affect lung function but do not increase tumor necrosis factor-alpha and prostacyclin production in lavaged rat lungs in vivo

BACKGROUND: Using an in vivo animal model of surfactant deficiency, the authors compared the effect of different ventilation strategies on oxygenation and inflammatory mediator release from the lung parenchyma. METHODS: In adult rats that were mechanically ventilated with 100% oxygen, acute lung injury was induced by repeated lung lavage to obtain an arterial oxygen partial pressure < 85 mmHg (peak pressure/positive end-expiratory pressure [PEEP] = 26/6 cm H2O). Animals were then randomly assigned to receive either exogenous surfactant therapy, partial liquid ventilation, ventilation with high PEEP (16 cm H2O), ventilation with low PEEP (8 cm H2O), or ventilation with an increase in peak inspiratory pressure (to 32 cm H2O; PEEP = 6 cm H2O). Two groups of healthy nonlavaged rats were ventilated at a peak pressure/PEEP of 32/6 and 32/0 cm H2O, respectively. Blood gases were measured. Prostacyclin (PGI2) and tumor necrosis factor-alpha (TNF-alpha) concentrations in serum and bronchoalveolar lavage fluid (BALF) as well as protein concentration in BALF were determined after 90 and 240 min and compared with mechanically ventilated and spontaneously breathing controls. RESULTS: Surfactant, partial liquid ventilation, and high PEEP improved oxygenation and reduced BALF protein levels. Ventilation with high PEEP at high mean airway pressure levels increased BALF PGI2 levels, whereas there was no difference in BALF TNF-alpha levels between groups. Serum PGI2 and TNF-alpha levels did not increase as a result of mechanical ventilation when compared with those of spontaneously breathing controls. CONCLUSIONS: Although alveolar protein concentration and oxygenation markedly differed with different ventilation strategies in this model of acute lung injury, there were no indications of ventilation-induced systemic PGI2 and TNF-alpha release, nor of pulmonary TNF-alpha release. Mechanical ventilation at high mean airway pressure levels increased PGI2 levels in the bronchoalveolar lavage-accessible space.     

Adaptive Lung Ventilation (ALV) Evaluierung eines neuen closed loop-gesteuerten Beatmungsalgorithmus bei Eingriffen in überstreckter Seitenlage

The lateral decubitus position is the standard position for nephrectomies. There is a lack of data about the effects of this extreme position upon respiratory mechanics and gas exchange. In 20 patients undergoing surgery in the nephrectomy position, we compared a new closed-loop-controlled ventilation algorithm, adaptive lung ventilation (ALV), which adapts the breathing pattern automatically, to the respiratory mechanics with conventionally controlled mandatory ventilation (CMV). The aims of our study were (1) to describe positioning effects on respiratory mechanics and gas exchange, (2) to compary ventilatory parameters selected by the ALV controller with traditional settings of CMV, and (3) to assess the individual adaptation of the ventilatory parameters by the ALV controller. The respirator used was a modified Amadeus ventilator, which is controlled by an external computer and possesses an integrated lung function analyzer. In a first set of measurements, we compared parameters of respiratory mechanics and gas exchange in the horizontal supine position and 20 min after changing to the nephrectomy position. In a second set of measurements, patients were ventilated with ALV and CMV using a randomized crossover design. The CMV settings were a tidal volume of 10 ml/kg body weight, a respiratory rate of 10 breaths/min, an I:E ratio of 1:1.5, and an end-inspiratory pause of 30% of inspiratory time. With both ventilation modes F_iO₂ was set to 0.5 and PEEP to 3 cm H₂O. During ALV a desired alveolar ventilation of 70 ml/kg?KG·min was preset. All other ventilatory parameters were determined by the ALV controller according to the instantaneously measured respiratory parameters. Positioning induced a reduction of compliance from 61.6 to 47.9 ml/cm H₂O; the respiratory time constant shortened from 1.2 to 1.08 s, whereas physiological dead space increased from 158.9 to 207.5 ml. On average, the ventilatory parameters selected by the ALV controller resembled very closely those used with CMV. However, an adaptation to individual respiratory mechanics was clearly evident with ALV. In conclusion, we found that the effects of positioning for nephrectomy are minor and may give rise to problems only in patients with restrictive lung disease. The novel ALV controller automatically selects ventilatory parameters that are clinically sound and are better adapted to the respiratory mechanics of ventilated patients than the standardized settings of CMV are.     

Sodium Nitrite Mitigates Ventilator-induced Lung Injury in Rats

BACKGROUND:: Nitrite (NO2) is a physiologic source of nitric oxide and protects against ischemia-reperfusion injuries. We hypothesized that nitrite would be protective in a rat model of ventilator-induced lung injury and sought to determine if nitrite protection is mediated by enzymic catalytic reduction to nitric oxide. METHODS:: Rats were anesthetized and mechanically ventilated. Group 1 had low tidal volume ventilation (LVT) (6 ml/kg and 2 cm H2O positive end-expiratory pressure; n = 10); group 2 had high tidal volume ventilation (HVT) (2 h of 35 cm H2O inspiratory peak pressure and 0 cm H2O positive end-expiratory pressure; n = 14); groups 3-5: HVT with sodium nitrite (NaNO2) pretreatment (0.25, 2.5, 25 μmol/kg IV; n = 6-8); group 6: HVT + NaNO2 + nitric oxide scavenger 2-(4-carboxyphenyl)-4,5dihydro-4,4,5,5-tetramethyl-1H-imidazolyl-1-oxy-3oxide(n = 6); group 7: HVT + NaNO2 + nitric oxide synthase inhibitor N-nitro-L-arginine methyl ester (n = 7); and group 8: HVT + NaNO2 + xanthine oxidoreductase inhibitor allopurinol (n = 6). Injury assessment included physiologic measurements (gas exchange, lung compliance, lung edema formation, vascular perfusion pressures) with histologic and biochemical correlates of lung injury and protection. RESULTS:: Injurious ventilation caused statistically significant injury in untreated animals. NaNO2 pretreatment mitigated the gas exchange deterioration, lung edema formation, and histologic injury with maximal protection at 2.5 μmol/kg. Decreasing nitric oxide bioavailability by nitric oxide scavenging, nitric oxide synthase inhibition, or xanthine oxidoreductase inhibition abolished the protection by NaNO2. CONCLUSIONS:: Nitrite confers protection against ventilator-induced lung injury in rats. Catalytic reduction to nitric oxide and mitigation of ventilator-induced lung injury is dependent on both xanthine oxidoreductase and nitric oxide synthases.     

Lung protective ventilation. Ventilatory modes and ventilator parameters

Mechanical ventilation has a considerable potential for injuring the lung tissue. Therefore, attention has to be paid to the proper choice of ventilatory mode and settings to secure lung-protective ventilation whenever possible. Such ventilator strategy should account for low tidal volume ventilation (6 ml/kg PBW), limited plateau pressure (30 to 35 cm H2O) and positive end-expiratory pressure (PEEP). It is unclear whether pressure controlled or volume controlled ventilation with square flow profile is beneficial. The adjustment of inspiration and expiration time should consider the actual breathing mechanics and anticipate the generation of intrinsic PEEP. Ventilatory modes with the possibility of supporting spontaneous breathing should be used as soon as possible.     

Intraoperative changes in arterial oxygenation during volume-controlled mechanical ventilation in modestly obese patients undergoing laparotomies with general anesthesia

BACKGROUND: In obese patients, arterial oxygenation can be greatly impaired during general anesthesia. Both avoidance of denitrogenation and application of positive end-expiratory pressure (PEEP) during mechanical ventilation may be effective in preventing such impairment of arterial oxygenation. METHODS: We studied 28 obese/overweight and seven non-obese (BMI < 25 kg x m-2) patients who underwent laparotomies with general anesthesia (i.e. isoflurane with or without nitrous oxide). During anesthesia, their lungs were mechanically ventilated at a rate of 10 breaths x min-1 with a constant flow, inspiratory-to-expiratory ratio 1 : 2, and tidal volume approximately 10 ml x kg-1. The obese/overweight patients were allocated to four different groups in terms of denitrogenation and application of PEEP (7 cm H2O) during the ventilation (n = 7 each). In the non-obese patients, their denitrogenated lungs were ventilated without application of PEEP. Arterial gas analyses were performed before induction of anesthesia, and 30, 90, 150 and 210 min after tracheal intubation. The ratio of PaO2 to FiO2 was calculated as an index of arterial oxygenation. RESULTS: No significant changes in the PaO2/FiO2 ratio were observed throughout the study in the non-obese patients and in the obese/overweight patients whose non-denitrogenated lungs were ventilated with PEEP. In the obese/overweight patients whose lungs were ventilated after denitrogenation or without application of PEEP, significant decreases in the PaO2/FiO2 ratio were observed 30 and 90 min after tracheal intubation. CONCLUSIONS: In obese or overweight patients under general anesthesia, it may be advisable to avoid denitrogenation and apply PEEP during mechanical ventilation in order to minimize the impairment of arterial oxygenation.