Low tidal volume reduces epithelial and endothelial injury in acid-injured rat lungs.

Using a rat model of acid-induced lung injury, we tested the hypothesis that tidal volume reduction at the same level of PEEP (10 cm H(2)O) would diminish the degree of pulmonary edema by attenuating injury to the alveolar epithelial and endothelial barriers. Tidal volume reduction from 12 to 6 to 3 ml/kg significantly reduced the rate of lung water accumulation from 690 microl/h to 310 microl/h to 210 microl/h. Ventilation with either 6 or 3 ml/kg reduced endothelial injury equally as measured by plasma vWf:Ag and permeability to albumin. Plasma RTI40, a marker of type I epithelial cell injury, decreased 46% when tidal volume was reduced from 12 to 6 ml/kg and decreased an additional 33% with 3 ml/kg (p < 0.05). The rate of alveolar epithelial fluid clearance was significantly faster in the 3-ml/kg group (24 +/- 7%/h) compared with 6 ml/kg (15 +/- 11%/h) and 12 ml/kg (3 +/- 6%/h). We conclude that low tidal volume ventilation protects both the alveolar epithelium and the endothelium in this model of acute lung injury. The additional decrease in pulmonary edema with a tidal volume of 3 ml/kg is partly accounted for by greater protection of the alveolar epithelium.     

Ventilatory effects of nasal continuous positive airway pressure

Nasal continuous positive airway pressure (nCPAP) improved arterial oxygenation in patients with sleep apnoea as well as those with acute pulmonary processes such as Pneumocystis carinii pneumonia. Despite an expanding pool of clinical information, little if any attempt seems to have been made to see whether nCPAP alters ventilatory patterns. The effect of nCPAP was assessed by respiratory inductance plethysmography in 14 healthy males. nCPAP reduced respiratory rate (14.3 +/- 1.47 to 9.7 +/- 1.98, p less than 0.0001) but increased tidal volume (0.483 +/- 0.090 to 0.602 +/- 0.140 l, p = 0.01). Accordingly, minute ventilation decreased (6.91 +/- 1.20 to 5.64 +/- 0.93 l.min-1, p = 0.0002). Duty cycle (TI/TTOT) decreased from 0.43 +/- 0.04 to 0.35 +/- 0.05 s during nCPAP (p less than 0.0001). Mean inspiratory time and mean expiratory time increased with nCPAP (1.79 +/- 0.19 to 2.20 +/- 0.41 and 2.44 +/- 0.38 to 4.27 +/- 1.07 s, respectively, p less than 0.02), but there were no significant changes in mean inspiratory flow rate or partitioning of rib cage and abdominal/diaphragmatic contributions to tidal volume. We conclude that nCPAP effects ventilatory pattern in a manner similar to that described for expiratory threshold loading; that is, by decreasing respiratory frequency and minute ventilation. nCPAP does not appear to stimulate healthy subjects to increase their level of ventilation.     

容许性高碳酸血症对急性肺损伤动物心肺影响的观察

观察不同水平的容许性高碳酸血症对油酸型急性肺损伤模型的心肺功能影响。复制猪ＡＬＩ模型，四腔热稀释漂浮导管监测血液动力学不同潮气量致不同程度的ＰＨＣ。     

Cyclic changes in arterial pulse during respiratory support revisited by Doppler echocardiography

It has long been known that there are cyclic changes in arterial pressure during mechanical ventilation. They are caused by cyclic changes in both the right and left ventricular stroke output, occurring in opposite phases. As a result, arterial pulse pressure is increased during inspiration and decreased during expiration. A cyclic improvement in left ventricular systolic function could thus be expected during mechanical lung inflation. We tested this hypothesis in 31 septic patients who were mechanically ventilated in controlled mode by combining left ventricular measurements by transesophageal echocardiography with invasive arterial pressure recordings and Doppler analysis of pulmonary venous flow and right and left ventricular stroke volume. Lung inflation by tidal ventilation significantly improved left ventricular stroke volume (26 +/- 0.4 cm3/m2 [mean +/- SEM] vs. 22.3 +/- 0.4 cm3/m2 at end deflation). Beat-to-beat analysis of pulmonary venous flow velocity illustrated the boosting effect of lung inflation on pulmonary venous return. The beneficial effect of inspiration thus appeared directly related to a significant increase in left ventricular diastolic volume (60.3 +/- 1.5 cm3/m2 vs. 53.3 +/- 1.4 cm3/m2 at end-expiration) and to a lesser extent to an improved left ventricular ejection fraction. We concluded that the transient beneficial hemodynamic effect of tidal ventilation on the left ventricular pump is essentially mediated by an improved left ventricular filling.     

High inflation pressure pulmonary edema. Respective effects of high airway pressure, high tidal volume, and positive end-expiratory pressure

The respective roles of high pressure and high tidal volume to promote high airway pressure pulmonary edema are unclear. Positive end-expiratory pressure (PEEP) was shown to reduce lung water content in this type of edema, but its possible effects on cellular lesions were not documented. We compared the consequences of normal tidal volume ventilation in mechanically ventilated rats at a high airway pressure (HiP-LoV) with those of high tidal volume ventilation at a high (HiP-HiV) or low (LoP-HiV) airway pressure and the effects of PEEP (10 cm H2O) on both edema and lung ultrastructure. Pulmonary edema was assessed by extravascular lung water content and microvascular permeability by the drug lung weight and the distribution space of 125I-labeled albumin. HiP-LoV rat lungs were not different from those of controls (7 cm H2O peak pressure ventilation). By contrast, the lungs from the groups submitted to high volume ventilation had significant permeability type edema. This edema was more pronounced in LoP-HiV rats. It was markedly reduced by PEEP, which, in addition, preserved the normal ultrastructural aspect of the alveolar epithelium. This was in striking contrast to the diffuse alveolar damage usually encountered in this type of edema. To our knowledge, this constitutes the first example of a protective effect of PEEP during permeability edema.     

气道压力释放通气应用于急性肺损伤/急性呼吸窘迫综合征患者的研究

目的评价气道压力释放通气(airway pressure release ventilation,APRV)对急性肺损伤(acute lung injury,ALI)/急性呼吸窘迫综合征(acute respiratory distress syndrome,ARDS)患者的疗效,评估其对患者呼吸机相关性肺损伤(Ventilator-Induced Lung Injury,VILI)程度,并探讨可能的机制。方法采用前瞻性研究方法,入组患者随机分为APRV组、小潮气量肺保护通气组。描记肺准静态压力-容积曲线(pressure-volume curve,P-V曲线),并据此设置呼吸机参数,通气24h、48h观察效果。结果两组患者氧合明显改善,血流动力学指标无明显变化,APRV组Pmean明显高于SIMV+PEEP组,准静态P-V曲线三角区Pflex容积(Vdelta)增加明显,血清SP-D浓度呈升高趋势。结论 APRV应用于急性肺损伤/急性呼吸窘迫综合征患者,相对于小潮气量肺保护性通气策略,氧合改善、呼吸力学类似;较高的平均气道压,能更有效地肺复张,未对血流动力学产生影响,但加重了肺损伤,导致呼吸机相关性肺损伤。     

Continuous negative extrathoracic pressure ventilation, lung water volume, and central blood volume. Studies in dogs with pulmonary edema induced by oleic acid.

The effect of continuous positive-pressure ventilation (CPPV) on extravascular lung water volume has been investigated, but there is only one report which studied the effect of continuous negative extrathoracic pressure ventilation (CNETPV). The effect of CNETPV on central blood volume (CBV) has not been studied. Changes in intrathoracic pressure by CNETPV may alter lung water volume and CBV. In this study the effects of CNETPV on lung water volume and CBV were compared with those of intermittent positive-pressure ventilation (IPPV) and CPPV in dogs with pulmonary edema induced by oleic acid. Nine mongrel dogs were anesthetized and given oleic acid at 0.06 ml/kg intravenously to induce pulmonary edema; CNETPV was applied with a cuirass and a negative thoracic pressure ventilator (Kimura OKT-100) for 1 h. Extravascular lung water volume (as extravascular thermal volume [EVTV]) and CBV were estimated with the double-indicator dilution method using thermal-sodium; PEEP and continuous negative extrathoracic pressure were matched to produce the same increments in FRC. The EVTV increased during CNETPV but did not change during CPPV. The CBV decreased during CPPV but did not change during CNETPV. An increase of transmural pulmonary microvascular pressure was thought to be one of the reasons for the increase in EVTV with CNETPV.     

小潮气量机械通气对海水淹溺急性肺损伤兔治疗作用的实验研究

目的 观察小潮气量机械通气在海水淹溺急性肺损伤应用时的治疗作用和安全性.方法 分别应用潮气量为6 ml/kg和12 ml/kg的机械通气对海水淹溺急性肺损伤兔进行分组救治.在不同时间点检测血气分析、呼吸动力学、血液动力学,观察血清和肺泡灌洗液肿瘤坏死因子a、白介素6以及肺HRCT变化,并进行肺病理学检查,以评价治疗效果和安全性.结果 采用6 ml/kg小潮气量机械通气不仅能改善SWD-ALI时的氧合,而且能有效控制气道峰压和气道平均压,从而在一定程度上避免呼吸机相关肺损伤.结论 小潮气量保护性机械通气策略应用治疗海水淹溺急性肺损伤兔,能够明显改善氧合,避免继发肺损伤,是一种安全有效的治疗海水淹溺急性肺损伤的机械通气手段.     

Dynamic determination of oxygenation and lung compliance in murine pneumonectomy

Thoracic surgical procedures in mice have been applied to a wide range of investigations, but little is known about the murine physiologic response to pulmonary surgery. Using continuous arterial oximetry monitoring and the FlexiVent murine ventilator, the authors investigated the effect of anesthesia and pneumonectomy on mouse oxygen saturation and lung mechanics. Sedation resulted in a dose-dependent decline of oxygen saturation that ranged from 55% to 82%. Oxygen saturation was restored by mechanical ventilation with increased rate and tidal volumes. In the mouse strain studied, optimal ventilatory rates were a rate of 200/minute and a tidal volume of 10 mL/kg. Sustained inflation pressures, referred to as a "recruitment maneuver," improved lung volumes, lung compliance, and arterial oxygenation. In contrast, positive end-expiratory pressure (PEEP) had a detrimental effect on oxygenation; an effect that was ameliorated after pneumonectomy. These results confirm that lung volumes in the mouse are dynamically determined and suggest a threshold level of mechanical ventilation to maintain perioperative oxygen saturation.     

beta-adrenergic stimulation restores rat lung ability to clear edema in ventilator-associated lung injury

Mechanical ventilation with high tidal volume (HVT) causes lung injury and decreases the lung's ability to clear edema in rats. beta-adrenergic agonists increase active Na(+) transport and lung edema clearance in normal rat lungs by stimulating apical Na(+) channels and basolateral Na,K-ATPase in alveolar epithelial cells. We studied whether beta-adrenergic agonists could restore lung edema clearance in rats ventilated with HVT (40 ml/kg, peak airway pressure of 35 cm H(2)O) for 40 min. The ability of rat lungs to clear edema decreased by approximately 50% after 40 min of HVT ventilation. Terbutaline (TERB) and isoproterenol (ISO) increased lung edema clearance in control nonventilated rats (from 0.50 +/- 0. 02 ml/h to 0.81 +/- 0.04 ml/h and 0.99 +/- 0.05 ml/h, respectively) and restored the lung's ability to clear edema in HVT ventilated rats (from 0.25 +/- 0.03 ml/h to 0.64 +/- 0.02 ml/h and 0.88 +/- 0. 09 ml/h, respectively). Disruption of cell microtubular transport system by colchicine inhibited the stimulatory effects of ISO in HVT ventilated rats, whereas beta-lumicolchicine did not affect beta-adrenergic stimulation. The Na,K-ATPase alpha(1)- and beta(1)-subunit mRNA steady state levels were not affected by incubation with ISO for 60 min in alveolar type II cells isolated from control and HVT ventilated rats. The data suggest that beta-adrenergic agonists increased alveolar fluid reabsorption in rats ventilated with HVT by promoting recruitment of ion-transporting proteins from intracellular pools to the plasma membrane of alveolar epithelial cells.     

Application of tracheal gas insufflation to acute unilateral lung injury in an experimental model

In unilateral lung injury, application of global positive end-expiratory pressure (PEEP) may cause overdistension of normal alveoli and redistribution of blood flow to diseased lung areas, thereby worsening oxygenation. We hypothesized that selective application of tracheal gas insufflation (TGI) will recruit the injured lung without causing overdistension of the normal lung. In eight anesthetized dogs, left lung saline lavage was performed until Pa(O(2))/FI(O(2)) fell below 100 mm Hg. Then, the dogs were reintubated with a Univent single lumen endotracheal tube that incorporates an internal catheter to provide TGI. After injury, increasing PEEP from 3 to 10 cm H(2)O did not change gas exchange, hemodynamics, or lung compliance. Selective TGI, while keeping end-expiratory lung volume (EELV) constant, improved Pa(O(2))/FI(O(2)) from 212 +/- 43 to 301 +/- 38 mm Hg (p < 0.01) while Pa(CO(2)) and airway pressures decreased (p < 0.01). During selective TGI, reducing tidal volume to 5.2 ml/kg while keeping EELV constant, normalized Pa(CO(2)), did not affect Pa(O(2))/FI(O(2)), and decreased end-inspiratory plateau pressure from 16.6 +/- 1.0 to 11.9 +/- 0.5 cm H(2)O (p < 0.01). In unilateral lung injury, we conclude that selective TGI (1) improves oxygenation at a lower pressure cost as compared with conventional mechanical ventilation, (2) allows reduction in tidal volume without a change in alveolar ventilation, and (3) may be a useful adjunct to limit ventilator-associated lung injury.     

Lung recruitment maneuvers in acute respiratory distress syndrome

In the experimental setting, repeated derecruitments of the lungs of ARDS models accentuate lung injury during mechanical ventilation, whereas open lung concept strategies can attenuate the injury. In the clinical setting, recruitment manuevers that use a continuous positive airway pressure of 40 cmH2O for 40 secs improve oxygenation in patients with early ARDS who do not have an impairment in the chest wall. High intermittent positive end-expiratory pressure (PEEP), intermitent sighs, or high-pressure controlled ventilation improves short-term oxygenation in ARDS patients. Both conventional and electrical impedance thoracictomography studies at the clinical setting indicate that high PEEP associated with low levels of pressure control ventilation recruit the collapsed portions of the ARDS lungs and that adequate PEEP levels are necessary to keep the ARDS lungs opened allowing a more homogenous ventilation. High PEEP/low tidal volume ventilation was seen to reduce inflammatory mediators in both bronchoalveolar lavage and plasma, compared to low PEEP/high tidal volume ventilation, after 36 hours of mechanical ventilation in ARDS patients. Recruitment maneuvers that used continuous positive airway pressure levels of 35-40 cmH2O for 40 secs, with PEEP set at 2 cmH2O above the lower inflection point of the pressure-volume curve, and tidal volume < 6 mL/kg were associated with a 28-day intensive care unit survival rate of 62%. This contrasted with a survival rate of only 29% with conventional ventilation (defined as the lowest PEEP for acceptable oxygenation without hemodynamic impairment with a tidal volume of 12 mL/kg), without recruitment manuevers (number needed to treat = 3; p < 0.001). In the near future, thoracic computed tomography associated with high-performance monitoring of regional ventilation may be used at the bedside to determine the optimal mechanical ventilation of the ARDS keeping an opened lung with a homogenous ventilation.     

Sigh in acute respiratory distress syndrome

Mechanical ventilation with plateau pressure lower than 35 cm H2O and high positive end-expiratory pressure (PEEP) has been recommended as lung protective strategy. Ten patients with ARDS (five from pulmonary [p] and five from extrapulmonary [exp] origin), underwent 2 h of lung protective strategy, 1 h of lung protective strategy with three consecutive sighs/min at 45 cm H2O plateau pressure, and 1 h of lung protective strategy. Total minute ventilation, PEEP (14.0 +/- 2.2 cm H2O), inspiratory oxygen fraction, and mean airway pressure were kept constant. After 1 h of sigh we found that: (1) PaO2 increased (from 92.8 +/- 18.6 to 137.6 +/- 23.9 mm Hg, p < 0.01), venous admixture and PaCO2 decreased (from 38 +/- 12 to 28 +/- 14%, p < 0.01; and from 52.7 +/- 19.4 to 49.1 +/- 18.4 mm Hg, p < 0.05, respectively); (2) end-expiratory lung volume increased (from 1.49 +/- 0.58 to 1.91 +/- 0.67 L, p < 0.01), and was significantly correlated with the oxygenation (r = 0.82, p < 0.01) and lung elastance (r = 0.76, p < 0.01) improvement. Sigh was more effective in ARDSexp than in ARDSp. After 1 h of sigh interruption, all the physiologic variables returned to baseline. The derecruitment was correlated with PaCO2 (r = 0.86, p < 0.01). We conclude that: (1) lung protective strategy alone at the PEEP level used in this study may not provide full lung recruitment and best oxygenation; (2) application of sigh during lung protective strategy may improve recruitment and oxygenation.     

急性呼吸窘迫综合征家兔肺不同区域有效血流灌注变化及肺保护性通气对其的影响

目的 通过观察家兔急性呼吸窘迫综合征(ARDS)模型肺不同区域有效血流灌注变化及肺保护性通气对其的影响,探讨ARDS所致严重低氧血症的发生机制。方法 采用静脉注射油酸的方法建立家兔ARDS模型,应用PIM-Ⅱ激光多普勒血流灌注扫描仪观察不同肺通气模式[(大潮气、小潮气 外源性呼气末正压(PEEP)、大潮气 俯卧位、俯卧位 小潮气 PEEP]下肺不同区域(肺上区、肺下区腹侧和肺下区背侧)局部有效血流灌注及动脉血气指标的变化。结果 家兔静脉注射油酸后,(1)肺不同区域氧合指数明显下降,应用肺保护性通气(小潮气 PEEP,俯卧位 小潮气 PEEP)后氧合指数明显改善;(2)肺不同区域局部有效血流灌注均有不同程度的下降,以肺下区背侧最为明显,肺下区腹侧次之,肺上区变化最小,应用肺保护性通气后,小潮气 PEEP对改善肺下区背侧胸膜下肺局部有效血流灌注的效果不如俯卧位 小潮气 PEEP。结论小潮气 PEEP、俯卧位 小潮气 PEEP均可良好改善肺局部有效血流灌注,其中俯卧位 小潮气 PEEP效果尤为明显;右-左分流导致的肺内分流可能是ARDS发生严重进行性低氧血症的主要原因之一。     

侧卧位和分侧肺通气对单侧急性肺损伤犬的影响

目的观察体位和分侧肺通气对单侧急性肺损伤(ALI)犬的影响,探讨单侧ALI时合理的机械通气方式。方法健康杂种犬28只,建立盐酸所致单侧ALI,行容量控制通气(VCV),分为常规通气组(A组)、常规通气+健侧卧位组(B组)、不同步分侧肺通气组(C组)、同步分侧肺通气组(D组)。通气240min后,每组随机选取4只犬行核素显像。监测氧合、血流动力学、呼吸力学和肺损伤指标。结果(1)通气30min后B、C、D组氧合指数(PaO2/FiO2)[(277±23)、(296±31)、(299±22)mmHg,1mmHg=0.133kPa]显著高于A组[(180±25)mmHg,P均<0.01],通气60min后C、D组PaO2/FiO2[(348±34)、(343±29)mmHg]显著高于B组[(314±33)mmHg,P均<0.05]。(2)通气120min后B组静态肺顺应性(Cst)[(23±4)ml/cmH2O]较A组[(19±2)ml/cmH2O]显著改善,通气60min后C、D组左侧Cst[(11±1)、(11±1)ml/cmH2O]均较ALI状态时显著改善[(7±2)、(6±1)ml/cmH2O,P均<0.01]。(3)B、C、D组损伤侧血流/总血流(Q损伤/Q总)[(31.3±4.6)%和(27.5±1.3)%、(27.3±2.8)%]与A组比较差异均有统计学意义[(38.3±2.2)%,P均<0.01]。结论健侧卧位和分侧肺通气均能明显改善单侧ALI犬的氧合和肺的顺应性,分侧肺通气改善氧合较健侧卧位更有效,改善氧合的机制可能与影响双侧血流分布有关。     

Mechanics and energetics of breathing in newly diagnosed infants with cystic fibrosis: effect of combined bronchodilator and chest physical therapy

Response to bronchodilator (BD) and chest physical therapy (CPT) was evaluated in newly diagnosed infants with cystic fibrosis (n = 13; age, 6.9 +/- 1.5 SE months) who were asymptomatic for lung disease at the time of the study. Lung function was assessed from the mechanics and energetics of breathing prior to and following combined BD and CPT. After therapy, respiratory rate, tidal volume, minute ventilation, and pulmonary compliance were not statistically different from values under baseline conditions. In contrast, there was a significant decrease in pulmonary resistance (-34%; P less than 0.05) and the resistive work of breathing (-26%; P less than 0.05) following the combined treatment. The effect of combined BD and CPT in decreasing the resistive respiratory load may be related to relief of subclinical bronchospasm, reduction in mucosal edema, and mobilization of mucous secretions.     

Effect of pentoxifylline on hemodynamics, alveolar fluid reabsorption, and pulmonary edema in a model of acute lung injury

We investigated the effect of pentoxifylline (PTX) on the development of pulmonary edema in a model of adult respiratory distress syndrome in rabbits. Lung injury was induced by repeated saline lavages in adult rabbits weighing 2.5 to 3.5 kg. Rabbits pretreated with PTX (20 mg/kg bolus followed by 20 mg/kg/h infusion) developed significantly lower amounts of lung edema 4 h after saline lavage (extravascular lung water to dry weight ratio [W/D], 6.9 +/- 0.6 SD versus 8.9 +/- 0.5 in control animals). PTX produced a 25% increase in cardiac output, but there were no differences between treated and untreated groups in calculated pulmonary vascular resistance or microvascular pressure. To determine whether PTX could have lowered pulmonary venous resistance and thus lowered effective microvascular pressure for fluid filtration, we directly measured pulmonary artery and left atrial pressures, and measured by micropuncture the pressure in 20 to 40 microns subpleural venules in four open-chested rabbits 3 to 4 h after lavage. Venous resistance was low (venous pressure drop 0.9 +/- 0.1 mm Hg) and was unchanged by PTX infusion. To determine if PTX decreased lung water by accelerating active alveolar fluid reabsorption, a single 60-ml aliquot of saline was instilled into the lungs of normal rabbits treated with saline or PTX. Both groups had a similar decrease in lung water content 1 and 4 h later. Our data indicate that PTX reduces edema formation in rabbits after saline lavage, not by lowering microvascular pressures for fluid filtration or by acceleration alveolar fluid reabsorption, but possibly by its anti-inflammatory effect on neutrophil function.     

Effects of High-Frequency Oscillatory Ventilation on Oleic Acid-Induced Lung Injury in Sheep

High-frequency oscillatory ventilation (HFOV) is a possible mechanical method for open lung strategies. The aim of this study was to examine whether HFOV has a beneficial effect on oleic acid-induced lung injury, with emphasis on changes in extravascular lung water. Thirteen anesthetized sheep prepared with a lung lymph fistula and vascular catheters for monitoring were randomly allocated to two experimental groups. In experiment 1, sheep (n = 6) were ventilated using conventional mechanical ventilation [CMV; 10 ml/kg of tidal volume, 70% oxygen, and positive end-expiratory pressure (PEEP) of 6 cmH(2)O after oleic acid administration (0.08 ml/kg)]. In experiment 2, sheep (n=7) were ventilated using HFOV (frequency=15 Hz, stroke volume=120 ml, mean airway pressure=15 cmH(2)O) after administration of the same dose of oleic acid as in experiment 1. Observation was continued for 4 h after oleic acid administration, then bronchoalveolar lavage (BAL) was performed and the lung wet-to-dry weight ratio was determined. Compared with CMV, HFOV significantly improved the deteriorated oxygenation during the late phase (2-4 h) of oleic acid-induced lung injury without any deterioration effects on pulmonary or systemic hemodynamics. HFOV showed significantly reduced lung lymph protein clearance, which paralleled significant decreases in wet-to-dry ratios and neutrophil counts in BAL fluid in the HFOV group. These findings suggest that HFOV could contribute to decreased lung lymph filtration in pulmonary microcirculation and improved oxygenation following oleic acid-induced lung injury in sheep.     

Pulmonary artery wedge pressure and extravascular lung water in patients with acute cardiogenic pulmonary edema requiring mechanical ventilation

This study describe the values of pulmonary artery wedge pressure (PAWP) and the extravascular lung water (EVLW) index in patients with acute cardiogenic pulmonary edema who require mechanical ventilation. Ten consecutive patients with acute cardiogenic pulmonary edema who required mechanical ventilation were studied. Cardiac index was determined with thermodilution. Central venous pressure and PAWP were measured with a pulmonary artery catheter. EVLW index was determined with the thermal dye dilution technique, using a commercially available computer system. Measurements were made at regular preset intervals after the initiation of mechanical ventilation. PAWP was normal at baseline (11.6+/-0.9 mm Hg, range 8 to 17) and did not change. EVLW index was elevated at baseline (13.7+/-1.5 ml/ kg) and decreased to a normal value after 24 hours (8.6+/-1.2 ml/kg, p = 0.02). Concomitantly cardiac index increased from 2.61+/-0.24 to 3.61+/-0.14 L/min/m2 (p = 0.05). There was no correlation between PAWP and EVLW index. Fluid balance was +1,221+/-908 ml after 24 hours and there was a weight gain of 0.88+/-1.06 kg after 24 hours. Thus, patients with acute cardiogenic pulmonary edema requiring mechanical ventilation may have a normal PAWP after mechanical ventilation has been initiated. In a hemodynamic unstable situation, these patients may require fluid challenges to improve cardiac output, despite the presence of pulmonary edema. The pulmonary edema, measured as EVLW index, resolves rapidly when cardiac performance improves, despite positive fluid balances and weight gain in the first 24 hours.     

肺复张手法联合双水平正压通气与小潮气量机械通气治疗急性呼吸窘迫综合征

目的观察肺复张手法联合双水平正压通气对急性呼吸窘迫综合征（ARDS）患者的治疗作用，并与小潮气量辅助／控制通气方式进行比较，以寻找更合理的机械通气方式。方法28例ARDS患者，男15例，女13例，平均年龄（37±9）岁。符合中华医学会呼吸病学分会制定的ARDS诊断标准。分为两组：（1）试验组14例：采用肺复张手法联合双水平正压机械通气；（2）对照组14例：采用美国ARDS协会推荐的小潮气量辅助／控制通气（潮气量设为6ml／kg，体重为标准体重）。分别观察两组患者上机后0、48和72h的氧合指数、肺顺应性（ml／cm H2O）、中心静脉压、镇静药物的用量以及28d的病死率和并发症等。结果试验组与对照组比较，氧合指数48h分别为（298±16）及（212±12）cm H2O（1cm H2O=0．098kPa），72h为（309±16）及（246±17）cm H2O；肺顺应性48h分别为（38．4±2．2）及（29．5±1．3）ml／cm H2O，72h为（42．0±1．3）及（29．0±1．0）ml／cm H2O；带机时间缩短为（14±3）及（19±3）d；试验组和对照组48h中心静脉压分别为（13．8±0．8）及（18．6±1．1）cm H2O，72h分别为（11．6±0．7）及（16．8±1．0）cm H2O。试验组仅在上机时应用少量镇静剂，而对照组则连续应用至通气方式转为自主通气方式。28d病死率和并发症的发生率两组比较差异无统计学意义（U=0．38，P〉0．05）。结论肺复张手法联合双水平正压通气方式比单纯小潮气量容量控制／辅助通气具有改善氧合迅速、肺顺应性增加明显、带机时间短、血液动力学稳定及所用镇静药物少等优点。