超声评估血管外肺水

血管外肺水(EVLW)是评估肺水肿的重要指标,与死亡率独立相关,积极治疗可改善患者预后.CT和MRI可准确评估肺水肿,但不适用于实时监测;而单次热稀释需要重复校准,易出错.由于空气的高声阻抗,传统上认为肺部不适于超声检查.超声B线是识别EVLW及观察其动态变化的灵敏方法,伴随研究的深入,超声越来越多地用于评估EVLW,...     

急性颅脑疾病患者血管外肺水指数的分布状况分析

目的 探讨急性颅脑疾病患者血管外肺水指数(EVLWI)的分布状况.方法 本研究回顾性调查了2009年1月至2014年12月共71例由于急性颅脑疾病而收住北京大学首钢医院ICU的病历资料,对所有研究对象于发病6 h内置入连续心输出量(PICCO)装置监测血流动力学指标.收集研究对象年龄、性别、急性生理和慢性健康Ⅱ(APA...     

血管外肺水的研究进展

血管外肺水（EVLW）是指肺血管腔以外的肺组织含水，包括肺间质含水、肺各种细胞含水以及肺泡腔内表面膜含水。狭义的EVLw仅指肺间质含水。EVLW是研究肺水肿的定量监测指标，可以早期、灵敏、直观地提供肺水肿发生发展及演变的病理过程，有助于指导治疗及预后评估，现将其研究综述如下。     

肺血管通透性指数对急性肺水肿的鉴别诊断价值探讨

目的探讨肺血管通透性指数鉴别诊断急性肺水肿中的价值。方法选取于2014年到我院治疗的急性肺水肿患者32例,经临床诊断而确诊,分为心源性肺水肿者(对照组)和非心源性肺水肿者(观察组),两组患者均给予相同的常规治疗、监测Pi CCO等,对比两组的PVPI均值、心脏指数、中心静脉压等血流动力学结果。结果观察组的PVPI均值高于对照组(P0.05);观察组的中心静脉压、体循环阻力指数明显低于对照组,而心脏指数明显高于对照组(P0.05)。结论 PVPI有助于重症患者肺水肿类型的鉴别,对于诊断与鉴别诊断急性肺水肿具有相当大的临床意义,具有可靠性,值得临床推广和广泛应用。     

脓毒性休克患者呼吸指数与血管外肺水指数的相关性

目的探讨脓毒性休克患者早期呼吸指数(RI)水平与血管外肺水指数(EVLWI)的相关性。方法选择入住ICU的脓毒性休克患者55例,根据预后分为死亡组20例和存活组35例,比较2组入院时和入院后第3、5天的RI、血管外肺水指数(ELWI)、肺血管通透性指数(PVPI)和心指数(CI)。结果与入院时比较,存活组患者第5天RI、EVLWI、PVPI水平明显下降(P0.05),而死亡组第5天RI、EVLWI、PVPI水平明显升高,CI明显下降(P0.05)。死亡组患者在入院第3、5天的RI、EVLWI、PVPI均显著高于同期的存活组患者(P0.05),CI则在入院第5天显著低于同期的存活组(P0.05)。2组患者RI与EVLWI呈显著正相关(r=0.526,P0.01)。结论脓毒性休克患者早期RI、EVLWI动态变化可预测患者的预后,并且RI与EVLWI具有显著相关性。     

血管外肺水含量指数对危重病患者预后的评价

目的:探讨用动脉轮廓曲线连续心排量(picco)技术测得的血管肺水含量指数对危重病患者预后的评估价值。方法:回顾性分析76例行picco检测的ICU患者临床资料,根据预后分为死亡组与存活组,分别记录0 h、24 h、72 h血流动力学参数,比较血管外肺水含量指数(EVLWI)在各时间点是否有差异。根据入ICU时EVLWI≤7.0,≥7.0,≥12.0,≥15.0分为四组,分别计算其死亡率。结果:0时死亡组的EVLWI明显高于存活组(P<0.05),24 h、72 h死亡组与存活组的EVWLI相比较无明显差异,P>0.05。入ICU时EVLWI≤7.0,>7.0,≥12.0,≥15.0的死亡率分别为21%,50%,69%,88%。结论:早期EVLWI可以作为危重病患者预后的评估指标之一,随EVLWI的升高患者的死亡率升高。     

急性呼吸窘迫综合征诊断新指标：血管外肺水和肺毛细血管通透性指数北大核心CSCD

1 ARDS诊断标准的历史演变 1967年Ashbaugh等[1]首先在Lancet杂志上报道了一组不同病因导致的以急性呼吸困难、顽固性低氧血症、双肺浸润性阴影、肺顺应性降低为特征的临床综合征.1994年欧美共识会议（Amercian-European Consensus Conference,AECC） 对急性呼吸窘迫综合征（acute respiratory sdistress syndrome,ARDS）的定义进行了规范和修订,提出了相应的诊断标准：①急性起病;②低氧血症,氧合指数（PaO2/FiO2）≤200 mmHg（1 mmHg =0.133 kPa）（不考虑呼吸末正压水平）;③正位X线胸片显示双肺浸润影;④肺毛细血管嵌压（PAWP）≤18mmHg或没有左心房压力增高的证据[2].     

血管外肺水指数在脓毒症相关性ALI/ARDS患者液体管理中的意义

目的 通过观察严重脓毒症/脓毒性休克患者血管外肺水指数(extravascular lung water index,EVLWI)与氧合指数(PaO2/FiO2)和胸腔内血容量指数(intrathoracic blood volume index,ITBVI)的相关性,探讨血管外肺水在脓毒症相关性急性肺损伤/急性呼吸窘迫综合征(ALI/ARDS)患者液体管理中的指导意义,为脓毒症相关性ALI/ARDS患者的液体管理提供新的临床策略.方法 选择2006年4月至2008年4月浙江大学医学院附属第二医院重症医学科符合严重脓毒症/脓毒性休克伴ALI/ARDS患者24例,应用PiCCO技术监测患者胸腔内血容量指数(ITBVI)和血管外肺水指数(EVLWI),用血气分析同时监测动脉血氧分压(PaO2),以PaO2/吸入氧浓度(FiO2)计算氧合指数.比较EVLWI与PaO2/FiO2和ITBVI与EVLWI之间的相关性.采用简单相关分析法进行统计学分析.结果 EVLWI与PaO2/FiO2呈明显负相关(r=-0.45,P＜0.01).进一步以EVLWI=14 mL/kg进行分层分析,当EVLWI≤14 mL/kg时,两者无明显相关性(r=0.12,P=0.243);当EVLWI＞14 mL/kg时,两者呈明显负相关(r=-0.47,P＜0.01).这可以提示对严重脓毒症/脓毒性休克伴ALI/ARDS患者,EVLW不是影响氧合的唯一因素,当EVLWI＞14 mL/kg时,可以通过降低EVLW来改善氧合,但更应综合考虑影响氧合指数的各种因素.ITBVI与EVLWI无明显相关性(r=0.02,P=0.84).进一步以ITBVI=1000 mL/m2进行分层分析,当ITBVI≤1000 mL/m2时,两者无明显相关性(r=0.13,P=0.17);当ITBVI＞1000 mL/m2时,两者呈明显正相关(r=0.40,P＜0.01).这提示我们对于脓毒症相关性ALI/ARDS,当ITBVI＞1000mL/m2时,可以通过降低ITBV来降低EVLW,但对于肺毛细血管通透性增高症引起的EVLW,不能通过降低ITBV来降低.结论 EVLW在脓毒症相关性ALI/ARDS的液体管理中具有重要指导意义.     

血管外肺水与肺血管通透性指数在急性呼吸窘迫综合征的研究进展

急性呼吸窘迫综合征（acute＆amp;respiratory＆amp;distress＆amp;syndrome,ARDS）是在严重感染、休克、创伤及烧伤等疾病的过程中,肺毛细血管内皮细胞和肺泡上皮细胞损伤,导致急性低氧性呼吸功能不全或衰竭。其病理生理特征为因肺泡膜通透性增加引起的渗出性肺水肿。 ARDS具有高患病率、高死亡率、临床预后差等特点,其死亡率高达35%～45%[1]。早期诊断ARDS非常困难,目前ARDS的临床诊断标准主要有1994年欧美联席会议标准[2]和2012年柏林定义[8],但两个标准中并没有一项直接体现ARDS病理生理过程中的肺水量化标准,这一缺陷可能会影响ARDS诊断的敏感性和特异性。随着脉搏指示剂连续心排血量监测（pulseC indicator＆amp;continous＆amp;output, PiCCO）技术的进步,用经肺热稀释法测得的血管外肺水指数（extravascularClungCwaterCindex,EVLWI）和肺血管通透性指数（pulmonaryCvascularCpermeabilityC index,PVPI）能较好地反映ARDS毛细血管通透性改变的特征性病理生理过程,对ARDS的早期诊断、早期干预及鉴别诊断等方面有重要意义。本次研究就血管外肺水（extravascularClungCwaterC,EVLW）和PVPI在ARDS的研究进展作一综述。     

大面积严重烧伤病人回吸收期血管外肺水指数变化与肺功能关系研究

[目的]观察大面积严重烧伤病人回吸收期血管外肺水指数(EVL-WI)的变化规律,探讨其与病人肺功能变化的关系。[方法]观察对象为我院收治入院的大面积严重烧伤的16例病人,于伤后第2个24h后期进行心肺容量监护仪(PiCCO)监测至伤后9d结束,监测指标包括EVLWI、肺血管通透性指数(PVPI)和氧合指数,同时观察病人肝、肾、心功能情况。[结果]休克期末(伤后2d)病人EV-LWI为6.71 mL/kg±1.07 mL/kg,均值处于正常上限,进入回吸收期后进一步升高,于伤后第5天达最高值7.75mL/kg±1.82mL/kg,至伤后第9天仍高于休克期末水平(EVLWI为6.92mL/kg±1.47mL/kg)。休克期末病人氧合指数为411.49mmHg±106.04 mmHg(1 mmHg=0.133kPa),均值处于正常下限,随后进行性下降,于伤后第5天达到最低值,为343.35mmHg±85.77mmHg,至伤后第9天仍低于休克期末水平为(368.51mmHg±64.13 mmHg);相关分析显示,病人EVLWI与氧合指数呈负相关(r=-0.16,P<0.05)。休克期末病人PVPI为1.60±0.28,随后下降,至伤后第7天达最低值1.29±0.25,与休克期末比较差异有统计学意义(P=0.006)。[结论]大面积严重烧伤病人血管外肺水在回吸收期进一步增高,可能是导致病人肺功能进行性下降的重要原因。     

Intravascular volume monitoring and extravascular lung water in septic patients with pulmonary edema

OBJECTIVE: To evaluate whether different indicators using for guiding volume expansion are valuable tools to assess edematous lung injury in patients with septic shock. DESIGN AND SETTING: Prospective observational clinical study in a university intensive care unit. PATIENTS: Sixteen consecutive mechanically ventilated patients developing septic shock with evidence of pulmonary edema on chest radiograph and severe hypoxemia (PaO(2)/FIO(2) <250 mmHg). MEASUREMENTS AND RESULTS: A pulmonary artery catheter was used for the measurement of cardiac index (CI), central venous pressure (CVP), and pulmonary artery occlusion pressure (PAOP). A fiberoptic catheter was placed in the descending aorta. Measurements of extravascular lung water index (EVLWI), intrathoracic blood volume index (ITBVI), and total end-diastolic volume index (TEDVI) were obtained using the thermal dye dilution technique. Measurements were taken just after placement of catheters and 24 h later. Fluid balance was also estimated within the first 24 h. TEDVI and ITBVI were significantly correlated with EVLWI, but not CVP and PAOP. Analysis of 24-h changes showed that the changes in TEDVI and in ITBVI reflected the change in EVLWI, whereas PAOP, CVP, and fluid balance did not. CONCLUSIONS: Volume variables (TEDVI, ITBVI) are more useful indicators than pressure variables (CVP, PAOP) for assessment of EVLWI in septic patients with pulmonary edema.     

血管外肺水和肺血管通透性的监测与临床应用

血管外肺水和肺血管通透性作为反映肺病理生理的指标，其测定的方法经不断的改进，从最初的离体动物实验到现在比较成熟的PICCO法。血管外肺水和胸腔内血容量比中心静脉压和肺小动脉楔压更能反映心脏前负荷的状况，血管外肺水和肺血管通透性可以反映肺损伤的程度，并对危重病患者的监测和治疗有较大的指导意义。随着PICCO技术的逐渐推广，今后两者在临床上的应用会更加广泛，在今后的研究上，如何降低血管外肺水和肺血管高通透性，减轻肺损伤，用何种方法或药物降是今后研究的方向。     

Extravascular lung water and the pulmonary vascular permeability index may improve the definition of ARDS

The recent Berlin definition has made some improvements in the older definition of acute respiratory distress syndrome (ARDS), although the concepts and components of the definition remained largely unchanged. In an effort to improve both predictive and face validity, the Berlin panel has examined a number of additional measures that may reflect increased pulmonary vascular permeability, including extravascular lung water. The panel concluded that although extravascular lung water has improved face validity and higher values are associated with mortality, it is infeasible to mandate on the basis of availability and the fact that it does not distinguish between hydrostatic and inflammatory pulmonary edema. However, the results of a multi-institutional study that appeared in the previous issue of Critical Care show that this latter reservation may not necessarily be true. By using extravascular lung water and the pulmonary vascular permeability index, both of which are derived from transpulmonary thermodilution, the authors could successfully differentiate between patients with ARDS and other patients in respiratory failure due to either cardiogenic edema or pleural effusion with atelectasis. This commentary discusses the merits and limitations of this study in view of the potential improvement that transpulmonary thermodilution may bring to the definition of ARDS.In the previous issue of Critical Care, Kushimoto and colleagues [1] reported on the clinical usefulness of transpulmonary thermodilution-derived extravascular lung water (EVLW) and the pulmonary vascular permeability index (PVPI) in the diagnosis of acute respiratory distress syndrome (ARDS). In an observational multi-institutional study, 266 mechanically ventilated patients with hypoxemic respiratory failure and bilateral infiltration on chest radiography were retrospectively allocated by three experts into three pathophysiological diagnostic categories: ARDS (including acute lung injury, or ALI), cardiogenic edema, and pleural effusion with atelectasis. As a first step in identifying true ARDS, a threshold value of EVLW of greater than 10 mL/kg (of predicted body weight) was used to exclude patients who had no pulmonary edema at all (the ''atelectasis and pleural effusion'' group). As a second step, the PVPI, which is the ratio of the EVLW to the pulmonary blood volume (PBV), was used to separate patients with true ARDS from those with cardiogenic edema, achieving a very high specificity in the overall diagnosis or exclusion of ARDS [1].The concept of the PVPI is based on the fact that although EVLW may be elevated in both permeability and cardiogenic edema, the latter will also be characterized by increased preload and, as a result, a lower PVPI ratio [2,3]. The PVPI was originally described in an experimental study as the ratio of the EVLW to the intrathoracic blood volume (ITBV) and was found to be significantly higher in permeability compared with hydrostatic pulmonary edema [4]. In a more recent clinical study, PVPI values were significantly higher in ALI/ARDS compared with hydrostatic pulmonary edema, and a PVPI value of at least 3 allowed the diagnosis of ALI/ARDS with high sensitivity and specificity [5]. This PVPI value is similar to the one found in the study by Kushimoto and colleagues [1] in a larger group of patients.However, the study by Kushimoto and colleagues [1] does have a number of limitations. The most disturbing one is that 14 patients, who were judged by the attending experts to have respiratory failure secondary to sepsis-induced increased pulmonary vascular permeability, were excluded from the study because ''their EVLW was less than 10 mL/kg due to hypovolemia'' [1]. This somewhat unclear exclusion is seemingly unjustified and, as the authors themselves readily admit, may have biased the results of the study. The authors claim that the experts were blinded to the PVPI but not to the EVLW and the ITBV. However, since the PBV is simply one fifth of the ITBV [2,3] and since the EVLW/ITBV ratio itself was originally used to calculate PVPI [4], one cannot exclude the possibility that the experts may have had some idea of the PVPI value during the exclusion and allocation processes. Other limitations of this study include the inclusion of mechanically ventilated patients only, the small size of the non-ARDS groups, the unclear pathophysiology of the atelectasis and pleural effusion group, and the absence of a calculated predictive validity of EVLW and PVPI regarding mortality.Despite its limitations, this study [1] presents an important addition to the mounting body of recent evidence showing that EVLW improves the diagnostic accuracy of lung injury and that it is a good predictor of mortality in ALI/ARDS [6-9]. Moreover, EVLW can predict progression to ALI more than 2 days before patients at increased risk for development of ALI meet American-European Consensus Conference (AECC) criteria, providing an early opportunity to initiate lung-protective ventilation and negative fluid balance [9]. The findings of these and other studies have already led to the suggestion that EVLW (>10 mL/kg) should be included in the definition of ARDS [9-11].The study of Kushimoto and colleagues [1] seems very relevant to the recent (''Berlin'') definition of ARDS [12,13], which was aimed at overcoming the limitations of the 1994 AECC definition [10,12-16]. The most important aspects of the new ''Berlin'' criteria include the introduction of three categories of ARDS (mild, moderate, severe), abandoning the term ''acute lung injury'' and removing the ''wedge pressure'' criterion [12-14]. Although these changes add a modicum of evidence and some simplification to the AECC definition, its concepts and components, including the reliance on the arterial partial pressure of oxygen/fraction of inspired oxygen (PaO₂/FiO₂) ratio as the major tool for identifying and stratifying patients with ARDS, remain practically unchanged. As a result, none of the key criteria of the new definition does directly reflect its conceptual model, namely that ''ARDS is a type of acute diffuse, inflammatory lung injury, leading to increased pulmonary vascular permeability, increased lung weight, and loss of aerated lung tissue'' [12]. Therefore, it is no wonder that neither the AECC nor the Berlin definition was found to be a particularly good predictor of death, with the Berlin definition offering only marginal improvement [12,14].The Berlin task force did indeed consider a number of additional measures to improve specificity and face validity for the increased pulmonary vascular permeability, including EVLW [12]. The panel concluded that although EVLW has improved face validity and higher values are associated with mortality, it is infeasible to mandate since (a) its technology is costly, invasive, and not widely available; (b) it has significant methodological limitations; and (c) it does not distinguish hydrostatic from inflammatory pulmonary edema [13]. This last reservation, at least, has now been refuted by Kushimoto and colleagues [1] and by others [5]. Previously, the AECC had used the pulmonary artery catheter (PAC) in the diagnosis of ARDS, even though it was (still is!) also invasive, costly, and not widely available and certainly had significant methodological limitations. Compared with the PAC, transpulmonary thermodilution is less invasive but provides better parameters for the diagnosis and management of ARDS. The technology has also become more available since it is not limited to one vendor anymore.The expanded rationale of the Berlin definition of ARDS [13] concludes by saying that the direct measurement of pulmonary vascular permeability or EVLW will be an important advance over current methods of assessing the presence and origin of lung edema and could be incorporated into the future definition of ARDS. The study of Kushimoto and colleagues [1] provides another justification for taking this step.     

The clinical usefulness of extravascular lung water and pulmonary vascular permeability index to diagnose and characterize pulmonary edema: a prospective multicenter study on the quantitative differential diagnostic definition for acute lung injury/acute respiratory distress syndrome

Introduction

Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is characterized by features other than increased pulmonary vascular permeability. Pulmonary vascular permeability combined with increased extravascular lung water content has been considered a quantitative diagnostic criterion of ALI/ARDS. This prospective, multi-institutional, observational study aimed to clarify the clinical pathophysiological features of ALI/ARDS and establish its quantitative diagnostic criteria.

Methods

The extravascular lung water index (EVLWI) and the pulmonary vascular permeability index (PVPI) were measured using the transpulmonary thermodilution method in 266 patients with PaO₂/FiO₂ ratio ≤ 300 mmHg and bilateral infiltration on chest radiography, in 23 ICUs of academic tertiary referral hospitals. Pulmonary edema was defined as EVLWI ≥ 10 ml/kg. Three experts retrospectively determined the pathophysiological features of respiratory insufficiency by considering the patients'' history, clinical presentation, chest computed tomography and radiography, echocardiography, EVLWI and brain natriuretic peptide level, and the time course of all preceding findings under systemic and respiratory therapy.

Results

Patients were divided into the following three categories on the basis of the pathophysiological diagnostic differentiation of respiratory insufficiency: ALI/ARDS, cardiogenic edema, and pleural effusion with atelectasis, which were noted in 207 patients, 26 patients, and 33 patients, respectively. EVLWI was greater in ALI/ARDS and cardiogenic edema patients than in patients with pleural effusion with atelectasis (18.5 ± 6.8, 14.4 ± 4.0, and 8.3 ± 2.1, respectively; P < 0.01). PVPI was higher in ALI/ARDS patients than in cardiogenic edema or pleural effusion with atelectasis patients (3.2 ± 1.4, 2.0 ± 0.8, and 1.6 ± 0.5; P < 0.01). In ALI/ARDS patients, EVLWI increased with increasing pulmonary vascular permeability (r = 0.729, P < 0.01) and was weakly correlated with intrathoracic blood volume (r = 0.236, P < 0.01). EVLWI was weakly correlated with the PaO₂/FiO₂ ratio in the ALI/ARDS and cardiogenic edema patients. A PVPI value of 2.6 to 2.85 provided a definitive diagnosis of ALI/ARDS (specificity, 0.90 to 0.95), and a value < 1.7 ruled out an ALI/ARDS diagnosis (specificity, 0.95).

Conclusion

PVPI may be a useful quantitative diagnostic tool for ARDS in patients with hypoxemic respiratory failure and radiographic infiltrates.

Trial registration

UMIN-CTR ID UMIN000003627     

Increased cardiac output increases lung water in canine permeability pulmonary edema

We investigated the effects of increased cardiac output (CO) on oleic acid pulmonary edema in 14 open-chest, anesthetized, mechanically ventilated dogs. Pulmonary artery wedge pressure (Pawp) was adjusted to approximately 9 mm Hg via a left atrial balloon and CO to 1.7 L · m⁻¹ via systemic arteriovenous fistulas (AVF); five minutes after oleic acid (0.08 mL · kg⁻¹), dogs were randomly divided into two groups, high CO and low CO. In the high CO group, CO was increased by opening the AVFs. Pawp was maintained at 9 mm Hg for four hours in all dogs. The average CO time in the high CO group was 3.9 L · min⁻¹ and 1.3 L · min⁻¹ in the low CO group (P < .01). Lung water accumulation was significantly increased in the high CO group with a wet weight/ body weight ratio of 29 g ò kg⁻¹v 21 g · kg ⁻¹ in the low CO group (P < .004). With time, mean pulmonary artery pressure increased significantly (P < .05) in both groups, but was not different between groups at any time. While pulmonary vascular resistance remained constant in the high CO group, it increased markedly (P < .05) in the low CO group, possibly due to a decrease in pulmonary vascular surface area. The increase in lung water accumulation in the high CO group is probably due to prevention of pulmonary vascular derecruitment and therefore a greater perfused pulmonary vascular surface area.     

Effects of furosemide versus isolated ultrafiltration on extravascular lung water in oleic acid-induced pulmonary edema

We studied the effects of no treatment, furosemide treatment, and isolated ultrafiltration on extravascular lung water (ETVL) in mongrel dogs in whom pulmonary edema was induced with oleic acid. In all treatment groups, ETVL was significantly elevated 90 min after oleic acid infusion. At 270 min, we found no difference between nontreatment and furosemide. There was, however, a significant difference between no treatment and ultrafiltration but not between furosemide and ultrafiltration. In spite of observations which suggest that ultrafiltration is of benefit in reducing ETVL, we could not demonstrate superiority of one therapy over another.     

Clinical measurement of extravascular lung water

The thermal-dye technique for the measurement of ELW is available for clinical and experimental use. This method is safe and can be performed serially in an individual patient. Although it is invasive, it requires only a central venous catheter and an arterial catheter, which are often already in place for routine hemodynamic monitoring and management. The procedure is accurate under a variety of conditions. Two obstacles argue against its routine application. First, the reliability of this approach appears to be seriously compromised when there are areas of edematous lung with poor blood perfusion. This includes aspiration and perhaps other forms of acute lung injury. Second, it remains to be demonstrated how useful routine measurements of ETVL, even if accurate, are in clinical management. However, regardless of the accuracy of the various methods for determination of ELW, the process of their development has significantly enhanced our knowledge of pulmonary edema formation and fluid distribution. We are at a transition point of soon being able to determine ELW easily. Techniques of reducing ELW can now be assessed directly in patients with pulmonary edema. As these therapies are developed and understood, the demand for the measurement of ELW will become a greater part of clinical medicine, and may stimulate further refinement of methods for quantitating lung water.     

Flow-dependance of extravascular thermal volume as an index of pulmonary edema

Using a double indicator (dye and heat) dilution technique of extravascular lung water measurement, we examined the effect of a reduction in cardiac output and positive pressures on the extravascular thermal volume (EVTV) in dogs. Following baseline EVTV measurements, cardiac output was lowered by inflation of balloons in the superior and inferior vena cavas, as well as by bleeding, and positive pressures were applied to the airways. There was good agreement between the baseline EVTV and post-mortem lung water; however, as the cardiac output was lowered there was a reduction in the measured EVTV. In other animals following application of positive airway pressure there was a decrease in the EVTV which appeared to be related to the reduction in cardiac output caused by positive airway pressure. At least in part, loss of thermal indicator appeared to explain the reduction in EVTV. Measurement of EVTV as an index of pulmonary edema may not be accurate in the face of a changing cardiac output.