Pulmonary edema is one of the most common complications and health burdens in critically ill patients [1,2]. Several recent reports have found that mortality reaches up to approximately 12% for cardiogenic  and 30%  for noncardiogenic pulmonary edema, the two major forms of this condition [1,2,4]. An increase in the pulmonary capillary hydrostatic pressure (usually paralleling an increase in blood volume in the pulmonary vessels) is the main determinant of cardiogenic (or hydrostatic) pulmonary edema. Typical causes include congestive heart failure due to left ventricular failure, fluid overload caused by inappropriate fluid infusion, and untreated renal failure. On the other hand, an increase in pulmonary capillary permeability (i.e., leaky lungs secondary to inflammatory mediators) is the hallmark of acute respiratory distress syndrome (ARDS), a representative type of noncardiogenic pulmonary edema [1,2,4].
A pair of human lungs contains about 700 million alveoli, with overall superficial area approximately 100 m2 (i.e., as large as half of a tennis court) . The alveoli consist of an epithelial layer, interstitium, and capillaries. The space outside the capillaries is known as the extravascular lung space. Correspondingly, the fluid in the alveoli and interstitium is called extravascular lung water (EVLW). Pulmonary edema, whether cardiogenic or noncardiogenic, is characterized by an increase in EVLW . Regardless of the cause, this EVLW accumulation impairs respiratory gas exchange, resulting in respiratory distress .
However, it is often difficult to evaluate pulmonary edema quantitatively in terms of severity and type of disease (cardiogenic versus increased permeability), especially in severely ill patients with multiple complications and extensive medical histories . In this article, we will review recent published papers and clarify why, how, and when EVLW measurements should be performed, especially in ARDS. In addition, we will suggest the quantitative diagnostic framework for evaluating pulmonary edema.
WHY IS THERE A NEED TO EVALUATE EXTRAVASCULAR LUNG WATER AND PULMONARY PERMEABILITY QUANTITATIVELY?
The existence and severity of pulmonary edema are generally evaluated based on physical examination, patient history, laboratory examination, and chest radiographic findings . However, the interpretation of these parameters, including chest X ray, is often affected by subjective factors that may cause interobserver error, even among experts [2,7,8▪▪,9▪▪]. Objective diagnosis of pulmonary edema can be made if EVLW is evaluated quantitatively at the bedside using the transpulmonary thermodilution (TPTD) technique [1,10] (Fig. 1).
Following the first description by Ashbaugh et al. in 1967 , the definition of ARDS was continuously reworked until the publication of the American-European Consensus Conference (AECC) definition in 1994 . The currently used Berlin definition was published in 2012, after minor revision from AECC definition . It has been shown to have only slightly better predictive validity for mortality than the AECC definition . Both the AECC and the Berlin definitions basically consist of four main components: (1) onset (acute), (2) chest radiography findings, (3) arterial blood gas results (PaO2/FiO2 ratio), and (4) absence of cardiogenic pulmonary edema [11,12].
Although the Berlin criteria are simple and widely used, significant criticisms of them have been published. First, accurate interpretation of chest radiography is required for the diagnosis. In a supplemental publication of the Berlin definition , expert panels (the ARDS Definition Task Force) presented typical examples of 12 chest radiographs, which were categorized into three groups: consistent with, inconsistent with, and equivocal for ARDS. However, the interpretation of chest radiography is often complicated and lacking in objectivity. Sjoding et al.[9▪▪] recently reported that clinicians showed only moderate interobserver agreement when diagnosing ARDS in patients with hypoxic respiratory failure according to the Berlin criteria. This result was driven primarily by the low reliability of the interpretation of chest images [9▪▪]. This conclusion was supported by a recent multicenter prospective study of interrater agreement, in which 286 intensivists independently reviewed the same 12 chest radiographs developed by the panels, before and after training. Radiographic diagnostic accuracy and interrater agreement were found to be poor when the Berlin radiographic definition was used and were not significantly improved by the training set of chest radiographs developed by the Task Force [8▪▪].
Second, although the severity of ARDS is determined by the PaO2/FiO2 ratio (i.e., mild, moderate, and severe ARDS for PaO2/FiO2 of 200–300, 100–200, and, < 100, respectively), this ratio depends strongly on FiO2, and the relationship between the numerator and denominator has been reported to be nonlinear . In addition, the level of positive end-expiratory pressure (PEEP) significantly impacts this ratio .
Third, the absence of cardiogenic pulmonary edema may not be an essential prerequisite for increased permeability pulmonary edema. Increased pulmonary permeability is the hallmark, but is not the only cause of accumulation of EVLW in ARDS. Patients with abnormal cardiac function may also have leaky lungs at the same time. For example, patients with a history of chronic cardiac disease and reduced cardiac function may develop abdominal sepsis due to bacterial peritonitis, and then increased lung permeability secondary to the generation of inflammatory mediators.
Finally, and most importantly, studies have shown only modest agreement between the pathologic findings for ARDS (primarily diffuse alveolar damage; DAD), and the AECC diagnostic criteria [16–19]. Even after the revision of the Berlin criteria, a recent autopsy study found that histopathologic findings of DAD were observed in only 45% of patients identified as having ARDS . This means that more than half of the patients were suffering from a wide range of respiratory failure symptoms without having DAD .
Therefore, there is also a need to evaluate pathophysiological hallmarks of the disease, pulmonary vascular permeability, for the diagnosis of the ARDS. Pulmonary vascular permeability index (PVPI) can be measured using the TPTD technique along with EVLW [1,21]. This information may help in assessing the severity of the disease and distinguishing the two types of pulmonary edema quantitatively, which may guide the selection of the correct therapeutic strategy .
HOW TO MEASURE EXCESS EXTRAVASCULAR LUNG WATER AND PULMONARY VASCULAR PERMEABILITY INDEX
The last 2 decades have witnessed the introduction and evolution of the TPTD technique for measuring EVLW and PVPI in a clinical setting. Currently, there are two similar commercially available TPTD systems, the PiCCO monitoring system [ProAQT platform or PiCCO2 monitoring (Pulsion/Getinge Medical Systems, Munich, Germany)]  and the EV1000 system (VolumeView, Edwards Lifesciences, Irvine, California, USA) . Both systems require a central venous catheter and a thermistor-tipped arterial catheter. After injection of 15 ml of cold isotonic saline into the central venous catheter, the arterial catheter detects thermodilutional changes, which allow for estimation of cardiac output, global end-diastolic volume (GEDV), global ejection fraction, EVLW, and PVPI (Fig. 1). The two devices (i.e., PiCCO or EV1000) measure almost the same sets of hemodynamic and pulmonary variables, including EVLW and PVPI. Although the details of the algorithms used by the proprietary software packages for the systems are not fully open to public, both work on generally the same principles. However, the PiCCO manufacturer frequently updates and revises their algorithm and software based on the results of published validation studies [23–25].
The accuracy of EVLW measurement by the PiCCO system was first validated against gold standard gravimetric measurement in animal models . Thermodilution measurement of EVLW values showed high accuracy in normal lungs, cardiogenic pulmonary edema, and ARDS models. In a human autopsy study, we observed a definite correlation between EVLW and postmortem lung weight from a wide range of normal and injured lungs . A recent study of brain-dead patients before organ transplantation suggested a close correlation between thermodilution EVLW and gravimetry EVLW .
Until recently, the reliability of the EVLW value among patients with impaired cardiac function and valvular disorders was only validated to a limited degree. Hilty et al.[28▪▪] evaluated patients undergoing elective left and right heart catheterization, along with left ventricular angiography. They found that TPTD measurement of blood flow was unaffected by differences in ventricular size and outflow obstruction.
WHEN TO EVALUATE EXTRAVASCULAR LUNG WATER AND PULMONARY VASCULAR PERMEABILITY INDEX
Several publications, and many experts in this field, recommend TPTD to evaluate EVLW and the PVPI during the treatment of critically ill patients . Accurate and objective diagnoses can be made for ARDS patients using EVLW and PVPI.
Several studies suggest that a normal EVLW value should be approximately 7 ml/kg and should not exceed 10 ml/kg (indexed by predicted body weight). Our clinical–pathological study showed mean EVLW values of approximately 7.3 ± 2.8 ml/kg to be the normal reference range for humans (n = 534) . This value was supported by Eichhorn et al., who published a meta-analysis of clinical studies (n = 687) in which they found a mean EVLW of 7.3 ml/kg (95% confidence interval, 6.8–7.6) in patients undergoing elective surgery, who were not supposed to have pulmonary edema. More recently, Wolf et al. obtained a similar result (8 ml/kg, interquartile range 7–9) in 101 elective brain tumor surgery patients.
In addition, Japanese nation-wide autopsy data (n = 1688) indicated that an EVLW more than 9.8 ml/kg represented the optimal discrimination threshold for a diagnosis of pulmonary edema from normal lungs, and an EVLW level of 14.6 ml/kg represents a 99% positive predictive value . The landmark study by Sakka et al. showed that the degree of initial EVLW on admission to the intensive care unit correlated with mortality, with a significant cut-off point of 14 ml/kg. The relationship between EVLW and prognosis was also clearly demonstrated in a systematic review of literature  and a recent large scales study .
The results of our multicenter study from Japan of 192 ARDS patients suggested that delta-EVLW (the decrease in EVLW during the first 48 h) was associated with 28-day survival in ARDS . Moreover, a recent retrospective study from China also found that the daily maximum values of EVLW in the 48 h after initial resuscitation were independent predictors of 28-day mortality in septic shock patients . With a cutoff value of 12.5 mL/kg, the daily maximum values of EVLW in septic shock patients after initial resuscitation were associated with a more positive fluid balance and increased mortality . Therefore, not only is the initial absolute value of EVLW useful for diagnosis of ARDS, but subsequent changes must also be taken into consideration in clinical practice .
Several experts have proposed that, based on the evidence, EVLW more than 10 ml/kg is a key criterion to include in a future definition of ARDS . According to pathological  and clinical  studies, EVLW values above 10 ml/kg represent higher than normal EVLW, and 15 ml/kg may be the key number to remember for severe pulmonary edema. By evaluating EVLW, we can (objectively at the bedside) accurately assess the initial severity of pulmonary edema as well as subsequent changes, thereby monitoring the ongoing therapeutic strategy.
We must always consider lung vascular permeability in addition to EVLW when we diagnose the cause of pulmonary edema, particularly with regard to fluid management. Giving fluids to a patient with high vascular permeability might result in very severe accumulation of EVLW . PVPI can be calculated from the relationship between EVLW and pulmonary blood volume. If the EVLW is elevated without increase in PVPI, the patient has cardiogenic pulmonary edema. On the other hand, an increase in EVLW along with an increase in PVPI means that the patient has increased permeability pulmonary edema.
Groeneveld and Verheij  demonstrated that lung vascular injury is associated with a rise in PVPI in mechanically ventilated patients with pneumonia or extrapulmonary sepsis-induced ARDS. Monnet et al. showed that PVPI allows differentiating hydrostatic pulmonary edema from increased permeability pulmonary edema, with a cut-off PVPI value of 3. A large-scale prospective multicenter study from Japan found almost the same results, in that a PVPI cut-off value between 2.6 and 2.85 provided a definitive diagnosis of ARDS (specificity, 0.90–0.95), and a value less than 1.7 ruled out an ARDS diagnosis (specificity, 0.95) . Among other recent studies that reported patients without increased permeability pulmonary edema, PVPI was reported to be less than 2  or 3 [28▪▪] in all of them. Taking all the evidence into account, PVPI less than approximately 2 may represent normal pulmonary permeability, and PVPI less than 3 indicates leaky lungs.
DIAGNOSTIC FRAMEWORK OF PULMONARY EDEMA
Synthesizing the results of the existing literature, we suggest the following diagnostic framework (Fig. 2). For diagnosing the existence of pulmonary edema, EVLW more than 10 ml/kg may be reasonable. EVLW more than 15 ml/kg indicates severe pulmonary edema. After quantitative diagnosis as pulmonary edema by EVLW more than 10 ml/kg, PVPI should be considered. PVPI less than 2 may represent normal pulmonary permeability, suggesting cardiogenic pulmonary edema. PVPI more than 3 (with EVLW > 10 ml/kg) represents increased permeability pulmonary edema, or ARDS. PVPI more than 3 and EVLW more than 15 suggest severe ARDS. Even if the initial EVLW and PVPI are high and indicate a high probability of mortality, if the values improve over time (especially during the first 48 h), a better outcome can be expected.
CLINICAL USE OF EXTRAVASCULAR LUNG WATER AND PULMONARY VASCULAR PERMEABILITY INDEX FOR EVALUATING ARDS AND OTHER DISEASES
There are many recent studies evaluating EVLW/PVPI in the field of ARDS research, from all over the world [44,45▪]. For example, a recent study evaluated potential treatments for ARDS, including recruitment maneuvers [45▪]. Currently, EVLW/PVPI evaluation is not restricted to patients with pulmonary edema, sepsis/septic shock, and pancreatitis, it is also expanding to other conditions, such as burns [46▪,47], lung surgery (endarterectomy [48▪] or lung transplant [50▪]), and postcardiac arrest syndrome . The clinical indications for measuring EVLW and PVPI may thus be expanding.
LIMITATIONS OF TRANSPULMONARY THERMODILUTION
TPTD has several limitations, mainly vascular obstruction and focal lung injury, which clinicians must bear in mind when interpreting the data. The amount of EVLW, the PaO2/FIO2 ratio, the tidal volume, and the PEEP level may affect the estimation of EVLW [21,52]. Although there has been a concern that the use of extracorporeal lung support may interfere with the accuracy and precision of the measurements, this support with a single-site jugular double-lumen cannula did not interfere with hemodynamic monitoring measurements using the TPTD method in ARDS patients . Other limitations are discussed elsewhere in detail [21,52].
EVLW and PVPI can be used to quantitatively establish the existence, evaluate the severity, and identify the nature of ARDS. EVLW-based criteria have been validated in several clinical and pathological studies: EVLW more than 10 ml/kg is a reasonable criterion for pulmonary edema, and EVLW more than 15 ml/kg for a high degree of severity. PVPI less than 2 may represent normal pulmonary permeability, and PVPI more than 3 suggests leaky lungs. These values of EVLW and PVPI have the potential to be included in the future definition of ARDS. EVLW and PVPI measurements will open the door to future ARDS clinical practice and research.
Financial support and sponsorship
Conflicts of interest
Disclosure: Dr Tagami is a member of the Medical Advisory Board of Pulsion Medical system. Dr. Ong has no conflict of interest to declare regarding this study.
REFERENCES AND RECOMMENDED READING
Papers of particular interest, published within the annual period of review, have been highlighted as:
- ▪ of special interest
- ▪▪ of outstanding interest
1. Sweeney RM, McAuley DF. Acute respiratory distress syndrome
. Lancet 2016; 388:2416–2430.
2. Ware LB, Matthay MA. Clinical practice. Acute pulmonary edema
. N Engl J Med 2005; 353:2788–2796.
3. Edoute Y, Roguin A, Behar D, Reisner SA. Prospective evaluation of pulmonary edema
. Crit Care Med 2000; 28:330–335.
4. Ashbaugh DG, Bigelow DB, Petty TL, Levine BE. Acute respiratory distress in adults. Lancet 1967; 2:319–323.
5. Corrin B, Nicholoson A. Pathology of the lungs. Edinburgh: Churchill Livingstone; 2011.
6. Assaad S, Kratzert WB, Shelley B, et al. Assessment of pulmonary edema
: principles and practice. J Cardiothorac Vasc Anesth 2018; 32:901–914.
7. Tagami T, Kushimoto S, Yokota H. Vincent J-L. Quantitative evaluation of pulmonary edema
. Annual Update in Intensive Care and Emergency Medicine 2014. Switzerland: Springer International Publishing; 2014. 257–267.
8▪▪. Peng JM, Qian CY, Yu XY, et al. Does training improve diagnostic accuracy and inter-rater agreement in applying the Berlin radiographic definition of acute respiratory distress syndrome
? A multicenter prospective study. Crit Care 2017; 21:12.
Multicenter prospective study reporting radiographic diagnostic accuracy and interrater agreement was found to be poor when the Berlin radiographic definition was used, and were not significantly improved by the training set of chest radiographs developed by the Task Force.
9▪▪. Sjoding MW, Hofer TP, Co I, et al. Interobserver Reliability of the Berlin ARDS definition and strategies to improve the reliability of ARDS diagnosis. Chest 2017; 153:361–367.
Study reporting only moderate inter-observer agreement when diagnosing ARDS in patients with hypoxic respiratory failure according to the Berlin criteria. The results were driven primarily by the low reliability of the interpretation of chest image.
10. Tagami T, Kushimoto S, Yamamoto Y, et al. Validation of extravascular lung water measurement by single transpulmonary thermodilution
: human autopsy study. Crit Care 2010; 14:R162.
11. Bernard GR, Artigas A, Brigham KL, et al. The American-European Consensus Conference on ARDS. Definitions, mechanisms, relevant outcomes, and clinical trial coordination. Am J Respir Crit Care Med 1994; 149:818–824.
12. Ranieri VM, Rubenfeld GD, Thompson BT, et al. Acute respiratory distress syndrome
: the Berlin definition
. JAMA 2012; 307:2526–2533.
13. Ferguson ND, Fan E, Camporota L, et al. The Berlin definition
of ARDS: an expanded rationale, justification, and supplementary material. Intensive Care Med 2012; 38:1573–1582.
14. Allardet-Servent J, Forel JM, Roch A, et al. FIO2 and acute respiratory distress syndrome
definition during lung protective ventilation. Crit Care Med 2009; 37:202–207. e204-e206.
15. Estenssoro E, Dubin A, Laffaire E, et al. Impact of positive end-expiratory pressure on the definition of acute respiratory distress syndrome
. Intensive Care Med 2003; 29:1936–1942.
16. Esteban A, Fernandez-Segoviano P, Frutos-Vivar F, et al. Comparison of clinical criteria for the acute respiratory distress syndrome
with autopsy findings. Ann Intern Med 2004; 141:440–445.
17. de Hemptinne Q, Remmelink M, Brimioulle S, et al. ARDS: a clinicopathological confrontation. Chest 2009; 135:944–949.
18. Ferguson ND, Frutos-Vivar F, Esteban As, et al. Acute respiratory distress syndrome
: Underrecognition by clinicians and diagnostic accuracy of three clinical definitions. Crit Care Med 2005; 33:2228–2234.
19. Sarmiento X, Guardiola JJ, Almirall J, et al. Discrepancy between clinical criteria for diagnosing acute respiratory distress syndrome
secondary to community acquired pneumonia with autopsy findings of diffuse alveolar damage. Respir Med 2011; 105:1170–1175.
20. Thille AW, Esteban A, Fernandez-Segoviano P, et al. Comparison of the Berlin definition
for acute respiratory distress syndrome
with autopsy. Am J Respir Crit Care Med 2013; 187:761–767.
21. Monnet X, Teboul JL. Transpulmonary thermodilution
: advantages and limits. Crit Care 2017; 21:147.
22. Bendjelid K, Giraud R, Siegenthaler N, Michard F. Validation of a new transpulmonary thermodilution
system to assess global end-diastolic volume and extravascular lung water. Crit Care 2010; 14:R209.
23. Berbara H, Mair S, Beitz A, et al. Pulmonary vascular permeability index and global end-diastolic volume: are the data consistent in patients with femoral venous access for transpulmonary thermodilution
: a prospective observational study. BMC Anesthesiol 2014; 14:81.
24. Beitz A, Berbara H, Mair S, et al. Consistency of cardiac function index and global ejection fraction with global end-diastolic volume in patients with femoral central venous access for transpulmonary thermodilution
: a prospective observational study. J Clin Monit Comput 2017; 31:599–605.
25. Saugel B, Umgelter A, Schuster T, et al. Transpulmonary thermodilution
using femoral indicator injection: a prospective trial in patients with a femoral and a jugular central venous catheter. Crit Care 2010; 14:R95.
26. Katzenelson R, Perel A, Berkenstadt H, et al. Accuracy of transpulmonary thermodilution
versus gravimetric measurement of extravascular lung water. Crit Care Med 2004; 32:1550–1554.
27. Venkateswaran RV, Dronavalli V, Patchell V, et al. Measurement of extravascular lung water following human brain death: implications for lung donor assessment and transplantation. Eur J Cardiothorac Surg 2013; 43:1227–1232.
28▪▪. Hilty MP, Franzen DP, Wyss C, et al. Validation of transpulmonary thermodilution
variables in hemodynamically stable patients with heart diseases. Ann Intensive Care 2017; 7:86.
This study found that TPTD measurement of blood flow was unaffected by differences in ventricular size and outflow obstruction.
29. Vieillard-Baron A, Matthay M, Teboul JL, et al. Experts’ opinion on management of hemodynamics in ARDS patients: focus on the effects of mechanical ventilation. Intensive Care Med 2016; 42:739–749.
30. Eichhorn V, Goepfert MS, Eulenburg C, et al. Comparison of values in critically ill patients for global end-diastolic volume and extravascular lung water measured by transcardiopulmonary thermodilution: a meta-analysis of the literature. Med Intensiva 2012; 36:467–474.
31. Wolf S, Riess A, Landscheidt JF, et al. How to perform indexing of extravascular lung water: a validation study. Crit Care Med 2013; 41:990–998.
32. Tagami T, Sawabe M, Kushimoto S, et al. Quantitative diagnosis of diffuse alveolar damage using extravascular lung water. Crit Care Med 2013; 41:2144–2150.
33. Sakka SG, Klein M, Reinhart K, Meier-Hellmann A. Prognostic value of extravascular lung water in critically ill patients. Chest 2002; 122:2080–2086.
34. Zhang Z, Lu B, Ni H. Prognostic value of extravascular lung water index in critically ill patients: a systematic review of the literature. J Crit Care 2012; 27:420.e1–420.e8.
35. Jozwiak M, Silva S, Persichini R, et al. Extravascular lung water is an independent prognostic factor in patients with acute respiratory distress syndrome
. Crit Care Med 2013; 41:472–480.
36. Tagami T, Nakamura T, Kushimoto S, et al. Early-phase changes of extravascular lung water index as a prognostic indicator in acute respiratory distress syndrome
patients. Ann Intensive Care 2014; 4:27.
37. Wang H, Cui N, Su L, et al. Prognostic value of extravascular lung water and its potential role in guiding fluid therapy in septic shock after initial resuscitation. J Crit Care 2016; 33:106–113.
38. Michard F, Fernandez-Mondejar E, Kirov MY, et al. A new and simple definition for acute lung injury. Crit Care Med 2012; 40:1004–1006.
39. Jozwiak M, Teboul JL, Monnet X. Extravascular lung water in critical care: recent advances and clinical applications. Ann Intensive Care 2015; 5:38.
40. Groeneveld AB, Verheij J. Extravascular lung water to blood volume ratios as measures of permeability in sepsis-induced ALI/ARDS. Intensive Care Med 2006; 32:1315–1321.
41. Monnet X, Anguel N, Osman D, et al. Assessing pulmonary permeability
by transpulmonary thermodilution
allows differentiation of hydrostatic pulmonary edema
from ALI/ARDS. Intensive Care Med 2007; 33:448–453.
42. Kushimoto S, Taira Y, Kitazawa Y, et al. 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
. Crit Care 2012; 16:R232.
43. Tagami T, Kushimoto S, Tosa R, et al. Plasma neutrophil elastase correlates with pulmonary vascular permeability: a prospective observational study in patients with pneumonia. Respirology 2011; 16:953–958.
44. Bhattacharjee A, Pradhan D, Bhattacharyya P, et al. How useful is extravascular lung water measurement in managing lung injury in intensive care unit? Indian J Crit Care Med 2017; 21:494–499.
45▪. Chung FT, Lee CS, Lin SM, et al. Alveolar recruitment maneuver attenuates extravascular lung water in acute respiratory distress syndrome
. Medicine (Baltimore) 2017; 96:e7627.
Study showing recruitment maneuver is a feasible method for improving oxygenation and the EVLW in patients with ARDS, as well as for decreasing ventilator days and intensive care unit stay duration.
46▪. Gong C, Zhang F, Li L, et al. The variation of hemodynamic parameters through PiCCO in the early stage after severe burns. J Burn Care Res 2017; 38:e966–e972.
A retrospective study evaluating hemodynamics of severely burned patients using PiCCO.
47. Soussi S, Deniau B, Ferry A, et al. Low cardiac index and stroke volume on admission are associated with poor outcome in critically ill burn patients: a retrospective cohort study. Ann Intensive Care 2016; 6:87.
48▪. Stephan F, Mazeraud A, Laverdure F, et al. Evaluation of reperfusion pulmonary edema
by extravascular lung water measurements after pulmonary endarterectomy. Crit Care Med 2017; 45:e409–e417.
Prospective observational study showing extravascular lung water values were significantly higher in patients with severe compared with nonsevere chronic thromboembolic pulmonary hypertension.
49. Tran-Dinh A, Augustin P, Dufour G, et al. Evaluation of cardiac index and extravascular lung water after single-lung transplantation using the transpulmonary thermodilution
technique by the PiCCO2 device. J Cardiothorac Vasc Anesth 2017; [Epub ahead of print].
50▪. Pottecher J, Roche AC, Degot T, et al. Increased extravascular lung water and plasma biomarkers of acute lung injury precede oxygenation impairment in primary graft dysfunction after lung transplantation. Transplantation 2017; 101:112–121.
This article found that immediate postreperfusion increases in EVLW and soluble receptor for advanced glycation end-products along with impaired PaO2/FiO2 ratios were early predictors of grade 3 pulmonary graft dysfunction in lung transplant patients.
51. Tagami T, Kushimoto S, Tosa R, et al. The precision of PiCCO measurements in hypothermic postcardiac arrest patients. Anaesthesia 2012; 67:236–243.
52. Michard F, Schachtrupp A, Toens C. Factors influencing the estimation of extravascular lung water by transpulmonary thermodilution
in critically ill patients. Crit Care Med 2005; 33:1243–1247.
53. Redwan B, Ziegeler S, Freermann S, et al. Single-site low-flow veno-venous extracorporeal lung support does not influence hemodynamic monitoring by transpulmonary thermodilution
. ASAIO J 2016; 62:454–457.