(Chest. 2002;121:942-950.)
© 2002
American College of Chest Physicians
Using the Chest Radiograph To Determine Intravascular Volume Status*
The Role of Vascular Pedicle Width
E. Wesley Ely, MD, MPH, FCCP and
Edward F. Haponik, MD, FCCP
*
From the Department of Medicine (Dr. Ely), Division of Allergy/Pulmonary/Critical Care Medicine, the Vanderbilt University School of Medicine, Nashville, TN; and the Department of Medicine (Dr. Haponik), the Johns Hopkins University School of Medicine, Baltimore, MD.
Correspondence to: E. Wesley Ely, MD, MPH, FCCP, Division of Allergy/Pulmonary/Critical Care Medicine, Center for Health Services Research, Sixth Floor Medical Center East, Vanderbilt University Medical Center, Nashville, TN 37232-8300; e-mail: wes.ely{at}mcmail.vanderbilt.edu
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Abstract
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Due to concerns about the efficacy and safety of using pulmonary artery catheterization to evaluate hemodynamic status, noninvasive diagnostic testing has gained increased importance. This article focuses on both the supportive evidence and the limitations of applying the vascular pedicle width (VPW), which is the mediastinal silhouette of the great vessels, as an aid in the assessment of patients’ intravascular volume status. The objective measurement of the VPW obtained from either upright or supine chest radiographs (CXRs which are often already available though not fully utilized) can increase the accuracy of the clinical and radiographic assessment of intravascular volume status by 15 to 30%, and this value may be even higher when VPW is used serially within the same patient. Regardless of the presence or absence of pulmonary edema, the best VPW cutoff for differentiating a high vs normal to low intravascular volume status is 70 mm. Patients with a VPW of > 70 mm coupled with a cardiothoracic ratio of > 0.55 are more than three times more likely to have a pulmonary artery occlusion pressure > 18 mm Hg than are patients without these radiographic findings. We suggest a management algorithm for utilizing the VPW, and whether or not such an approach will offer superior patient outcomes requires prospective investigation. Reappraisal of the VPW and other roentgenographic signs should be incorporated into newly implemented studies of the Swan-Ganz catheter, ICU echocardiography, portable CT scans, and other costlier technologies. While such investigations may refine the optimum application of the portable CXR, conventional and digital supine radiographs should retain an important role in the diagnosis and management of critically ill patients. Lastly, the measurement of the VPW should be incorporated into the training of chest clinicians and radiologists.
Key Words: ARDS • congestive heart failure • ICU • intravascular volume • myocardial infarction • pneumonia • pulmonary edema • radiography • sepsis
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Introduction
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In a timely investigation published in CHEST, Duane and Colice1
addressed the impact of substituting noninvasive diagnostic studies for Swan-Ganz catheter placement in evaluating acutely ill patients. We strongly agree that the nonintrusive assessment of a patient’s intravascular volume status has gained increased importance, due to appropriate concerns about the efficacy and safety of pulmonary artery catheters,2
3
4
and that coupling clinical assessment and echocardiography has particular appeal and value in this setting.5
We also believe that another, lower cost opportunity to enhance the noninvasive appraisal of intravascular volume status entails the improved utilization of information already available on frequently acquired portable, supine chest radiographs (CXRs) of ICU patients.6
We would like to draw the attention of readers to the vascular pedicle, which is the mediastinal silhouette of the great vessels, and its relevance to this clinical dilemma. For the purposes of this article, we will focus on both the evidence supporting the application of the portable CXR in clinical practice as well as its limitations.
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Measuring the Vascular Pedicle
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Described in detail by Milne and colleagues7
8
nearly 2 decades ago as well as in another recent publication,6
the vascular pedicle width (VPW) is measured by dropping a perpendicular line from the point at which the left subclavian artery exits the aortic arch and measuring across to the point at which the superior vena cava crosses the right mainstem bronchus (Fig 1 ). When the right border of the pedicle is indistinct, the vertical lateral border of the superior vena cava or right brachiocephalic vein have been used in VPW measurements.7
9
On CXRs made with patient in the upright posteroanterior position (n = 83), Milne and colleagues7
reported the mean (± SC) normal VPW to be 48 ± 5 mm.
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Figure 1. The VPW is measured by (1) dropping a perpendicular line from the point at which the left subclavian artery exits the aortic arch and (2) measuring across to the point at which the superior vena cava crosses the right mainstem bronchus.
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Chest clinicians are aware of the many factors that might influence VPW and artifactually alter its predictive value. This measurement varies with patient height and body build, and technical variations such as patient rotation, poor inspiratory effort, or supine vs upright positioning of the patient will also modify the VPW in predictable ways. VPW measured with the patient in a supine posture is approximately 17% greater than that with the patient in an upright posture.7
The rotation of the patient to the right (ie, a left anterior oblique projection) increases VPW, whereas the rotation of the patient to the left (ie, a right anterior oblique projection) decreases this measurement. Accordingly, ICU CXRs should be taken in a reproducible fashion, with similar body positioning and focal film distance (40 inches from the chestwall is the standard focal-film difference). The usefulness of this sign also might be expected to vary in circumstances in which the components of the silhouette have been altered by vascular or other mediastinal disease or as a result of the effects of prior thoracic surgery, radiation therapy, or trauma. For example, in their careful review of 261 patients, Chiou et al10
found that a widening of the ascending aorta and vascular pedicle is a normal postoperative CXR finding following cardiac transplantation. Increased VPW also may occur in patients experiencing extravascular bleeding. While elevated intravascular volume predominantly causes widening to the right of the midline, aortic injury causes widening predominantly to the left of the midline, together with the "vanishing" of the right paratracheal stripe and azygous vein.11
The impact of variations in oncotic pressure (eg, the development of hypoalbuminemia) on serial VPW assessments is not known. Milne et al7
observed little change in VPW with inspiration and expiration. Although mechanical ventilation may have profound effects on other roentgenographic findings such as the pattern and severity of parenchymal infiltrates,12
13
we have found that VPW measurements are relatively consistent between spontaneous and positive-pressure breaths (unpublished observations from previously reported cohort12
)
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Differentiating Patterns of Pulmonary Edema
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In a series of classic investigations, Milne and coworkers8
14
15
determined roentgenographic criteria with which to differentiate among cardiogenic, renal, and injury patterns of edema that pivoted around the pattern of infiltrates and the measurement of the VPW. Using 216 CXRs made predominantly with the patient in an upright posteroanterior position, these investigators8
observed that assessments of the distribution of pulmonary flow, the distribution of pulmonary edema, and the width of the vascular pedicle had particular usefulness. A VPW < 43 mm was most predictive of patients with an injury pattern of edema, whereas a widened VPW (ie, a VPW > 53 mm in CXRs made with the patient in an upright position) was predictive of volume overload states such as cardiac or renal failure (Fig 2
).8
Interestingly, the widening of the vascular pedicle has also been observed in patients with polycythemia vera11
and laryngospasm-induced, "negative-pressure" pulmonary edema (mean VPW, 67 mm).16
In the latter example, these roentgenographic findings support the theory that negative-pressure pulmonary edema occurs due to increased intravascular volume via a hydrostatic mechanism as well as capillary leak derangements.17
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Figure 2. Measurements of the VPW are significantly larger in patients with pulmonary edema due to congestive heart failure (p < 0.01) or renal failure (p < 0.001) compared to patients with pulmonary edema due to acute lung injury. PA = posteroanterior. Reproduced with permission from Milne et al.8
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In a retrospective analysis of 119 patients,14
a standardized approach to reading CXRs was found to differentiate reliably among patients with pulmonary edema due to left heart decompensation, renal failure, and lung microvascular injury. A stepwise method of discriminant analysis resulted in correct classification in 86.6% of the patients, with VPW having the second highest discriminating power among 15 radiographic findings.14
The implementation of these roentgenographic criteria by intensivists and cardiologists in ICU patients, however, has been limited in part due to the use of clinical diagnoses rather than data derived from pulmonary artery catheterization and to postural variations in radiographic technique (ie, the use of CXRs made with the patient in the upright position rather than the supine position) by previous investigators. Other factors contributing to the general under-recognition and underuse of the VPW by the medical community might relate either to an overexpectation of its clinical utility or to general unfamiliarity with this roentgenographic sign.
Thomason et al18
assessed the role of portable, supine, conventional CXRs in differentiating ARDS from pulmonary edema due to volume overload. The accuracy of CXR interpretation could be improved by > 30% (from 41 to 73%) by incorporating the VPW and/or cardiothoracic ratio (CTR). Taken by itself, the optimal cutoff for VPW to balance sensitivity and specificity in distinguishing between the permeability and hydrostatic forms of pulmonary edema was found to be 68 mm. The VPW correlated with pulmonary artery occlusion pressure (PAOP) [r = 0.45; p = 0.008] and CTR (r = 0.52; p = 0.01), and VPW and CTR correlated with one another (r = 0.49; p = 0.003). Importantly, we encountered the following two clinical scenarios (both familiar to intensivists and radiologists) in which the use of the VPW would offer an accurate estimate of current intravascular volume status as measured by the PAOP, but the explanation would be predictably different from the original explanation of the patient’s pulmonary edema: (1) diuresis of patients with cardiogenic edema; and (2) volume loading of hypotensive patients experiencing ARDS. In these two scenarios, the VPW had become reduced and enlarged in size, respectively, as a result of the antecedent therapy.
In a subsequent prospective investigation using newer computer-generated, digital CXRs in 100 supine patients (all of whom had volume status assessed by pulmonary artery catheters), logistic regression and receiver operating characteristic curve analyses confirmed that the VPW and CTR were the most important individual roentgenographic predictors of volume status.6
19
Regardless of the presence (66%) or absence (33%) of pulmonary edema, the best VPW cutoff for differentiating a high intravascular volume status from a normal-to-low intravascular volume status was 70 mm.
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Usefulness of Serial Measurements
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Changes in the VPW have been associated with altered intravascular volume status, but anecdotal observations suggest that many clinicians are unaware of this relationship, and there have been a limited number of clinical reports in which such measurements have been applied serially. Pistolesi et al15
determined in upright, non-mechanically ventilated patients who were undergoing cardiac catheterization that the VPW and total blood volume (TBV) were highly correlated (r = 0.80; p < 0.001) and that a change in volume status also correlated with a change in VPW (r = 0.93; p < 0.001) [Fig 3
]. In fact, an increase of 1 L in TBV was associated with an increase of 5 mm in VPW when CXRs were obtained with the patient in the upright position (Fig 4
).15
Thus, while a single measurement of the VPW may be informative, we believe that serial measurements obtained on CXRs performed with similar patient posture and radiographic technique have particular clinical usefulness (Fig 5
). As evidenced in Figure 4
, veins are much more compliant than arteries, and alterations in intravascular fluid volume are reflected by a greater change in the right side of the pedicle compared with the left side.7
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Figure 3. Correlation between TBV and VPW in 71 radiographs made with the patient in an erect posture (r = 0.80; p < 0.001). Open plus closed circles = linear regression line a. Thirty-eight of the radiographs were of patients with rheumatic valvular disease (r = 0.90; p < 0.001; closed circles = linear regression line b), and 33 radiographs were of patients with ischemic heart disease (r = 0.67; p < 0.001; open circles = linear regression line c). Reproduced with permission from Pistolesi et al.15
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Figure 4. Top, a: changes in VPW vs changes in TBV. This graph compares changes in VPW with changes in TBV in 10 cardiac patients (closed circles) and 3 healthy subjects (crosses). Two of the healthy subjects had been given 2 L normal saline solution, and one healthy subject had 450 mL blood removed. Equation a represents the linear correlation for 10 cardiac patients only (r = 0.93; p < 0.001; solid line), and the dashed extended portion shows how closely the three healthy subjects fit the same line. Recalculating the regression (equation b) to include the healthy subjects shows the data virtually unchanged (r = 0.97; p < 0.001). Reproduced with permission from Pistolesi et al.15
Bottom, b: linear regression in 8 of the same 10 cardiac patients in whom pulmonary blood volume (PBV) also had been measured. The change in VPW is now correlated with systemic blood volume (ie, TBV - PBV) (r = 0.96; p < 0.001). Reproduced with permission from Pistolesi et al.15
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Figure 5. Top: portable digital CXR of a 52-year-old woman who had experienced a tricyclic antidepressant overdose and developed ARDS and subsequent nosocomial pneumonia, with Pseudomonas aeruginosa growth on cultures made from both blood and bronchoscopic protected-specimen brush biopsy specimen. Multiorgan dysfunction syndrome and profound septic shock necessitating vasopressor support developed in the patient. Shortly after this CXR, the patient was intubated and underwent placement of a pulmonary artery catheter because her managing clinicians were unsure of her intravascular volume status due to ongoing hypotension despite, having received a net 8,400 mL fluid resuscitation (ie, 8.4 L more fluid in than out), and because of the presence of anasarca and worsening renal function. Her body weight at the time of this CXR was 84 kg. After the placement of the pulmonary artery catheter (within 2 h of the CXR shown), the following hemodynamic parameters were obtained: PAOP, 26 mm Hg; cardiac index, 4.56 L/min/m2. This supine, digital CXR showed diffuse airspace disease, a widened CTR (ie, > 0.55), and a VPW of 79 mm. Bottom: Portable digital CXR. The same patient shown in the top panel is shown here 10 days later after marked resolution of her ARDS, acute tubular necrosis, and septic shock. In the interim, she had 10,900 mL net fluid diuresis recorded (not including insensible losses) and a marked reduction in her anasarca. Her body weight at the time of this CXR was 67 kg. While the pulmonary artery catheter had already been removed, this portable, supine CXR showed near complete resolution of her airspace infiltrates and only minimal interstitial disease, a normal CTR (ie, < 0.55), and a VPW of 56 mm.
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These observations are consistent with serial clinical findings in populations that have been treated with intravascular volume expansion or contraction. A widening of the vascular pedicle on serial CXRs in burn patients has preceded the development of pulmonary edema following fluid resuscitation.20
Among 42 patients with cutaneous burns and risks for inhalation injury, the development of pulmonary edema during the first 3.3 days after the injury was associated with increased VPW during the initial 24 h of fluid resuscitation (Fig 6
). Patients who later developed pulmonary edema had received more IV fluid (16 vs 8.9 L) during this period. While 12 of 13 patients with VPW increases of 
1 cm later developed pulmonary edema, no patient with a decrease in VPW developed this problem (Fig 7
). Don and colleagues9
reviewed 36 pairs of CXRs immediately before and after hemodialysis in 22 patients with chronic renal failure. VPW decreased significantly and was recorded as a useful indicator of volume status. Reductions of VPW and the transverse diameter of the heart correlated with the percentage reduction in body weight following dialysis. These authors suggested that VPW and CTR may provide useful estimates of dry weight when the clinical assessment is difficult. In patients with renal failure and pulmonary edema due to missed dialysis, we often have observed a decrease of an enlarged VPW after the reinstitution of dialysis.
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Figure 6. Serial VPW measurements in 42 patients with cutaneous burns. The VPW increased significantly in patients who subsequently developed pulmonary edema (p < 0.01) but was unchanged in those without this complication. Reproduced with permission from Haponik et al.20
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Figure 7. Changes in the VPWs of burn patients. VPW enlargement was associated with pulmonary edema. Twelve of 13 patients with pedicle enlargements 1.0 cm developed pulmonary edema, and no patients with reductions of the VPW developed pulmonary edema. Reproduced with permission from Haponik et al.20
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These reports are complemented by recent comparisons of serial VPW measurements to prospectively measured changes in net fluid intake and patient weight. Martin and colleagues21
studied 133 portable, supine CXRs in 36 mechanically ventilated patients who had experienced acute lung injury and noted that a clinically detectable and significant reduction in VPW over a 5-day period (p = 0.02) was associated with a mean net diuresis of 3.3 L and a mean weight loss of 10 kg. Another recently report22
roentgenographic sign, the ratio of the pulmonary artery to the bronchus, also may contribute to estimates of intravascular volume status using the portable CXR. However, this sign is likely to be more difficult to measure than the VPW, and it has not been established whether coupling this sign with VPW assessment improves intravascular volume estimates.
The clinical use of each of these roentgenographic signs requires an awareness of the potentially confounding effects of the variations in patient posture, radiographic technique, and ventilator-patient interactions that confront physicians (discussed above). Limitations imposed by these and other factors should not deter the use of the portable CXR, but rather should fuel the need for the standardization of the interpretation of the CXR23
24
so that we can optimize the use of the pertinent information that is present on the CXRs of our patients. The reproducibility of the technique of serial CXRs (ie, using the same body position, focal film distance, and exposure) underlies the potential clinical application of VPW measurements.
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Applying Assessment of VPW to Patient Care
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Portable, supine CXRs are the most commonly used noninvasive studies to identify the presence, severity, or change in pulmonary edema in the ICU,25
26
and they may promote a therapeutic change in up to two thirds of patients.27
Accordingly, optimizing the use of portable, supine CXRs is imperative. Despite several limitations, the portable CXR offers some utility in appraising volume status (although it is not to be relied on exclusively). It is important to acknowledge that we are not proposing the measurement of VPW as a substitute for pulmonary artery catheterization. This procedure will clearly retain a diagnostic role in carefully selected patients, but the definition of who will benefit from such invasive monitoring requires further study. On the other hand, there are patients in whom the intensivist may have no intention of using invasive techniques to determine volume status because the risks outweigh the benefits. In such patients in particular, the information already available on the patient’s CXR should be used to its maximum potential. Despite the standard use of the PAOP as a measure of intravascular volume status, this measure remains controversial and unreliable in inexperienced hands.19
28
Although the reading of CXRs made in the ICU is typically imbedded within ICU rounds, the relative lack of a uniform approach to this daily event increases even further the appeal and potential impact of simplifying and/or standardizing the application of this tool.23
24
Clinicians and radiologists should be encouraged by the fact that the VPW and CTR are highly reproducible, with intrareader and interreader correlation coefficients ranging from 0.84 to 0.96.6
18
In their comprehensive analysis of radiographic findings, Milne et al8
found the least interobserver variability (2%) in the assessment of the VPW. In clinical reports,6
9
20
21
VPW measurement has been feasible in approximately three fourths of patients. It is also important to note that measurements obtained from the portable, supine CXR have had predictive values that were superior to those of any of the more commonly used, conventional roentgenographic criteria, such as edema pattern or distribution, air bronchograms, peribronchial cuffing, septal lines, or pleural effusions. The VPW and CTR have likelihood ratios of > 3 in differentiating ARDS from volume overload. By contrast, the likelihood ratios of other roentgenographic signs that often are used in this determination were unacceptably close to 1.0.6
18
While able to provide modest but not large shifts from pretest to posttest probability, the test performance of the VPW measurement is as good or better than many other widely accepted diagnostic tests that are used in pulmonary and critical care medicine.6
29
30
Interestingly, neither the analyses of CXRs obtained during major multicenter investigations of respiratory failure, nor the classic pulmonary and critical care textbooks used by intensivists and cardiologists alike, nor some publications instructing physicians how to use the CXR in their research or clinical practices have addressed the use of the VPW.23
24
31
32
Although CT scans of the chest and other advanced imaging modalities have increasingly been extended to the ICU setting, more investigations of their correlative relationships to hemodynamic data also are needed. We have observed that radiologists and chest clinicians have varying degrees of awareness of (and confidence in) this roentgenographic sign and its potential roles in noninvasive patient evaluation. Informal surveys of experienced chest radiologists of three major medical centers revealed that two thirds of physicians had received no formal training in the measurement of the VPW, yet they admitted that without such an objective measurement they had little to no confidence in using the CXR to determine the etiology of pulmonary edema or volume status. Considering that most patients already receive numerous portable CXRs while in the ICU, the added information available to the clinician is essentially "cost-free" and offers the potential for enhanced decision making. Often the mere subjective assessment of VPW (eg, as normal vs wide and increasing vs decreasing), rather than rigorous objective measurement of its value, suffices as a worthwhile clinical tool. We suspect that such an subjective impression has been used unconsciously for decades by clinicians as they view and interpret CXRs.
How Might These Observations Be Translated to Patient Care?
We think that the VPW provides one other validated roentgenographic sign that radiologists and clinicians should incorporate into their routine examination of the CXR and should relate to the clinical context in which the CXR has been obtained. A potential although simplistic approach to the use of the VPW is outlined in Figure 8
. It has not been established whether a reduction of the VPW (suggesting diuresis or blood loss) or an expansion of the VPW (suggesting volume overload) in patients without parenchymal opacities should influence care. However, evidence supports the notion that the VPW is of similar value both in the presence or absence of pulmonary edema.6
VPW enlargement, especially as seen on serial CXRs, should trigger a review of the patient’s fluid intake and output, alerting the physician to the possibility of intravascular volume expansion. The cumulative effects of days of repetitive net fluid intake often go unnoticed otherwise, progressing insidiously until the patient succumbs to abrupt airspace flooding and hypoxemic respiratory failure. In such circumstances, the VPW could heighten the clinician’s awareness of the increased likelihood of a hydrostatic mechanism for a patient’s decline or, ideally, could prompt earlier intervention, avoiding the problem altogether. On the contrary, a narrow vascular pedicle should suggest an alternative explanation for pulmonary opacities such as ARDS, atelectasis, or infection and may influence thresholds for empiric therapy or the performance of confirmatory diagnostic procedures. A narrow VPW on a supine CXR is an unlikely finding in the setting of increased systemic blood volume and hydrostatic edema.
Complex, critically ill patients often have varying mechanisms of pulmonary edema, which evolve throughout the course of their illnesses and are modified by therapy and/or supervening problems (Fig 5)
. Considering the size of the VPW may provide further insight into such multiphasic courses, as well as in initial diagnostic efforts, and may assist in the clinical evaluation of patients who have sequential or simultaneous hydrostatic and permeability etiologies for their pulmonary edema. For example, in heart-lung transplantation patients with septal lines and new or increasing pleural effusions, the stability of the VPW and the CTR has been suggestive of acute lung rejection and has had an overall accuracy of 83%.33
Among immunocompromised hosts with unexplained bilateral pulmonary infiltrates, we have occasionally found that VPW enlargement prompted diuresis with the subsequent clearing of infiltrates, obviating the need for the biopsy procedures under consideration.
In conclusion, the objective measurement of the VPW obtained from CXRs made with the patient in either the upright or the supine position (which often are already available, although not utilized) can increase the accuracy of the clinical and radiographic assessment of intravascular volume status by 15 to 30%,6
18
and this value may be even higher when the VPW is used serially within the same patient. Whether management approaches such as that proposed in Figure 8
offer superior outcomes requires prospective investigation. When intravascular volume status remains unclear after this assessment, echocardiography, pulmonary artery catheter placement, or empiric therapy as dictated by the patient’s clinical status and risk/benefit considerations must be pursued. We believe that reappraisal of the VPW and other roentgenographic signs should be incorporated into newly implemented studies of the Swan-Ganz catheter, ICU echocardiography, portable CT scans, and other costlier technologies. While such investigations may refine the optimum application of the portable CXR, we believe that conventional (and digital) supine CXRs, though old-fashioned, will retain an important role in the diagnosis and management of critically ill patients.
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Footnotes
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Abbreviations: CTR = cardiothoracic ratio; CXR = chest radiograph; PAOP = pulmonary artery occlusion pressure; TBV = total blood volume; VPW = vascular pedicle width
Received for publication February 5, 2001.
Accepted for publication October 10, 2001.
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Abstract
Introduction
