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Research Article | Volume 11 Issue 5 (May, 2025) | Pages 95 - 101
Radiological Evaluation of Cardiogenic vs Non-Cardiogenic Pulmonary Edema: A Comparative Prospective Study
 ,
 ,
1
Assistant Professor, Department of Radiodiagnosis, Mamata Medical College, Khammam, Telangana, India
2
Assistant Professor, Department of General Medicine, Mamata Medical College, Khammam, Telangana, India
Under a Creative Commons license
Open Access
Received
March 20, 2025
Revised
April 5, 2025
Accepted
April 25, 2025
Published
May 9, 2025
Abstract

Background: Pulmonary edema is a critical clinical condition with two major etiologies: cardiogenic pulmonary edema (CPE), caused by elevated hydrostatic pressure, and non-cardiogenic pulmonary edema (NCPE), resulting from increased capillary permeability. Differentiation between the two is essential for guiding appropriate treatment. This study evaluates the diagnostic value of clinical parameters, chest X-ray, high-resolution computed tomography (HRCT), and lung ultrasound (LUS) in distinguishing CPE from NCPE. To compare clinical, biochemical, and radiological findings in patients with CPE and NCPE, and to determine the diagnostic accuracy of specific imaging and laboratory parameters. Material and Methods: A prospective observational study was conducted on 50 patients with radiologically confirmed pulmonary edema at the Departments of Medicine and Radiology, Mamata Medical College, Khammam. Patients were classified into CPE and NCPE groups based on clinical, echocardiographic, and biomarker data. All underwent chest X-ray, HRCT, and lung ultrasound. Data were analyzed using independent t-tests, Fisher’s exact test, and ROC curve analysis to assess statistical and diagnostic significance. Results: BNP levels were significantly higher in the CPE group (751.75 ± 152.78 pg/mL) compared to NCPE (140.28 ± 36.46 pg/mL), with an AUC of 1.0 and an optimal cut-off of 498.8 pg/mL. Chest X-ray showed cardiomegaly (88% vs. 4%) and Kerley B lines (84% vs. 28%) significantly more in CPE. HRCT revealed interlobular septal thickening (80%) and central opacities predominantly in CPE, while NCPE showed peripheral ground-glass opacities (88%). LUS findings showed diffuse B-lines in 84% of CPE and focal B-lines in 72% of NCPE. Most categorical imaging features showed p < 0.01. Conclusion: BNP is a reliable biomarker for differentiating CPE from NCPE. Chest X-ray and HRCT remain important diagnostic tools, while LUS offers rapid bedside evaluation with high diagnostic value. A combined clinical and radiological approach improves diagnostic accuracy and guides timely management.

Keywords
INTRODUCTION

Pulmonary edema, characterized by fluid accumulation in the alveolar spaces and interstitium of the lungs, is a common yet potentially life-threatening condition encountered in clinical practice. It is broadly classified into cardiogenic pulmonary edema (CPE), resulting from elevated hydrostatic pressure due to left ventricular dysfunction, and non-cardiogenic pulmonary edema (NCPE), primarily caused by increased capillary permeability due to factors such as acute respiratory distress syndrome (ARDS), sepsis, trauma, or inhalation injury (1). Accurate and timely differentiation between CPE and NCPE is crucial as the underlying etiology significantly influences management strategies and prognosis. Chest radiography, being the first-line imaging modality in evaluating pulmonary edema, provides valuable clues in distinguishing between these two types based on specific radiologic patterns such as cardiomegaly, vascular redistribution, septal lines, and pleural effusions in CPE, compared to a more peripheral or patchy alveolar distribution in NCPE (2, 3). However, significant overlap exists in imaging findings, especially in early or atypical presentations, thereby necessitating the use of advanced imaging techniques such as high-resolution computed tomography (HRCT) and point-of-care ultrasound (POCUS) for improved diagnostic accuracy.

 

Previous studies have attempted to correlate imaging features with clinical and hemodynamic parameters to improve diagnostic confidence. Earlier studies have evaluated HRCT features distinguishing CPE from NCPE, noting peribronchial cuffing and interlobular septal thickening more often in CPE (4). Similarly, Lichtenstein et al. (2009) demonstrated the utility of lung ultrasound in differentiating interstitial syndrome etiologies using B-line patterns (5). Despite these advancements, a clear consensus or diagnostic algorithm integrating imaging features across modalities remains underdeveloped, especially in settings lacking invasive hemodynamic monitoring. Additionally, many studies are either retrospective or limited by small sample sizes and lack of standardization in imaging interpretation.

 

The current research gap lies in the lack of a comprehensive, prospective evaluation comparing radiographic, ultrasonographic, and tomographic findings in CPE and NCPE across diverse patient populations and clinical contexts. There is also a need for standardized radiological criteria or scoring systems validated against gold standard diagnoses such as pulmonary capillary wedge pressure measurements or echocardiographic findings.

This study aims to systematically compare the radiological characteristics of cardiogenic and non-cardiogenic pulmonary edema using chest X-ray, HRCT, and lung ultrasound, to identify reliable imaging markers that aid in accurate differentiation. It also seeks to address the existing research gap by correlating imaging findings with clinical parameters and establishing a potential diagnostic framework for frontline clinicians.

MATERIALS AND METHODS

This prospective, observational study was conducted in the Department of Medicine in collaboration with the Department of Radiology at Mamata Medical College and General Hospital, Khammam. The study spanned a period of 12 months after obtaining approval from the Institutional Ethics Committee. Informed written consent was obtained from all participants prior to enrolment.

 

A total of 50 patients presenting with clinical features of acute pulmonary edema were included. Patients aged 18 years and above, admitted with symptoms such as dyspnea, orthopnea, and hypoxia, with radiographic evidence suggestive of pulmonary edema, were eligible. Patients with pre-existing chronic lung diseases (e.g., pulmonary fibrosis, COPD), active pulmonary infections, or recent thoracic trauma were excluded to avoid confounding findings.

 

Clinical Assessment:

Each patient underwent a thorough clinical evaluation including history, physical examination, and assessment of vital parameters. Laboratory investigations included complete blood count, renal function tests, serum electrolytes, arterial blood gases, cardiac biomarkers (troponin, BNP), and echocardiography to determine cardiac function.

Radiological Evaluation:

 

All patients underwent:

Chest X-ray (CXR):

Performed in the posteroanterior view (or anteroposterior in bedridden patients), interpreted by two independent radiologists. Key findings such as cardiomegaly, upper lobe venous diversion, Kerley B lines, perihilar bat-wing opacities, and pleural effusions were recorded.

 

High-Resolution Computed Tomography (HRCT):

HRCT was done for all patients using a 64-slice CT scanner. Features such as interlobular septal thickening, ground-glass opacities, distribution pattern (central vs peripheral), and presence of consolidation or air bronchograms were documented.

 

Lung Ultrasound (LUS):

LUS was conducted using a portable ultrasound machine with a curvilinear probe. Presence and pattern of B-lines, pleural line abnormalities, and effusions were noted. A standardized scanning protocol covering anterior, lateral, and posterior chest zones was used.

 

Classification of Pulmonary Edema:

Based on clinical parameters, echocardiography findings, and BNP levels, patients were classified into:

  • Cardiogenic Pulmonary Edema (CPE): Confirmed left ventricular dysfunction or elevated BNP >500 pg/mL.
  • Non-Cardiogenic Pulmonary Edema (NCPE): Normal cardiac function with evidence of underlying conditions like sepsis, ARDS, or aspiration.

 

Data Analysis:

Radiological findings were compared between the two groups (CPE vs NCPE). Interobserver agreement was calculated for radiographic interpretation. Descriptive statistics were used to summarize baseline characteristics. Chi-square test was applied for categorical variables and t-test for continuous variables. A p-value <0.05 was considered statistically significant.

RESULTS

Table 1: Comparison of Clinical Parameters between Cardiogenic and Non-Cardiogenic Pulmonary Edema

Parameter

CPE (Mean ± SD)

NCPE (Mean ± SD)

Age (years)

63.36 ± 9.57

55 ± 11.11

Heart Rate (bpm)

99.27 ± 11.84

103.94 ± 11.33

Respiratory Rate (/min)

24.16 ± 3.10

25.47 ± 4.04

Systolic BP (mmHg)

152.89 ± 17.11

130.42 ± 16.99

Diastolic BP (mmHg)

93.01 ± 12.17

80.01 ± 9.52

SpO2 (%)

87.18 ± 6.31

85.72 ± 5.20

BNP (pg/mL)

751.75 ± 152.78

140.28 ± 36.46

This table 1 summarizes the mean and standard deviation of key clinical and physiological parameters in patients diagnosed with cardiogenic pulmonary edema (CPE) and non-cardiogenic pulmonary edema (NCPE). Notable differences are observed in systolic and diastolic blood pressure, BNP levels, and age, reflecting the differing underlying mechanisms of each condition.

 

Table 2: Comparison of Laboratory Parameters between Cardiogenic and Non-Cardiogenic Pulmonary Edema

Parameter

CPE (Mean ± SD)

NCPE (Mean ± SD)

Hemoglobin (g/dL)

12.88 ± 0.93

11.86 ± 1.51

WBC (×10^3/μL)

8.86 ± 1.96

9.51 ± 2.82

Serum Creatinine (mg/dL)

1.34 ± 0.40

1.20 ± 0.35

Serum Sodium (mEq/L)

135.4 ± 3.34

132.16 ± 4.86

Serum Potassium (mEq/L)

4.22 ± 0.38

4.00 ± 0.46

This table 2 presents the mean and standard deviation values of key laboratory investigations in CPE and NCPE groups. Hemoglobin and serum sodium levels were slightly higher in CPE, while WBC count was marginally elevated in NCPE, suggesting an inflammatory component. Creatinine values indicate mildly compromised renal function in both groups, which may reflect underlying comorbidities or acute dysfunction.

 

Table 3: Arterial Blood Gases, Cardiac Biomarkers, and Echocardiographic Findings in CPE vs NCPE

Parameter

CPE (Mean ± SD)

NCPE (Mean ± SD)

pH

7.37 ± 0.03

7.33 ± 0.04

PaO2 (mmHg)

59.59 ± 9.34

55.84 ± 8.77

PaCO2 (mmHg)

44.18 ± 6.18

40.79 ± 6.34

Troponin I (ng/mL)

1.36 ± 0.56

0.20 ± 0.08

BNP (pg/mL)

751.75 ± 152.78

140.28 ± 36.46

LVEF (%)

39.49 ± 7.11

60.28 ± 4.86

This table 3 shows comparative mean and standard deviation values for arterial blood gas parameters, cardiac biomarkers, and left ventricular ejection fraction (LVEF) in CPE and NCPE groups. Significantly elevated BNP and troponin levels in CPE suggest underlying cardiac dysfunction. Lower pH and PaO2 values in NCPE reflect hypoxemia and possible respiratory compromise. LVEF clearly differentiates the two groups, with reduced values in CPE indicative of systolic heart failure.

 

Table 4: Comparison of Key Diagnostic Parameters between Cardiogenic and Non-Cardiogenic Pulmonary Edema

Parameter

CPE (Mean ± SD)

NCPE (Mean ± SD)

Troponin I (ng/mL)

1.36 ± 0.56

0.2 ± 0.08

PaO2 (mmHg)

59.59 ± 9.34

55.84 ± 8.77

PaCO2 (mmHg)

44.18 ± 6.18

40.79 ± 6.34

pH

7.37 ± 0.03

7.33 ± 0.04

BNP (pg/mL)

751.75 ± 152.78

140.28 ± 36.46

LVEF (%)

39.49 ± 7.11

60.28 ± 4.86

This table 4 shows critical physiological and biochemical indicators that aid in differentiating cardiogenic pulmonary edema (CPE) from non-cardiogenic pulmonary edema (NCPE). Troponin I and BNP levels were markedly elevated in CPE, reflecting myocardial stress and ventricular dysfunction. LVEF was significantly reduced in CPE, supporting systolic heart failure as the underlying cause. Arterial blood gas parameters revealed lower pH and PaO₂ in NCPE, indicating more pronounced respiratory compromise.

 

Table 5: Chest X-ray Findings in Cardiogenic vs Non-Cardiogenic Pulmonary Edema

Chest X-ray Finding

CPE (%)

NCPE (%)

Cardiomegaly

88

4

Upper Lobe Diversion

96

16

Kerley B Lines

84

28

Bat-wing Opacity

88

12

Pleural Effusion

72

32

This table 5 presents the frequency of characteristic chest X-ray findings in patients with cardiogenic (CPE) and non-cardiogenic pulmonary edema (NCPE). Cardiomegaly and upper lobe venous diversion were predominantly observed in CPE, indicating elevated left atrial pressures. Kerley B lines and bat-wing opacities were also more frequent in CPE, reflecting interstitial and alveolar fluid accumulation. Pleural effusion was seen in both groups but more common in CPE. These imaging features remain essential for the initial evaluation and differentiation of pulmonary edema etiology.

 

Table 6: High-Resolution CT Findings in Cardiogenic vs Non-Cardiogenic Pulmonary Edema

HRCT Finding

CPE (%)

NCPE (%)

Interlobular Septal Thickening

80

24

Ground-glass Opacities

36

76

Central Distribution

72

20

Peripheral Distribution

16

88

Consolidation

60

60

Air Bronchograms

32

60

This table 6 compares HRCT findings between CPE and NCPE groups. Interlobular septal thickening and central distribution of opacities were more common in CPE, consistent with hydrostatic pulmonary edema. In contrast, NCPE frequently showed ground-glass opacities and peripheral distribution, reflecting increased capillary permeability and diffuse alveolar damage. Interestingly, consolidation and air bronchograms were observed in both groups, with higher air bronchogram presence in NCPE.

Table 7: Lung Ultrasound Findings in Cardiogenic vs Non-Cardiogenic Pulmonary Edema

Lung Ultrasound Finding

CPE (%)

NCPE (%)

Diffuse B-lines (bilateral)

84.0

28.00

Focal B-lines (patchy)

16.0

72.0

Pleural Line Irregularity

20.0

68.0

Pleural Effusion

80.0

32.0

This table 7 outlines the distribution of key lung ultrasound (LUS) features in patients with CPE and NCPE. Diffuse bilateral B-lines were highly prevalent in CPE, reflecting widespread interstitial fluid due to raised hydrostatic pressure. In contrast, NCPE was associated with focal B-lines and pleural line irregularities, which are suggestive of patchy alveolar involvement and inflammatory processes like ARDS. Pleural effusion was more common in CPE. These LUS patterns provide a rapid, bedside diagnostic tool to distinguish between types of pulmonary edema with considerable accuracy.

Table 8: Comparative Analysis of Continuous Variables between CPE and NCPE

Variable

CPE Mean ± SD

NCPE Mean ± SD

Normality(p-value)

p-value

BNP (pg/mL)

751.75 ± 152.78

140.28 ± 36.46

CPE: 0.792, NCPE: 0.791

0

Heart Rate (bpm)

99.27 ± 11.84

103.94 ± 11.33

CPE: 0.322, NCPE: 0.732

0.1608

LVEF (%)

39.49 ± 7.11

60.28 ± 4.86

CPE: 0.150, NCPE: 0.205

0

This table 8 summarizes the statistical comparison of key continuous parameters between cardiogenic and non-cardiogenic pulmonary edema groups. BNP levels and LVEF showed statistically significant differences (p = 0.000), with elevated BNP and reduced LVEF strongly favoring a cardiogenic cause. Heart rate did not differ significantly between groups (p = 0.1608). Normality testing using the Shapiro-Wilk test confirmed that all variables followed a normal distribution in both groups, justifying the use of the independent t-test.

Table 9: Categorical Imaging Findings in CPE vs NCPE with Statistical Significance

Variable

CPE (%)

NCPE (%)

p-value

Kerley B Lines

84

28

0.0001

Pleural Effusion

80

32

0.0014

Diffuse B-lines (bilateral)

84

28

0.0001

Focal B-lines (patchy)

16

72

0.0001

Pleural Line Irregularity

20

68

0.0014

This table 9 compares the prevalence of key imaging features between cardiogenic pulmonary edema (CPE) and non-cardiogenic pulmonary edema (NCPE), along with corresponding p-values. Kerley B lines, pleural effusion, and diffuse bilateral B-lines were significantly more frequent in CPE, reflecting hydrostatic pressure changes. Conversely, focal B-lines and pleural line irregularity were predominant in NCPE, consistent with inflammatory or permeability-related pathology. All listed variables demonstrated statistically significant differences (p < 0.01), reinforcing their diagnostic utility in differentiating CPE from NCPE using chest X-ray and lung ultrasound.

DISCUSSION

The present study aimed to evaluate and compare radiological, clinical, and laboratory parameters in patients with cardiogenic (CPE) and non-cardiogenic pulmonary edema (NCPE), involving 50 patients at Mamata Medical College, Khammam. Differentiating CPE from NCPE is clinically significant as it guides targeted therapeutic strategies and improves outcomes. The results of this prospective study reaffirm key diagnostic features while also providing new insights into the utility of multi-modality imaging in real-world hospital settings.

 

In our cohort, BNP levels were significantly higher in CPE patients (mean 751.75 ± 152.78 pg/mL) compared to NCPE (140.28 ± 36.46 pg/mL), consistent with earlier studies by Maisel et al. (2002), who demonstrated BNP as a strong biomarker for heart failure-related dyspnea with diagnostic accuracy exceeding 90% (6). ROC curve analysis in our study confirmed excellent diagnostic performance of BNP with an AUC of 1.0 and an optimal cut-off value of 498.8 pg/mL, aligning closely with the threshold proposed in prior literature (>500 pg/mL) (7).

 

Echocardiographic findings, particularly left ventricular ejection fraction (LVEF), also significantly differed between groups, with CPE patients showing reduced LVEF (~39.5%), in line with cardiogenic pathophysiology. Although LVEF showed statistical significance, the ROC curve showed poor discrimination (AUC 0.01), likely due to inverse distribution or overlap with NCPE cases where cardiac function was preserved but mildly compromised in systemic illnesses like sepsis.

 

Chest X-ray findings were markedly different between groups. Cardiomegaly (88% in CPE vs 4% in NCPE) and Kerley B lines (84% in CPE vs 28% in NCPE) were significantly associated with CPE, reaffirming classical radiographic features. These findings are consistent with earlier studies (8), who identified vascular redistribution and cardiomegaly as key differentiators. Similarly, bat-wing pattern and pleural effusions were predominantly seen in CPE, supporting prior reports (9).

 

In terms of HRCT imaging, interlobular septal thickening and central distribution were more frequent in CPE, whereas ground-glass opacities and peripheral distribution were common in NCPE. This aligns earlier study which emphasized peribronchial cuffing and septal thickening in CPE versus patchy, diffuse infiltrates in NCPE (10). Our findings reinforce the value of HRCT in uncertain or overlapping cases where CXR findings are inconclusive.

 

Lung ultrasound (LUS) further emerged as a highly useful bedside modality. In our study, diffuse bilateral B-lines were observed in 84% of CPE cases, while focal patchy B-lines and pleural line irregularities were significantly more common in NCPE. These findings are in agreement with Lichtenstein et al. (2009), who demonstrated LUS could effectively differentiate between hydrostatic and permeability edema, particularly in emergency settings (5).

 

Statistical analysis showed significant differences in most clinical and imaging parameters between CPE and NCPE, with categorical features like Kerley B lines, pleural effusion, and B-line patterns on LUS showing p-values <0.001. These results not only confirm known diagnostic patterns but also highlight the incremental value of combining modalities for greater diagnostic confidence.

CONCLUSION

The current study demonstrates that integrating clinical data with imaging modalities like chest X-ray, HRCT, and lung ultrasound significantly enhances diagnostic accuracy in distinguishing cardiogenic from non-cardiogenic pulmonary edema. BNP emerged as a robust biomarker with high sensitivity and specificity. Chest radiography and HRCT retained their relevance in identifying classical signs of CPE, while LUS provided a rapid, non-invasive alternative with practical utility in acute settings. These findings support a multimodal approach in clinical practice and underscore the need for standard diagnostic algorithms incorporating radiologic and biochemical markers.

REFERENCES
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