Pleural effusion is a common clinical problem that can cause dyspnea [1]. Symptom improvement after thoracentesis has been noted, though there is currently discussion about the mechanism of improvement. Some have postulated that fluid removal improves ventilation-perfusion matching [2], while others have suggested that symptom improvement occurs through changes in respiratory mechanics [3].

A new technology non-invasively measures the partial pressure of expired oxygen (PAO2) [4]. By using the alveolar gas equation, this device provides a non-invasive measurement of the oxygen content in the arteries (gPaO2). The difference between the measured PAO2 and gPaO2 represents the oxygen deficit. While this has been used to demonstrate larger oxygen deficits in patients with lung disease, it has not been studied in patients with pleural effusions [5]. The primary objective of this study is to evaluate the differences in oxygen deficit after thoracentesis.

Patients undergoing outpatient thoracentesis were enrolled in a single academic center. Participants were excluded if they were under the age of 18, if they were too weak to form a tight seal around the mouthpiece, or if they were on supplemental oxygen.

Immediately prior to thoracentesis, gas exchange measurements were taken using the MediPines AGM100 Alveolar Gas Monitor (Medipines Corporation, Yorba Linda, CA) at sea level. Nose clips were used while the patient breathed normal tidal volumes of room air. Gas exchange parameters and oxygen deficits were collected. Normal oxygen deficit as defined by the device is 0–30, moderate oxygen deficit is 30–60, and severe oxygen deficit is greater than 60, though there may be age-related variations [6].

Patients underwent thoracentesis in the usual fashion, immediately followed by a second measurement of the above parameters. One-sample t-tests and linear and logistic regressions were performed using Stata 13 [7].

A total of 19 patients were included, from which 20 measurements were taken. One patient was not able to complete the post-procedure measurements. The median age was 67.1 years (59.7–78.1 interquartile range (IQR)), and 35.0% of the participants were female (Table 1). Nine patients (45.0%) had malignant pleural effusions, and 60% of patients had systolic or diastolic heart failure.

Table 1: Demographic and Procedural Variables.

A median of 1100mL (650 – 1400 IQR) was removed during the procedure. Prior to the procedure, the median oxygen deficit was 10.5 (3.5 – 18.0 IQR). After the thoracentesis, the oxygen deficit did not change significantly (mean difference 1.42, p=0.58, Table 2). 47.4% of patients had improvements in oxygen deficit, while 31.6% of patients had worsening of their oxygen deficits (Figure 1a).

Figure 1a: Graph of oxygen deficits of all patients before and after thoracentesis.

Table 2: Gas Exchange Variables Before and After Thoracentesis.

Comparing patients who had worsened oxygen deficit after thoracentesis (n=6) to those that had stable or improved oxygen deficit showed that these patients had a lower ejection fraction, a larger proportion with malignant effusions, and a higher proportion presenting with recurrent effusions. Among those that had worsened oxygen deficit, while the PAO2 increased from a median of 111.5 mmHg to 117.0 mmHg, the gPaO2 decreased from 102.0 mmHg to 77.0 mmHg.

Logistic regression using improved oxygen deficit as the outcome showed that patients with malignancy were more likely to have a worsened oxygen deficit after thoracentesis, but this was not statistically significant (OR 0.50, p=0.47). Linear regression using the difference in oxygen deficit before and after thoracentesis as a continuous outcome was not associated with amount of fluid removed (p=0.75, Figure 1b).

Figure 1b: Scatter plot of the changes in oxygen deficit by the total amount of pleural fluid removed.

Multiple studies have shown improvements in dyspnea scores following thoracentesis, with ongoing discussion about the mechanism of improvement [2,3]. Using a novel device to noninvasively measure the oxygen deficit, we found no statistically significant difference in gas exchange before and after thoracentesis.

In our study, 31.6% of patients had a worsened oxygen deficit after thoracentesis. In these patients, while the PAO2 increased, the gPaO2 decreased by a larger proportion, suggesting the possibility of dead space ventilation immediately after thoracentesis. All of these patients had recurrent pleural effusion, whereas 30.8% of patients with a stable or improved oxygen deficit after thoracentesis presented for their first procedure. This raises the question of whether chronic effusions with a resultant trapped lung may impact gas exchange after thoracentesis. Since trapped lung was not evaluated in our study, we are unable to draw conclusions, but future studies may be able to evaluate this further.

The timeline of improvement after thoracentesis may also be a relevant factor. In our study, we measured the oxygen deficit immediately before and after the procedure. Prior studies have shown that after 3 hours, functional reserve capacity improves by 320 mL and vital capacity improves by 120 mL [8]. When looking at more immediate assessments, however, the results are mixed. For instance, Brown et al. found no improvement in gas exchange when measuring immediately after thoracentesis [8].

Our study suggests that the improvement in dyspnea may be related to improvements in respiratory mechanics. Studies have shown improvements in lung volumes after thoracentesis [9]. Patients with chronic effusions and trapped lungs may not have improvements in gas exchange after thoracentesis due to the lack of lung expansion [10]. Since 80.0% of patients in our study presented for recurrent effusions, our lack of significant improvement in oxygen deficit may be due to inadequate lung expansion, though we did not specifically evaluate this.

Our study has been limited to those patients not on oxygen, which may preclude generalization to the larger population with pleural effusions. The rapidity with which fluid was removed during the procedure was not standardized. Given that this may impact the rate of expansion of the affected lung, this may impact the effect that the procedure has on gas exchange. Next, given the nature of the study being a pilot study, we did not have the sample size needed to adequately evaluate the patient-level factors associated with improvements in oxygen deficit.

Future studies should evaluate the correlation of the oxygen deficit with symptoms and the changes in the oxygen deficit over time. Comparisons between patients with initial and recurrent pleural effusions, as well as by diagnosis, may also help determine which patients are most likely to have improvements in gas exchange.

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