Changes In Pleural Pressure Research Articles

Estimating the change in pleural pressure using the change in central venous pressure in various clinical scenarios: a pig model study

BackgroundWe have previously reported a simple correction method for estimating pleural pressure (Ppl) using central venous pressure (CVP). However, it remains unclear whether this method is applicable to patients with varying levels of intravascular volumes and/or chest wall compliance. This study aimed to investigate the accuracy of our method under different conditions of intravascular volume and chest wall compliance.ResultsTen anesthetized and paralyzed pigs (43.2 ± 1.8 kg) were mechanically ventilated and subjected to lung injury by saline lung lavage. Each pig was subjected to three different intravascular volumes and two different intraabdominal pressures. For each condition, the changes in the esophageal pressure (ΔPes) and the estimated ΔPpl using ΔCVP (cΔCVP-derived ΔPpl) were compared to the directly measured change in pleural pressure (Δd-Ppl), which was the gold standard estimate in this study. The cΔCVP-derived ΔPpl was calculated as κ × ΔCVP, where “κ” was the ratio of the change in airway pressure to the change in CVP during the occlusion test. The means and standard deviations of the Δd-Ppl, ΔPes, and cΔCVP-derived ΔPpl for all pigs under all conditions were 7.6 ± 4.5, 7.2 ± 3.6, and 8.0 ± 4.8 cmH2O, respectively. The repeated measures correlations showed that both the ΔPes and cΔCVP-derived ΔPpl showed a strong correlation with the Δd-Ppl (ΔPes: r = 0.95, p < 0.0001; cΔCVP-derived ΔPpl: r = 0.97, p < 0.0001, respectively). In the Bland–Altman analysis to test the performance of the cΔCVP-derived ΔPpl to predict the Δd-Ppl, the ΔPes and cΔCVP-derived ΔPpl showed almost the same bias and precision (ΔPes: 0.5 and 1.7 cmH2O; cΔCVP-derived ΔPpl: − 0.3 and 1.9 cmH2O, respectively). No significant difference was found in the bias and precision depending on the intravascular volume and intraabdominal pressure in both comparisons between the ΔPes and Δd-Ppl, and cΔCVP-derived ΔPpl and Δd-Ppl.ConclusionsThe CVP method can estimate the ΔPpl with reasonable accuracy, similar to Pes measurement. The accuracy was not affected by the intravascular volume or chest wall compliance.

Expiratory Muscle Activity Counteracts Positive End-Expiratory Pressure and Is Associated with Fentanyl Dose in Patients with Acute Respiratory Distress Syndrome.

Rationale: Hypoxemia during mechanical ventilation might be worsened by expiratory muscle activity, which reduces end-expiratory lung volume through lung collapse. A proposed mechanism of benefit of neuromuscular blockade in acute respiratory distress syndrome (ARDS) is the abolition of expiratory efforts. This may contribute to the restoration of lung volumes. The prevalence of this phenomenon, however, is unknown. Objectives: To investigate the incidence and amount of end-expiratory lung impedance (EELI) increase after the administration of neuromuscular blocking agents (NMBAs), clinical factors associated with this phenomenon, its impact on regional lung ventilation, and any association with changes in pleural pressure. Methods: We included mechanically ventilated patients with ARDS monitored with electrical impedance tomography (EIT) who received NMBAs in one of two centers. We measured changes in EELI, a surrogate for end-expiratory lung volume, before and after NMBA administration. In an additional 10 patients, we investigated the characteristic signatures of expiratory muscle activity depicted by EIT and esophageal catheters simultaneously. Clinical factors associated with EELI changes were assessed. Measurements and Main Results: We included 46 patients, half of whom showed an increase in EELI of >10% of the corresponding Vt (46.2%; IQR, 23.9-60.9%). The degree of EELI increase correlated positively with fentanyl dosage and negatively with changes in end-expiratory pleural pressures. This suggests that expiratory muscle activity might exert strong counter-effects against positive end-expiratory pressure that are possibly aggravated by fentanyl. Conclusions: Administration of NMBAs during EIT monitoring revealed activity of expiratory muscles in half of patients with ARDS. The resultant increase in EELI had a dose-response relationship with fentanyl dosage. This suggests a potential side effect of fentanyl during protective ventilation.

Understanding cardiopulmonary interactions through esophageal pressure monitoring.

Esophageal pressure is the closest estimate of pleural pressure. Changes in esophageal pressure reflect changes in intrathoracic pressure and affect transpulmonary pressure, both of which have multiple effects on right and left ventricular performance. During passive breathing, increasing esophageal pressure is associated with lower venous return and higher right ventricular afterload and lower left ventricular afterload and oxygen consumption. In spontaneously breathing patients, negative pleural pressure swings increase venous return, while right heart afterload increases as in passive conditions; for the left ventricle, end-diastolic pressure is increased potentially favoring lung edema. Esophageal pressure monitoring represents a simple bedside method to estimate changes in pleural pressure and can advance our understanding of the cardiovascular performance of critically ill patients undergoing passive or assisted ventilation and guide physiologically personalized treatments.

An approach to study recruitment/derecruitment dynamics in a patient-specific computational model of an injured human lung.

We present a new approach for physics-based computational modeling of diseased human lungs. Our main object is the development of a model that takes the novel step of incorporating the dynamics of airway recruitment/derecruitment into an anatomically accurate, spatially resolved model of respiratory system mechanics, and the relation of these dynamics to airway dimensions and the biophysical properties of the lining fluid. The importance of our approach is that it potentially allows for more accurate predictions of where mechanical stress foci arise in the lungs, since it is at these locations that injury is thought to arise and propagate from. We match the model to data from a patient with acute respiratory distress syndrome (ARDS) to demonstrate the potential of the model for revealing the underlying derangements in ARDS in a patient-specific manner. To achieve this, the specific geometry of the lung and its heterogeneous pattern of injury are extracted from medical CT images. The mechanical behavior of the model is tailored to the patient's respiratory mechanics using measured ventilation data. In retrospective simulations of various clinically performed, pressure-driven ventilation profiles, the model adequately reproduces clinical quantities measured in the patient such as tidal volume and change in pleural pressure. The model also exhibits physiologically reasonable lung recruitment dynamics and has the spatial resolution to allow the study of local mechanical quantities such as alveolar strains. This modeling approach advances our ability to perform patient-specific studies in silico, opening the way to personalized therapies that will optimize patient outcomes.

The impact of spontaneous cough on pleural pressure changes during therapeutic thoracentesis

Cough during therapeutic thoracentesis (TT) is considered an adverse effect. The study was aimed to evaluate the relationship between cough during TT and pleural pressure (Ppl) changes (∆P). Instantaneous Ppl was measured after withdrawal of predetermined volumes of pleural fluid. Fluid withdrawal (FW) and Ppl measurement (PplM) periods were analyzed separately using the two sample Kolmogorov–Smirnov test and the nonparametric skew to assess differences between ∆P distributions in periods with and without cough. The study involved 59 patients, median age 66 years, median withdrawn fluid volume 1800 mL (1330 ÷ 2400 mL). In total, 1265 cough episodes were recorded in 52 patients, in 24% of FW and 19% of PplM periods, respectively. Cough was associated with significant changes in ∆P distribution (p < 0.001), decreasing the left tail of ∆P distribution for FW periods (the skew = − 0.033 vs. − 0.182) and increasing the right tail for PplM periods (the skew = 0.182 vs. 0.088). Although cough was more frequent in 46 patients with normal pleural elastance (p < 0.0001), it was associated with significantly higher ∆P in patients with elevated elastance (median Ppl increase 2.9 vs. 0.2 cmH2O, respectively). Cough during TT is associated with small but beneficial trend in Ppl changes, particularly in patients with elevated pleural elastance, and should not be considered solely as an adverse event.

Effect of intrabronchial administration of autologous adipose-derived mesenchymal stem cells on severe equine asthma

BackgroundSevere equine asthma (SEA) is a common chronic respiratory disease and a significant health and well-being problem in horses. Current therapeutic strategies improve pulmonary function and clinical signs in some horses, but in the long-term, return to full athletic function appears to be rare. The aim of this study was to assess the safety and the effect of intrabronchial administration of adipose-derived mesenchymal stem cells (AD-MSC) on pulmonary inflammatory and clinical parameters in horses with SEA.MethodsThis was a randomized controlled trial. Twenty adult horses diagnosed with SEA were randomly divided into two groups (n = 10), and treated either with a single intrabronchial application of autologous AD-MSC or oral dexamethasone for three weeks. A targeted clinical examination with determination of clinical score, maximal change in pleural pressure during the breathing cycle, and an endoscopic examination of the airways were performed at baseline and three weeks after treatment. Bronchoalveolar lavage fluid was analyzed cytologically, and IL-1β, IL-4, IL-8, IL-17, TNFα and IFNγ mRNA and protein concentrations were measured at baseline and three weeks. The horses were then monitored over one year for recurrence of SEA. A non-inferiority analysis and a linear mixed-effects model were performed to assess differences between treatments.ResultsThe non-inferiority of AD-MSC treatment was not established. However, AD-MSC administration significantly ameliorated the clinical score (P = 0.01), decreased the expression of IL-17 mRNA (P = 0.05) and IL-1β (P ≤ 0.001), IL-4 (P ≤ 0.001), TNFα (P = 0.02) protein levels, and had a positive long-term effect on SEA-associated clinical signs (P = 0.02).ConclusionsIntrabronchial administration of AD-MSC had limited short-term anti-inflammatory effects but improved the clinical signs of SEA at one year.

Impact of therapeutic thoracentesis and pleural pressure changes on breathing pattern, dyspnea, lung function, and arterial blood gases.

Therapeutic thoracentesis is highly effective in providing symptomatic improvement in patients with large volume pleural effusion (PE). However, some physiological effects of pleural fluid (PF) withdrawal are still not fully elucidated. The study aimed to evaluate alterations in the breathing pattern, pulmonary function, and arterial blood gases (ABG) in relation to both withdrawn PF volume and pleural pressure (Ppl) changes in patients undergoing therapeutic thoracentesis. This prospective, observational, cross‑sectional study included 37 patients with large volume PE. Respiratory rate (RR), dyspnea, pulmonary function, and ABG were assessed before the thoracentesis, at the termination of the PF withdrawal and 1, 3, and 24 hours after the procedure. The volume of PF drained, Ppl, and tidal volume (TV) were monitored during the thoracentesis. Thoracentesis resulted in a transient but significant increase in RR directly after the procedure, and a transient decrease, followed by subsequent increase in TV. There was a significant and constant increase in forced vital capacity up to 24 hours after thoracentesis (P = 0.001). Oxygen partial pressure (PaO2) significantly improved directly after PF withdrawal (P = 0.01) and returned to baseline values after 24 hours. Thoracentesis was invariably associated with a significant increase in the amplitude of Ppl (Ppl_ampl) changes during the respiratory cycle (P <0.001). Therapeutic thoracentesis results in a modest improvement in pulmonary function, tran-sient increase in PaO2 and increase in Ppl_ampl. The improvement in pulmonary function and ABG is closely related to the volume of PF drained and pleural elastance. The increase in Ppl_ampl probably represents a more efficient work of the respiratory muscles.

Effect of Trendelenburg position during prone ventilation in fifteen COVID-19 patients. Observational study

Background Prone position ventilation has shown to improve oxygenation and mortality in severe ARDS. The data of prone position ventilation during severe ARDS secondary to COVID-19 have shown similar benefit in oxygenation and mortality. Usually, patient placed in prone position are placed flat or in reverse Trendelenburg positioning to decrease risk of aspiration and abdominal girth compressing the chest. To date, no studies are available to compare the effects of positioning the bed in different angles during the prone position ventilation. Methods An observational study in fifteen patients with severe ARDS secondary to COVID-19 who were placed in the prone position for the first time. All the patients were sedated and chemically paralyzed with no spontaneous effort. All patients were ventilated with the pressure-controlled mode with set PEEP according to the pressure-volume curves. Five patients had esophageal balloon manometry to estimate pleural pressures and trans-pulmonary pressures. Patients were initially placed in reverse Trendelenburg position and later in Trendelenburg position. Tidal volume and respiratory compliance were observed for 30 minutes after bed positioning has been achieved. Tidal volume and total respiratory compliance in both Trendelenburg and reverse Trendelenburg position were compared. Ventilator settings were not changed during the observation. No patients were suspected of increased intra-cranial or intra-ocular pressures. T-test was done to compare the values. Results Tidal volume significantly increased by 80.26 ± 23.4 ml/breath (95% CI 37.7 - 122.9) from 391.3 ± 52.7 to 471.6 ± 60.9 (20.5%) P 0.001. The respiratory system compliance significantly increased by 4.9 ml/cmH2O (95% CI 1.4 - 8.4) from 34.6 ± 4.7 to 39.5 ± 4.6 (14%) P 0.001. Of the five patients with esophageal balloon, the lung compliance significantly increased by 16.7 ml/cmH2O (95% CI 12.8 – 20.6) from 66.6 ± 1.7 to 83.3 ± 3.3 (25%) P 0.001. The chest wall compliance had small but non-significant increase by 1.5 ml/cmH2O (95% CI -1.3 – 4.3) from 65 ± 1.4 to 66.5 ± 2.3 (2%) P 0.085. Conclusion In this study, statistically significant increase in tidal volume, lung and respiratory system compliance were observed in patients placed in the Trendelenburg position during prone position ventilation. The results reflect the effect of body positioning during prone position ventilation. These effects may be the reflection of altered ventilation distribution throughout the lungs and change in pleural pressure as well as trans-pulmonary pressure during body positioning. More studies need to be done to confirm and examine this phenomenon. Precautions should be taken as this maneuver can increase the intra-cranial and intra-ocular pressures. Keywords: COVID-19, Trendelenburg, Reverse Trendelenburg, ARDS

PPV May Be a Starting Point to Achieve Circulatory Protective Mechanical Ventilation.

Pulse pressure variation (PPV) is a mandatory index for hemodynamic monitoring during mechanical ventilation. The changes in pleural pressure (Ppl) and transpulmonary pressure (PL) caused by mechanical ventilation are the basis for PPV and lead to the effect of blood flow. If the state of hypovolemia exists, the effect of the increased Ppl during mechanical ventilation on the right ventricular preload will mainly affect the cardiac output, resulting in a positive PPV. However, PL is more influenced by the change in alveolar pressure, which produces an increase in right heart overload, resulting in high PPV. In particular, if spontaneous breathing is strong, the transvascular pressure will be extremely high, which may lead to the promotion of alveolar flooding and increased RV flow. Asynchronous breathing and mediastinal swing may damage the pulmonary circulation and right heart function. Therefore, according to the principle of PPV, a high PPV can be incorporated into the whole respiratory treatment process to monitor the mechanical ventilation cycle damage/protection regardless of the controlled ventilation or spontaneous breathing. Through the monitoring of PPV, the circulation-protective ventilation can be guided at bedside in real time by PPV.

Estimation of change in pleural pressure in assisted and unassisted spontaneous breathing pediatric patients using fluctuation of central venous pressure: A preliminary study.

It is important to evaluate the size of respiratory effort to prevent patient self-inflicted lung injury and ventilator-induced diaphragmatic dysfunction. Esophageal pressure (Pes) measurement is the gold standard for estimating respiratory effort, but it is complicated by technical issues. We previously reported that a change in pleural pressure (ΔPpl) could be estimated without measuring Pes using change in CVP (ΔCVP) that has been adjusted with a simple correction among mechanically ventilated, paralyzed pediatric patients. This study aimed to determine whether our method can be used to estimate ΔPpl in assisted and unassisted spontaneous breathing patients during mechanical ventilation. The study included hemodynamically stable children (aged <18 years) who were mechanically ventilated, had spontaneous breathing, and had a central venous catheter and esophageal balloon catheter in place. We measured the change in Pes (ΔPes), ΔCVP, and ΔPpl that was calculated using a corrected ΔCVP (cΔCVP-derived ΔPpl) under three pressure support levels (10, 5, and 0 cmH2O). The cΔCVP-derived ΔPpl value was calculated as follows: cΔCVP-derived ΔPpl = k × ΔCVP, where k was the ratio of the change in airway pressure (ΔPaw) to the ΔCVP during airway occlusion test. Of the 14 patients enrolled in the study, 6 were excluded because correct positioning of the esophageal balloon could not be confirmed, leaving eight patients for analysis (mean age, 4.8 months). Three variables that reflected ΔPpl (ΔPes, ΔCVP, and cΔCVP-derived ΔPpl) were measured and yielded the following results: -6.7 ± 4.8, - -2.6 ± 1.4, and - -7.3 ± 4.5 cmH2O, respectively. The repeated measures correlation between cΔCVP-derived ΔPpl and ΔPes showed that cΔCVP-derived ΔPpl had good correlation with ΔPes (r = 0.84, p< 0.0001). ΔPpl can be estimated reasonably accurately by ΔCVP using our method in assisted and unassisted spontaneous breathing children during mechanical ventilation.

Determinants of the esophageal-pleural pressure relationship in humans.

Esophageal pressure has been suggested as adequate surrogate of the pleural pressure. We investigate after lung surgery the determinants of the esophageal and intrathoracic pressures and their differences. The esophageal pressure (through esophageal balloon) and the intrathoracic/pleural pressure (through the chest tube on the surgery side) were measured after surgery in 28 patients immediately after lobectomy or wedge resection. Measurements were made in the nondependent lateral position (without or with ventilation of the operated lung) and in the supine position. In the lateral position with the nondependent lung, collapsed or ventilated, the differences between esophageal and pleural pressure amounted to 4.4 ± 1.6 and 5.1 ± 1.7 cmH2O. In the supine position, the difference amounted to 7.3 ± 2.8 cmH2O. In the supine position, the estimated compressive forces on the mediastinum were 10.5 ± 3.1 cmH2O and on the iso-gravitational pleural plane 3.2 ± 1.8 cmH2O. A simple model describing the roles of chest, lung, and pneumothorax volume matching on the pleural pressure genesis was developed; modeled pleural pressure = 1.0057 × measured pleural pressure + 0.6592 (r2 = 0.8). Whatever the position and the ventilator settings, the esophageal pressure changed in a 1:1 ratio with the changes in pleural pressure. Consequently, chest wall elastance (Ecw) measured by intrathoracic (Ecw = ΔPpl/tidal volume) or esophageal pressure (Ecw = ΔPes/tidal volume) was identical in all the positions we tested. We conclude that esophageal and pleural pressures may be largely different depending on body position (gravitational forces) and lung-chest wall volume matching. Their changes, however, are identical.NEW & NOTEWORTHY Esophageal and pleural pressure changes occur at a 1:1 ratio, fully justifying the use of esophageal pressure to compute the chest wall elastance and the changes in pleural pressure and in lung stress. The absolute value of esophageal and pleural pressures may be largely different, depending on the body position (gravitational forces) and the lung-chest wall volume matching. Therefore, the absolute value of esophageal pressure should not be used as a surrogate of pleural pressure.

Assessment of Diaphragm Function and Pleural Pressures During Thoracentesis

This prospective observational study reports on diaphragm excursion, velocity of diaphragm contraction, and changes in pleural pressure that occur with thoracentesis. Twenty-eight patients with pleural effusion underwent therapeutic thoracentesis. Diaphragm excursion and velocity of diaphragm contraction were measured with M-mode ultrasonography of the affected hemidiaphragm. Pleural pressure was measured at each aliquot of 250mL of fluid removal. Fluid removal was continued until no more fluid could be withdrawn, unless there was evidence of nonexpandable lung defined as a pleural elastance greater > 14.5cm H2O/L and/or ipsilateral anterior chest discomfort. Twenty-three patients had expandable lung, and five patients had nonexpandable lung. Velocity of diaphragm contraction (mean ± SD) increased from 1.5 ± 0.4cm/s to 2.8 ± 0.4cm/s pre-thoracentesis and post-thoracentesis, respectively (CI, 0.93-1.61; P< .001) in subjects with expandable lung. Velocity of diaphragm contraction (mean ± SD) increased from 2.0 ± 0.4cm/s to 2.3 ± 0.4cm/s pre-thoracentesis and post-thoracentesis (P= .45) in subjects with nonexpandable lung. Diaphragm excursion was significantly increased in subjects with expandable lung at the end of thoracentesis; diaphragm excursion did not increase to a significant extent in patients with nonexpandable lung. The velocity of diaphragm contraction and diaphragm excursion increased in association with fluid removal with thoracentesis in patients with expandable lung, whereas it did not significantly change in patients with nonexpandable lung. This may derive from improvement in loading conditions of the diaphragm in patients with expandable lung related to its preload and length-tension characteristics.

A novel method for transpulmonary pressure estimation using fluctuation of central venous pressure.

The objective of the study is to develop a correction method for estimating the change in pleural pressure (ΔPpl) and plateau transpulmonary pressure (PL) by using the change in central venous pressure (ΔCVP). Seven children (aged < 15years) with acute respiratory failure (PaO2/FIO2 < 300mmHg), who were paralyzed and mechanically ventilated with a PEEP of < 10 cmH2O and had central venous catheters and esophageal balloon catheters placed for clinical purposes, were enrolled prospectively. We compared change in esophageal pressure (ΔPes), ΔCVP, and ΔPpl calculated using a corrected ΔCVP (cΔCVP-derived ΔPpl). cΔCVP-derived ΔPpl was calculated as κ × ΔCVP, where κ was the ratio of the change in airway pressure (ΔPaw) to ΔCVP during the occlusion test. cΔCVP-derived ΔPpl correlated better than ΔCVP with ΔPes (R2 = 0.48, p = 0.08 vs. R2 = 0.14, p = 0.4) with lesser bias and precision in Bland-Altman analysis. The plateau PL calculated using the cΔCVP-derived ΔPpl (17.6 ± 2.6 cmH2O) correlated well with the ΔPes-derived plateau PL (18.1 ± 2.3 cmH2O) (R2 = 0.90, p = 0.001). Our correction method can estimate ΔPpl and plateau PL from ΔCVP with a reasonable accuracy in paralyzed and mechanically ventilated pediatric patients with respiratory failure.

Physiologic Basis of Symptoms in Pleural Disease.

Pleural effusions are commonly encountered and have a significant impact on the respiratory system. The reported effect of thoracentesis on physiologic parameters including oxygenation, lung volumes, and respiratory mechanics is variable likely owing to studies with a small, heterogeneous population of patients.Most patients who are short of breath from pleural effusion experience relief following drainage due to improvement in the length-tension relationship of the respiratory muscles. An observed increase in oxygenation following thoracentesis is likely due to improved ventilation and perfusion matching. Recent advances in methods of measuring pleural pressure provide a greater understanding of the impact of pleural effusion on pleural pressure and changes in pleural pressure with thoracentesis; however, there has been no demonstrated benefit of routine monitoring of pleural pressure to reduce complications from thoracentesis. Manometry does allow for the identification of patients with unexpandable lung which is useful when determining options for pleural palliation. The following article will review the pathophysiological effects of pleural effusion and thoracentesis.

Heart-Lung interaction in spontaneous breathing subjects: the basics

Heart-lung interactions occur primarily because of two components of lung inflation, changes in pleural pressure and changes in transpulmonary pressure. Of these, changes in pleural pressure dominate during spontaneous breathing. Because the heart is surrounded by pleural pressure, during inspiration the environment of the heart falls relative to the rest of the body. This alters inflow into the right heart and outflow from the left heart. Alterations in transpulmonary pressure can alter the outflow from the right heart and the inflow to the left heart. These interactions are modified by the cardiac and respiratory frequency, ventricular function and magnitude of the respiratory efforts.

Physiology-guided management of hemodynamics in acute respiratory distress syndrome.

Skillfully implemented mechanical ventilation (MV) may prove of immense benefit in restoring physiologic homeostasis. However, since hemodynamic instability is a primary factor influencing mortality in acute respiratory distress syndrome (ARDS), clinicians should be vigilant regarding the potentially deleterious effects of MV on right ventricular (RV) function and pulmonary vascular mechanics (PVM). During both spontaneous and positive pressure MV (PPMV), tidal changes in pleural pressure (PPL), transpulmonary pressure (PTP, the difference between alveolar pressure and PPL), and lung volume influence key components of hemodynamics: preload, afterload, heart rate, and myocardial contractility. Acute cor pulmonale (ACP), which occurs in 20-25% of ARDS cases, emerges from negative effects of lung pathology and inappropriate changes in PPL and PTP on the pulmonary microcirculation during PPMV. Functional, minimally invasive hemodynamic monitoring for tracking cardiac performance and output adequacy is integral to effective care. In this review we describe a physiology-based approach to the management of hemodynamics in the setting of ARDS: avoiding excessive cardiac demand, regulating fluid balance, optimizing heart rate, and keeping focus on the pulmonary circuit as cornerstones of effective hemodynamic management for patients in all forms of respiratory failure.

Changes of pleural pressure after thoracic surgery.

The negative pressure of the pleural cavity is critical to maintain lung expansion. However, the actual values of pleural pressure according to the phase of respiration after various types of pulmonary resection have not been well reported. The aim of this study was to measure the pleural pressure directly and to compare the results according to the extent of pulmonary resection. We manufactured a high-resolution digital manometer with which pleural pressure can be measured directly. A total of 43 patients who underwent thoracic surgery (lobectomy in 23, minimal resections in 20) were enrolled. The maximum, minimum, and mean pleural pressure was recorded during normal quiet breathing, forced breathing, and coughing, separately. During normal quiet breathing, the average values of pleural pressure at end inspiration, end expiration, and the mean pleural pressure were -17.7, -7.0 and -11.2 cmH2O in lobectomy group, and -14.3, -4.6, -8.3 cmH2O in the minimal/no-resection group, respectively. The mean pleural pressure was significantly lower in lobectomy group compared to the minimal/no-resection group (P=0.026). During forced respiration, the same values were -44.0, -4.2 and -18.9 cmH2O in the lobectomy group, and -29.8, -0.1 and -12.7 cmH2O in the minimal/no-resection group. All of the pleural pressure values in lobectomy group were significantly lower compared to minimal/no-resection group (P=0.029, P=0.015, P=0.019, respectively). The maximal pressures during coughing were not statistically different between the two groups (38.4 vs. 34.4 cmH2O, P=0.687). We reported the actual pleural pressure changes according to the phase of respiration and type of surgery using a digital manometer. In lobectomy patients, the pleural pressure was highly negative compared to the minimal/no-resection group, especially during deep inspiration.

Pleural manometry in patients with pleural diseases - the usefulness in clinical practice.

Although pleural manometry is a relatively simple medical procedure it is only occasionally used to follow pleural pressure (Ppl) changes during a therapeutic thoracentesis and pneumothorax drainage. As some studies showed that pleural pressure monitoring might be associated with significant advantages, pleural manometry has been increasingly evaluated in the last decade. The major clinical applications of pleural pressure measurements include: the prevention of complications associated with large volume thoracentesis, diagnosis and differentiation between various types of an unexpandable lung and a possible prediction of the efficacy of chest tube drainage in patients with spontaneous pneumothorax. It is well known that the therapeutic thoracentesis might be complicated by cough, chest discomfort, and rarely, by a life threatening condition called reexpansion pulmonary edema (RPE). The serious adverse events of thoracentesis are related to pleural pressure drop rather than to the volume of removed pleural effusion. The use of pleural manometry during pleural fluid withdrawal enables the evaluation of the relationship between withdrawn pleural fluid volume, pleural pressure changes and procedure related complications. Pleural pressure measurement is also an important tool to study the different mechanism of pneumothorax complicating the thoracentesis. Pleural manometry is critical for measurement of pleural elastance, diagnosis of an unexpandable lung and differentiation between trapped lung and lung entrapment. This usually has significant clinical implications in terms of further management of patients with pleural effusion. The paper is a comprehensive review presenting different aspects of pleural pressure measurement in clinical practice.

Pleural manometry-historical background, rationale for use and methods of measurement.

Subatmospheric pleural pressure (Ppl), which is approximately -3 to -5 cmH2O at functional residual capacity (FRC) makes pleura a unique organ in the human body. The negative Ppl is critical for maintaining the lungs in a properly inflated state and for proper blood circulation within the thorax. Significant and sudden pleural pressure changes associated with major pleural pathologies, as well as therapeutic interventions may be associated with life-threatening complications. The pleural pressure may show two different values depending on the measurement method applied. These are called pleural liquid pressure and pleural surface pressure. It should also be realized that there are significant differences in pleural pressure distribution in pneumothorax and pleural effusion. In pneumothorax, the pressure is the same throughout the pleural space, while in pleural effusion there is a vertical gradient of approximately 1 cm H2O/cm in the pleural pressure associated with the hydrostatic pressure of the fluid column. Currently, two main methods of pleural pressure measurement are used: simple water manometers and electronic systems. The water manometers are conceptually simple, cheap and user-friendly but they only allow the estimation of the mean values of pleural pressure. The electronic systems for pleural pressure measurement are based on pressure transducers. Their major advantages include precise measurements of instantaneous pleural pressure and the ability to display and to store a large amount of data. The paper presents principles and details of pleural pressure measurement as well as the rationale for its use.

Correlation of Changes in Pleural Pressure With Velocity of Diaphragmatic Contraction Measured With Ultrasonography During Thoracentesis

Correlation of Changes in Pleural Pressure With Velocity of Diaphragmatic Contraction Measured With Ultrasonography During Thoracentesis