Pleural manometry enables the assessment of physiological abnormalities of lung mechanics associated with pleural effusion. Applying pleural manometry, we found small pleural pressure curve oscillations resembling the pulse tracing line. The aim of our study was to characterize the oscillations of pleural pressure curve (termed here as the pleural pressure pulse, PPP) and to establish their origin and potential significance. This was an observational cross-sectional study in adult patients with pleural effusion who underwent thoracentesis with pleural manometry. The pleural pressure curves recorded prior to and during fluid withdrawal were analyzed. The presence of PPP was assessed in relation to the withdrawn pleural fluid volume, lung expandability, vital and echocardiographic parameters, and pulmonary function testing. A dedicated device was developed to compare the PPP to the pulse rate. Fifty-four patients (32 women) median age 66.5 (IQR 58.5-78.7) years were included. Well visible and poorly visible pressure waves were detected in 48% and 35% of the patients, respectively. The frequency of PPP was fully concordant with the pulse rate and the peaks of the oscillations reflected the period of heart diastole. PPP was more visible in patients with a slower respiratory rate (p = 0.008), a larger amount of pleural effusion, and was associated with a better heart systolic function assessed by echocardiography (p < 0.05). This study describes a PPP, a new pleural phenomenon related to the cyclic changes in the heart chambers volume. Although the importance of PPP remains largely unknown, we hypothesize that it could be related to lung atelectasis or lower lung and visceral pleura compliance.

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.

Tension hydrothorax is a rare complication of pneumonectomy for pleural mesothelioma and an exceptionally rare cause of heart failure. We describe a patient who had undergone extrapleural pneumonectomy, chemotherapy, and radiation for pleural mesothelioma and who developed heart failure symptoms within months of the completion of treatment. Investigation showed a massive left pleural effusion resulting in tension hydrothorax, mediastinal shift, and evidence of right heart failure with constrictive physiology and low cardiac output. Therapeutic thoracentesis resulted in increase in cardiac output and symptomatic improvement.

The close relationship between pleural space and pericardial space and the dependence of their pressure kinetics are well known. This study evaluates the effects of increased intra pleural pressure due to pleural effusion on cardiovascular system.

Forty patients above the age of 12 who had massive unilateral/bilateral pleural effusion due to non-cardiac etiology were included in the study. Therapeutic thoracocentesis was done for massive pleural effusion. The echocardiographic parameters measured before and after thoracocentesis were compared.

Mean age of the patients 46.6 years. Out of 40 patients 8 were females (20%). 7 patients had right atrial collapse on echo. 85% of patients had significant flow velocity changes across both tricuspid valve and mitral valve during phases of respiration.11 patients (47.82%) had IVC compressibility of <50% during inspiration. Mean flow velocity respiratory variations across tricuspid valve before thoracocentesis and after thoracocentesis E 45.04 ± 10.3,32 ± 11.3% (p value <0.001), A 53.71 ± 28%, 32.08 ± 12.5% (p < 0.001) across mitral valve E 32.30 ± 12%, 19.78 ± 7.8% (p < 0.001), A 26 ± 11.2%, 21 ± 9.3% (p 0.006) across pulmonary artery 42.63 ± 31.3%, 17.70 ± 6.2% (p < 0.001), across aorta 21.57 ± 11.4%, 14.08 ± 7.6% (p < 0.001).

Large pleural effusion has a potential to cause adverse impact on the cardiovascular hemodynamics, which could manifest as tamponade physiology. Altered cardiac hemodynamics could be an important contributor in the mechanism of dyspnea in patients with large pleural effusion.

Despite 50-60% of intensive care patients demonstrating evidence of pleural effusions, there has been little emphasis placed on the role of effusions in the aetiology of weaning failure. Critical illness and mechanical ventilation lead to multiple perturbations of the normal physiological processes regulating pleural fluid homeostasis, and consequently, failure of normal pleural function occurs. Effusions can lead to deleterious effects on respiratory mechanics and gas exchange, and when extensive, may lead to haemodynamic compromise. The widespread availability of bedside ultrasound has not only facilitated earlier detection of pleural effusions but also safer fluid sampling and drainage. In the majority of patients, pleural drainage leads to improvements in lung function, with data from spontaneously breathing individuals demonstrating a consistent symptomatic improvement, while a meta-analysis in critically ill patients shows an improvement in oxygenation. The effects on respiratory mechanics are less clear, possibly reflecting heterogeneity of underlying pathology. Limited data on clinical outcome from pleural fluid drainage exist; however, it appears to be a safe procedure with a low risk of major complications. The current level of evidence would support a clinical trial to determine whether the systematic detection and drainage of pleural effusions improve clinical outcomes.

No consensus exists as to the benefit of pleural drainage in mechanically ventilated patients with conflicting data concerning the effects on gas exchange. We determined the effects on gas exchange over a 48-hour period of draining, by thoracocentesis, large volume pleural effusions.

A total of 15 thoracocenteses were performed in 10 mechanically ventilated patients with ultrasound evidence of pleural effusions predicted to be greater than 800 mL in volume. Gas exchange, mixed expired CO2, dynamic lung compliance, ventilator settings before procedure and at 30 min, 4, 8, 24 and 48 h were determined. Data were analysed using paired t-tests and repeated-measure anova.

Following thoracocentesis there was a 40% increase in the PaO(2) from 82.0 +/- 10.6 mm Hg to 115.2 +/- 31.1 mm Hg (P < 0.05) with a 34% increase in the P:F ratio from 168.9 +/- 55.9 mm Hg to 237.8 +/- 72.6 mm Hg (P < 0.05). These effects were maintained for a period of 48 h. There was a correlation between the amount of fluid drained and the effects on oxygenation with an increase in the PaO(2) of 4 mm Hg for each 100 mL of pleural fluid drained. A-a gradients continued to improve over the course of the study together with a reduction in the dead space fraction and improved dynamic compliance.

Drainage of large pleural effusions in mechanically ventilated patients leads to a significant improvement in gas exchange, and these effects are sustained for 48 h after the procedure supporting a role in the discontinuation of mechanical ventilation.

A 16-month-old, female German shepherd dog was presented with severe bicavitary effusions. A diaphragmatic hernia was diagnosed by thoracic radiography. An echocardiogram performed prior to surgical repair of the hernia revealed signs of cardiac tamponade, with right atrial collapse, in the absence of pericardial effusion. Right atrial collapse was presumed to be secondary to severe pleural effusion. At surgery, no pericardial disease was identified. Surgical correction of the diaphragmatic hernia resulted in resolution of the pleural and peritoneal effusions. Follow-up echocardiography demonstrated resolution of the signs of cardiac tamponade.

We report on two patients who developed large left-sided pleural effusions in association with hemodynamic compromise. In both cases transthoracic echocardiography demonstrated left ventricular diastolic collapse confirming our clinical suspicion of cardiac tamponade. Large-volume thoracentesis in the first case and thoracotomy with drainage of the pleural collection in the second case resulted in immediate hemodynamic improvement. Our report shows that large pleural effusions can result in impaired cardiac filling and a tamponade-like physiology. Thoracentesis in this setting can lead to rapid improvement of the hemodynamic profile.

Pleural effusion(s) can increase the pressure of an otherwise insignificant pericardial effusion to a degree that can result in cardiac tamponade. The case histories presented here illustrate the importance of recognizing this phenomenon and altering our treatment algorithm to drain the pleural effusions instead of the pericardial collections.

To investigate the cardiorespiratory effects of graded bilateral pleural effusions in the anesthetized pig.

Prospective, randomized, controlled, laboratory study.

Animal laboratory.

Eleven male Yorkshire pigs.

Animals were anesthetized using inhaled isoflurane. Orotracheal intubation was followed by mechanical ventilation. Bilateral chest tubes were inserted, and graded increasing pleural effusions were created using saline of 0, 20, 40, and 80 mL/kg, divided equally between each side. At each pleural volume, intravascular volume was randomly altered (by phlebotomy or transfusion of colloid) to normal (unchanged), low (decreased by 10 mL/kg), or high (increased by 10 mL/kg).

Hemodynamic parameters, intrapleural pressures, hemoglobin, and blood gases were measured. At the lowest volume of pleural fluid, PaO2 was reduced by approximately 50% vs. baseline, whereas systemic hemodynamics were unchanged. PaO2 was reduced in a dose-dependent fashion as pleural volume increased but was not affected by alterations in intravascular volume. Intrapulmonary shunt was increased both by intrapleural volume in a dose-dependent fashion and by increases in intravascular volume at high levels of pleural volume. Cardiac output and systemic mean arterial pressure increased with elevated intravascular volume but were not influenced by lower levels of intrapleural volume. Mean pulmonary arterial pressure, central venous pressure, and pulmonary artery occlusion pressure were increased by elevations in both intrapleural volume and intravascular volume. Intrapleural pressure and pulmonary vascular resistance were related to intrapleural volume only.

Hypoxemia occurs as an early event in acute bilateral pleural effusions and precedes hemodynamic decompensation. Oxygenation is independent of intravascular filling pressures, but hemodynamics are preserved with elevated filling pressures. Clinical studies should be undertaken to examine the risks/benefits of careful removal of pleural fluid in patients with pleural effusions, when oxygenation is impaired during mechanical ventilation.