Functions of the Respiratory System
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2020
The lungs lie within the thorax, covered by the visceral pleura and separated from the parietal pleura on the inside of the chest wall by the (potential) intrapleural space. The diaphragm separates the lungs from the abdominal contents. The elastic forces of the lung and the chest wall are in equilibrium; the tendency of the lung is to collapse (contract down), and the tendency of the chest wall is to expand (muscle tone in the diaphragm also contributes to this), resulting in a negative intrapleural pressure (Figure 15.1). Therefore, the transmural pressure gradient that tends to distend the alveolar wall (called the transpulmonary pressure) increases. Transpulmonary pressure is the difference between alveolar and intrapleural pressures. At the end of a normal expiration, the two opposing forces balance and the lung volume is at FRC.
Respiratory physiology
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2015
The lungs lie within the thorax, covered by the visceral pleura and separated from the parietal pleura on the inside of the chest wall by the (potential) intrapleural space. The diaphragm separates the lungs from the abdominal contents. The elastic forces of the lung and the chest wall are in equilibrium; the tendency of the lung is to contract down and the tendency of the chest wall is to expand (muscle tone in the diaphragm also contributes to this), resulting in a negative intrapleural pressure (Figure 3.1). Therefore, the transmural pressure gradient that tends to distend the alveolar wall (called the transpulmonary pressure) increases. Transpulmonary pressure is the difference between alveolar and intrapleural pressures. At the end of a normal expiration, the two opposing forces balance and the lung volume is at FRC.
Lung Compliance
Lara Wijayasiri, Kate McCombe, Paul Hatton, David Bogod in The Primary FRCA Structured Oral Examination Study Guide 1, 2017
Draw a pressure–volume curve of the lung. Lung compliance is best described using pressure–volume curves of the lungs under static conditions (i.e. when there is no gas flow and the respiratory muscles are relaxed). Under these conditions the transpulmonary pressure reflects in magnitude the elastic recoil pressure of the lungs. The slope of the pressure–volume curve equates to lung compliance. Normal lung compliance is 200 mL/cm H2O.In neonatal respiratory distress syndrome, lung compliance is greatly reduced due to insufficient surfactant.Conversely, in hypothetical saline-filled lungs, compliance is greatly increased as the lack of an air–fluid interface means that no surface tension exists.
Controversies when using mechanical ventilation in obese patients with and without acute distress respiratory syndrome
Published in Expert Review of Respiratory Medicine, 2019
Giulia Bonatti, Chiara Robba, Lorenzo Ball, Pedro Leme Silva, Patricia Rieken Macêdo Rocco, Paolo Pelosi
A schematic representation of the overall changes in regional transpulmonary pressures, with potential effects on alveolar recruitment and overdistension, at different tidal volumes and PEEP are shown in Figure 1. Obese patients with ARDS should be mechanically ventilated with low VT. However, they may require higher PEEP levels, in the range of 12–14 cmH2O [69]. In obese patients with increased pleural pressure, high peak airway pressures (>30 cmH2O) can be applied without lung overdistension, since transpulmonary pressures (<25 cmH2O) at end-inspiration have been considered safe. Transpulmonary pressure at end-expiration is higher in obese compared to non-obese patients, and especially so in those with ARDS. Furthermore, low-to-negative values of transpulmonary pressure have been shown to predict lung collapse and intratidal recruitment/derecruitment in obese patients [70]. This is in line with recent findings suggesting that optimisation of PEEP is not achieved by using conventional mechanical parameters in ARDS patients, particularly in those cases with high intra-abdominal pressure and obesity [71]. Overall, these recent studies support the importance of transpulmonary pressure monitoring in obese patients with ARDS. Moreover, unlike in non-obese patients with ARDS, driving pressure was not associated with mortality in the obese [72] (Table 1).
Does the antisecretory peptide AF-16 reduce lung oedema in experimental ARDS?
Published in Upsala Journal of Medical Sciences, 2019
Annelie Barrueta Tenhunen, Fabrizia Massaro, Hans Arne Hansson, Ricardo Feinstein, Anders Larsson, Anders Larsson, Gaetano Perchiazzi
The PV relation was measured by delivering eight monotonically decreasing lung volumes, from PAW 25 cmH2O to 0 cmH2O over PEEP. Each volume was delivered during steady-state ventilation, in volume control mode, and followed by an inspiratory hold manoeuvre (IHM) and an expiratory hold manoeuvre. Before the beginning of the decreasing ramp, in order to standardise the history of volume, we performed a recruitment manoeuvre applying a PAW of 40 cmH2O for 40 s (25). Having the oesophageal catheter in place, we could measure the variation of transpulmonary pressure (PTP) as: AW,plat is airway pressure during IHM, PESO,plat is the oesophageal pressure at the same time, and PAW,EE and PESO,EE are the corresponding airway and oesophageal pressures at the end of expiration (26). This way we could draw the PV curve of the lung in the different mentioned conditions.
Prognostic value of pulmonary artery pulsatility index in chronic heart failure patients with reduced ejection fraction
Published in Acta Cardiologica, 2022
At the end of expiration following parameters were measured one after the other: pulmonary capillary wedge pressure (PCWP), pulmonary artery systolic and diastolic pressure (PASP and PADP), and RAP. MAP was recorded. By utilising Fick's equation, we calculated cardiac output (CO), then dividing by body surface area, we obtained the cardiac index (CI). The transpulmonary pressure gradient (TPG) was computed as mean PA pressure minus PCWP and reported in mm Hg. Dividing TPG by CO, the pulmonary vascular resistance (PVR) was calculated and represented in units of dynxsec/cm5. PAPG was calculated as PASP minus PADP and reported in mm Hg. The right ventricular function was assessed by calculation of PAPi according to the following formula: PAPi = PAPG/RAP.
Related Knowledge Centers
- Alveolar Pressure
- Apnea
- Elastic Recoil
- Intrapleural Pressure
- Esophagus
- Pleural Cavity
- Spirometry
- Pulmonary Alveolus
- Pneumothorax