Ilaria Algieri

Mechanical Power and Development of Ventilator-induced Lung Injury.

Background:The ventilator works mechanically on the lung parenchyma. The authors set out to obtain the proof of concept that ventilator-induced lung injury (VILI) depends on the mechanical power applied to the lung. Methods:Mechanical power was defined as the function of transpulmonary pressure, tidal volume (TV), and respiratory rate. Three piglets were ventilated with a mechanical power known to be lethal (TV, 38 ml/kg; plateau pressure, 27 cm H2O; and respiratory rate, 15 breaths/min). Other groups (three piglets each) were ventilated with the same TV per kilogram and transpulmonary pressure but at the respiratory rates of 12, 9, 6, and 3 breaths/min. The authors identified a mechanical power threshold for VILI and did nine additional experiments at the respiratory rate of 35 breaths/min and mechanical power below (TV 11 ml/kg) and above (TV 22 ml/kg) the threshold. Results:In the 15 experiments to detect the threshold for VILI, up to a mechanical power of approximately 12 J/min (respiratory rate, 9 breaths/min), the computed tomography scans showed mostly isolated densities, whereas at the mechanical power above approximately 12 J/min, all piglets developed whole-lung edema. In the nine confirmatory experiments, the five piglets ventilated above the power threshold developed VILI, but the four piglets ventilated below did not. By grouping all 24 piglets, the authors found a significant relationship between the mechanical power applied to the lung and the increase in lung weight (r2 = 0.41, P = 0.001) and lung elastance (r2 = 0.33, P < 0.01) and decrease in PaO2/FIO2 (r2 = 0.40, P < 0.001) at the end of the study. Conclusion:In piglets, VILI develops if a mechanical power threshold is exceeded.

Lung inhomogeneities and time course of ventilator-induced mechanical injuries.

Background:During mechanical ventilation, stress and strain may be locally multiplied in an inhomogeneous lung. The authors investigated whether, in healthy lungs, during high pressure/volume ventilation, injury begins at the interface of naturally inhomogeneous structures as visceral pleura, bronchi, vessels, and alveoli. The authors wished also to characterize the nature of the lesions (collapse vs. consolidation). Methods:Twelve piglets were ventilated with strain greater than 2.5 (tidal volume/end-expiratory lung volume) until whole lung edema developed. At least every 3 h, the authors acquired end-expiratory/end-inspiratory computed tomography scans to identify the site and the number of new lesions. Lung inhomogeneities and recruitability were quantified. Results:The first new densities developed after 8.4 ± 6.3 h (mean ± SD), and their number increased exponentially up to 15 ± 12 h. Afterward, they merged into full lung edema. A median of 61% (interquartile range, 57 to 76) of the lesions appeared in subpleural regions, 19% (interquartile range, 11 to 23) were peribronchial, and 19% (interquartile range, 6 to 25) were parenchymal (P < 0.0001). All the new densities were fully recruitable. Lung elastance and gas exchange deteriorated significantly after 18 ± 11 h, whereas lung edema developed after 20 ± 11 h. Conclusions:Most of the computed tomography scan new densities developed in nonhomogeneous lung regions. The damage in this model was primarily located in the interstitial space, causing alveolar collapse and consequent high recruitability.

Effect of body mass index in acute respiratory distress syndrome.

BACKGROUND Obesity is associated in healthy subjects with a great reduction in functional residual capacity and with a stiffening of lung and chest wall elastance, which promote alveolar collapse and hypoxaemia. Likewise, obese patients with acute respiratory distress syndrome (ARDS) could present greater derangements of respiratory mechanics than patients of normal weight. METHODS One hundred and one ARDS patients were enrolled. Partitioned respiratory mechanics and gas exchange were measured at 5 and 15 cm H2O of PEEP with a tidal volume of 6-8 ml kg(-1) of predicted body weight. At 5 and 45 cm H2O of PEEP, two lung computed tomography scans were performed. RESULTS Patients were divided as follows according to BMI: normal weight (BMI≤25 kg m(-2)), overweight (BMI between 25 and 30 kg m(-2)), and obese (BMI>30 kg m(-2)). Obese, overweight, and normal-weight groups presented a similar lung elastance (median [interquartile range], respectively: 17.7 [14.2-24.8], 20.9 [16.1-30.2], and 20.5 [15.2-23.6] cm H2O litre(-1) at 5 cm H2O of PEEP and 19.3 [15.5-26.3], 21.1 [17.4-29.2], and 17.1 [13.4-20.4] cm H2O litre(-1) at 15 cm H2O of PEEP) and chest elastance (respectively: 4.9 [3.1-8.8], 5.9 [3.8-8.7], and 7.8 [3.9-9.8] cm H2O litre(-1) at 5 cm H2O of PEEP and 6.5 [4.5-9.6], 6.6 [4.2-9.2], and 4.9 [2.4-7.6] cm H2O litre(-1) at 15 cm H2O of PEEP). Lung recruitability was not affected by the body weight (15.6 [6.3-23.4], 15.7 [9.8-22.2], and 11.3 [6.2-15.6]% for normal-weight, overweight, and obese groups, respectively). Lung gas volume was significantly lower whereas total superimposed pressure was significantly higher in the obese compared with the normal-weight group (1148 [680-1815] vs 827 [686-1213] ml and 17.4 [15.8-19.3] vs 19.3 [18.6-21.7] cm H2O, respectively). CONCLUSIONS Obese ARDS patients do not present higher chest wall elastance and lung recruitability.

Cycling-off criteria during pressure support ventilation: What do we have to monitor?

In this issue of the Journal, Hoff et al [1] evaluated the effect of 2 cycling-off termination flow criteria: a fixed at 5% of the peak inspiratory flow and an automatic real-time breath-by-breath adjustement, in 16 patients during pressure support ventilation (PSV). The automatic adjustement (AA) caused a significantly higher flow termination (31% vs 12% of the peak inspiratory flow). Compared with the fixed criteria, the AA was associated to a significantly higher

The Prone Position in the Treatment of Patients with ARDS: Problems and Real Utility

Prone positioning is a life-saving treatment used in ARDS patients in order to improve oxygenation and reduce lung injury due to mechanical ventilation. The beneficial effects of this procedure are the result of complex mechanisms that cooperate in improving gas exchange and in reducing global “stress” and “strain” of the lung. Prone positioning seems to be more effective in extrapulmonary form of ARDS, where the main feature of the disease is represented by compression atelectasis in dependent lung regions caused by the gain in lung weight due to pulmonary edema. To date, it is recommended in ARDS patients that maintain a PaO2/FiO2 ratio lower than 150 mmHg even after optimization of mechanical ventilation. However, only the patients who react to prone positioning with a decrease in PaCO2 show a real benefit in terms of survival rate. The relationship between improvement in gas exchange and patient outcome still remains unclear. This is not a maneuver free of complications, and it is important to balance risks and benefits associated with the procedure. An expert team is required to safely prone the patient and to reduce the incidence of adverse effects.

Dissipated energy during protective mechanical ventilation

From literature we know that a cornerstone of the protective lung ventilation in Acute Respiratory Distress Syndrome (ARDS) patients[1] and during general anesthesia[2] is a low tidal volume. On the other hand, driving pressure seems to be the variable that best stratifies mortality risk[3]. Our hypothesis is that the combination of volume and pressure, that is the energy dissipated into respiratory system, is the main determinant of a ventilator-induced lung injury (VILI).

0994. Development of ventilatory-induced lung injury depends on energy dissipated into respiratory system

Mechanical ventilation with high volumes/pressures induces ventilatory induced lung injury (VILI). During each breath, part of the energy transmitted from ventilator to respiratory system is given back as elastic recoil and part is dissipated into the respiratory system; this amount of energy is measured by the hysteresis area of the pressure-volume (PV) curve of the respiratory system. Total dissipated energy into respiratory system, or dissipated inspiratory potency, equals to energy dissipated during every single breath multiplied by the respiratory rate (RR).

0894. Time course of VILI development: a CT scan study

Mechanical Ventilation at high tidal volumes and pressures induces in lung oedema which is undistinguishable from ARDS. It is possible that pleura, bronchi and vessels act as a natural stress raiser playing as local stress multipliers. [1]