Miriam Gotti

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.

Body temperature affects cerebral hemodynamics in acutely brain injured patients: an observational transcranial color-coded duplex sonography study

IntroductionTemperature changes are common in patients in a neurosurgical intensive care unit (NICU): fever is frequent among severe cases and hypothermia is used after cardiac arrest and is currently being tested in clinical trials to lower intracranial pressure (ICP). This study investigated cerebral hemodynamics when body temperature varies in acute brain injured patients.MethodsWe enrolled 26 patients, 14 with acute brain injury who developed fever and were given antipyretic therapy (defervescence group) and 12 who underwent an intracranial neurosurgical procedure and developed hypothermia in the operating room; once admitted to the NICU, still under anesthesia, they were re-warmed before waking (re-warming group). We measured cerebral blood flow velocity (CBF-V) and pulsatility index (PI) at the middle cerebral artery using transcranial color-coded duplex sonography (TCCDS).ResultsIn the defervescence group mean CBF-V decreased from 75 ± 26 (95% CI 65 to 85) to 70 ± 22 cm/s (95% CI 61 to 79) (P = 0.04); the PI also fell, from 1.36 ± 0.33 (95% CI 1.23 to 1.50) to 1.16 ± 0.26 (95% CI 1.05 to 1.26) (P = 0.0005). In the subset of patients with ICP monitoring, ICP dropped from 16 ± 8 to 12 ± 6 mmHg (P = 0.003). In the re-warming group mean CBF-V increased from 36 ± 10 (95% CI 31 to 41) to 39 ± 13 (95% CI 33 to 45) cm/s (P = 0.04); the PI rose from 0.98 ± 0.14 (95% CI 0.91 to 1.04) to 1.09 ± 0.22 (95% CI 0.98 to 1.19) (P = 0.02).ConclusionsBody temperature affects cerebral hemodynamics as evaluated by TCCDS; when temperature rises, CBF-V increases in parallel, and viceversa when temperature decreases. When cerebral compliance is reduced and compensation mechanisms are exhausted, even modest temperature changes can greatly affect ICP.

High-Flow Nasal Cannula Oxygen Therapy: Physiological Effects and Clinical Data

In patients with mild to moderate acute respiratory failure the commonly used techniques to ameliorate gas exchange are oxygen therapy and non-invasive ventilation (NIV). However due to mask intolerance, hypercapnia, respiratory acidosis, muscle fatigue and hypoxemia, intubation and invasive mechanical ventilation are frequently required. High-flow nasal cannulas, originally developed to improve gas exchange in neonatal and pediatric settings, have recently been evaluated in various groups of adult critically ill patients. High-flow nasal cannulas deliver a high humidified air/oxygen gas flow (up to 60 l/min) via a nasal cannula. The main advantages of high-flow nasal cannulas are the ability to deliver a very high flow of humidified gas, exceeding, in the majority of patients, the peak inspiratory flow, with a constant oxygen fraction and the use, as interface, of a nasal cannula which can insure patient comfort. Several studies have shown that use of high-flow nasal cannulas was able to improve gas exchange and reduce the respiratory rate and, in selected patients, also to improve outcomes.

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).

Ventilator-Induced Lung injury: a preliminary morphological study

In this study we aimed at characterizing by morphological methods the effect of ventilator-induced lung injury (VILI) on lung structure, and we analyzed collagen and elastin content to understand the possible role of the main components of lung connective tissue in the development of VILI. For this purpose four female piglets (21.7±4.5 kg) were sedated, intubated and mechanically ventilated with high pressure to induce VILI. After death, lungs were excised inflated; each lung was divided in four regions, and lung fragments were obtained from each region of both lungs: three samples from subpleural regions, one sample from the medial portion of the lung. Lung fragments were immediately fixed in 4% formalin in 0.1M phosphate buffered saline (PBS), pH 7.4, routinely dehydrated, paraffin embedded, and serially cut (thickness 5 μm). Lung structure was analyzed in haematoxylin-eosin stained sections using a semiquantitative grading scale to assess the injury grade. To study collagen and elastin content, sections were stained by Sirius red and Weigert’s resorcin-fuchsin, respectively, and analyzed by a specific software. Collagen and elastin content were expressed as a percent of the stained area relative to the lung tissue. Light microscopy analysis of hematoxylin-eosin stained sections revealed that VILI induced several lung injuries such as hyaline membranes, interstitial and septal infiltrate, vascular congestion and intra-alveolar hemorraging, alveoli rupturing and basophilic material deposition. These lesions were diffuse and involved the whole lung parenchyma without any preferential localization. Image analysis of Sirius red and Weigert’s resorcin-fuchsin stained sections showed that lung injury was more evident where elastin was less abundant, but was also evident where elastin content was high and collagen was concomitantly less abundant. These preliminary data suggest that lung extracellular matrix could influence the response to damaging ventilation, and that both

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]