scholarly journals Bedside quantification of dead-space fraction using routine clinical data in patients with acute lung injury: secondary analysis of two prospective trials

Critical Care ◽  
2010 ◽  
Vol 14 (4) ◽  
pp. R141 ◽  
Author(s):  
Hassan Siddiki ◽  
Marija Kojicic ◽  
Guangxi Li ◽  
Murat Yilmaz ◽  
Taylor B Thompson ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Clinical Data ◽  
Dead Space ◽  
Secondary Analysis ◽  
Prospective Trials

scholarly journals Correction: Bedside quantification of dead-space fraction using routine clinical data in patients with acute lung injury: secondary analysis of two prospective trials

Critical Care ◽  
2011 ◽  
Vol 15 (2) ◽  
pp. 410
Author(s):  
Hassan Siddiki ◽  
Marija Kojicic ◽  
Guangxi Li ◽  
Murat Yilmaz ◽  
Taylor B Thompson ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Clinical Data ◽  
Dead Space ◽  
Secondary Analysis ◽  
Prospective Trials

Effect of inhaled nitric oxide on pulmonary hemodynamics after acute lung injury in dogs

1994 ◽  
Vol 76 (3) ◽  
pp. 1356-1362 ◽  
Author(s):  
J. A. Romand ◽  
M. R. Pinsky ◽  
L. Firestone ◽  
H. A. Zar ◽  
J. R. Lancaster
Keyword(s):  
Nitric Oxide ◽  
Acute Lung Injury ◽  
Gas Exchange ◽  
Lung Injury ◽  
Dead Space ◽  
Left Ventricular ◽  
Right Atrial ◽  
Adrenergic Blockade ◽  
Pulmonary Hemodynamics ◽  
Beta Adrenergic

Increased pulmonary vascular resistance (PVR) and mismatch in ventilation-to-perfusion ratio characterize acute lung injury (ALI). Pulmonary arterial pressure (Ppa) decreases when nitric oxide (NO) is inhaled during hypoxic pulmonary vasoconstriction (HPV); thus NO inhalation may reduce PVR and improve gas exchange in ALI. We studied the hemodynamic and gas exchange effects of NO inhalation during HPV and then ALI in eight anesthetized open-chest mechanically ventilated dogs. Right atrial pressure, Ppa, and left ventricular and arterial pressures were measured, and cardiac output was estimated by an aortic flow probe. Shunt and dead space were also estimated. The effect of 5-min exposures to 0, 17, 28, 47, and 0 ppm inhaled NO was recorded during hyperoxia, hypoxia, and oleic acid-induced ALI. During ALI, partial beta-adrenergic blockade (propranolol, 0.15 mg/kg i.v.) was induced and 74 ppm NO was inhaled. Nitrosylhemoglobin (NO-Hb) and methemoglobin (MetHb) levels were measured. During hyperoxia, NO inhalation had no measurable effects. Hypoxia increased Ppa (from 19.8 +/- 6.1 to 28.3 +/- 8.7 mmHg, P < 0.01) and calculated PVR (from 437 +/- 139 to 720 +/- 264 dyn.s.cm-5, P < 0.01), both of which decreased with 17 ppm NO. ALI decreased arterial PO2 and increased airway pressure, shunt, and dead space ventilation. Ppa (19.8 +/- 6.1 vs. 23.4 +/- 7.7 mmHg) and PVR (437 +/- 139 vs. 695 +/- 359 dyn.s.cm-5, P < 0.05) were greater during ALI than during hyperoxia. No inhalation had no measureable effect during ALI before or after beta-adrenergic blockade. MetHb remained low, and NO-Hb was unmeasurable. Bolus infusion of nitroglycerin (15 micrograms) induced an immediate decrease in Ppa and PVR during ALI.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Management of Phosgene-Induced Acute Lung Injury (ALI) by Personalized Protective PEEP-ECMO: What Can We Learn from Animal Bioassays?

2019 ◽  
pp. 1-9
Author(s):  
Chunli Yang ◽  
Chunli Yang ◽  
Yang Xiaogang ◽  
Zhaohui He
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Dead Space ◽  
Extravascular Lung Water ◽  
Lung Mechanics ◽  
Lung Edema ◽  
Lung Water ◽  
Extravascular Lung Water Index ◽  
Water Index ◽  
Arterial Blood

Background: Phosgene (carbonyl dichloride) gas is an indispensable chemical intermediate used in numerous industrial processes. Acute lung injury (ALI) caused by accidental inhalation exposure to phosgene is characterized pulmonary edema being phenotypically manifested after an asymptomatic or more precisely phrased “clinical occult” period. Opposite to common clinical practice, protective treatment should be given preference to curative treatment. Treatment initiated already during the asymptomatic phase shortly after exposure requires prognostic endpoints preceding the lung edema for triage and re-triage. Treatment strategies need to be personalized and exposure-dose related. The objective of this post-hoc analysis of published data is to assess prognostic value of ventilation dead-space (Vd/Vt) and extravascular lung water index (EVLWI) to guide treatment by protective PEEP supplemented by venovenous (vv) ECMO. Methods: This paper aims to compare the overarching published framework from systematic toxicological research of phosgene in animal bioassays with the clinical evidence from four accidentally phosgenepoisoned workers admitted to hospital with life-threatening lung edema. Treatment focused on a combination of protective PEEP and ECMO to reverse phosgene-induced deterioration in lung mechanics by personalized mechanical ventilation. Endpoints selected for titration PEEP focused on endpoints indicative of decoupling cardiopulmonary and vascular functions. To better understand any cardiogenic and vascular disturbances, titration endpoints included calculated ventilation dead-space (Vd/Vt), measured extravascular lung water index (EVLWI), arterial blood gases and acid-base status, systemic vascular resistance index (SVRI), and cardiac index (CI). EVLWI and APACHE II criteria guided the course of treatment in adjusting plateau pressure (Pplat), positive end-expiratory pressure (PEEP), and driving pressure (ΔP). Results: Remarkable equivalence of human data and those from controlled inhalation studies with phosgene on rats and dogs was found. The endpoint of choice guiding PEEP ventilation and implementation of ECMO was EVLWI. This maker of lung edema precisely reflects the increased wet lung weights in animals. Conclusions: ECMO-supplemented PEEP not only mitigates hypoxemia at conditions of severe ARDS and it also provides a means to reduce driving and plateau pressures minimizing ventilatorassociated lung injury.

scholarly journals Effects of inspiratory pause on CO2 elimination and arterial Pco2 in acute lung injury

2008 ◽  
Vol 105 (6) ◽  
pp. 1944-1949 ◽  
Author(s):  
Jérôme Devaquet ◽  
Björn Jonson ◽  
Lisbet Niklason ◽  
Anne-Gaëlle Si Larbi ◽  
Leif Uttman ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Dead Space ◽  
Gas Diffusion ◽  
Arterial Pco2 ◽  
Mechanically Ventilated ◽  
Alveolar Plateau ◽  
Single Breath ◽  
Single Breath Test ◽  
Airway Dead Space

A high respiratory rate associated with the use of small tidal volumes, recommended for acute lung injury (ALI), shortens time for gas diffusion in the alveoli. This may decrease CO2 elimination. We hypothesized that a postinspiratory pause could enhance CO2 elimination and reduce PaCO2 by reducing dead space in ALI. In 15 mechanically ventilated patients with ALI and hypercapnia, a 20% postinspiratory pause (Tp20) was applied during a period of 30 min between two ventilation periods without postinspiratory pause (Tp0). Other parameters were kept unchanged. The single breath test for CO2 was recorded every 5 min to measure tidal CO2 elimination (VtCO2), airway dead space (VDaw), and slope of the alveolar plateau. PaO2, PaCO2, and physiological and alveolar dead space (VDphys, VDalv) were determined at the end of each 30-min period. The postinspiratory pause, 0.7 ± 0.2 s, induced on average <0.5 cmH2O of intrinsic positive end-expiratory pressure (PEEP). During Tp20, VtCO2 increased immediately by 28 ± 10% (14 ± 5 ml per breath compared with 11 ± 4 for Tp0) and then decreased without reaching the initial value within 30 min. The addition of a postinspiratory pause significantly decreased VDaw by 14% and VDphys by 11% with no change in VDalv. During Tp20, the slope of the alveolar plateau initially fell to 65 ± 10% of baseline value and continued to decrease. Tp20 induced a 10 ± 3% decrease in PaCO2 at 30 min (from 55 ± 10 to 49 ± 9 mmHg, P < 0.001) with no significant variation in PaO2. Postinspiratory pause has a significant influence on CO2 elimination when small tidal volumes are used during mechanical ventilation for ALI.

Prognostic Value of Different Dead Space Indices in Mechanically Ventilated Patients With Acute Lung Injury and ARDS

CHEST Journal ◽  
2008 ◽  
Vol 133 (1) ◽  
pp. 62-71 ◽  
Author(s):  
Umberto Lucangelo ◽  
Francesca Bernabè ◽  
Sara Vatua ◽  
Giada Degrassi ◽  
Ana Villagrà ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Dead Space ◽  
Prognostic Value ◽  
Mechanically Ventilated ◽  
Mechanically Ventilated Patients ◽  
Ventilated Patients

scholarly journals Neutrophils disturb pulmonary microcirculation in sepsis-induced acute lung injury

2019 ◽  
Vol 53 (3) ◽  
pp. 1800786 ◽  
Author(s):  
Inwon Park ◽  
Mingyo Kim ◽  
Kibaek Choe ◽  
Eunjoo Song ◽  
Howon Seo ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Dead Space ◽  
Imaging System ◽  
Early Stage ◽  
Circulating Cells ◽  
Custom Made ◽  
Pulmonary Microcirculation ◽  
Functional Deterioration

The lung is highly vulnerable during sepsis, yet its functional deterioration accompanied by disturbances in the pulmonary microcirculation is poorly understood. This study aimed to investigate how the pulmonary microcirculation is distorted in sepsis-induced acute lung injury (ALI) and reveal the underlying cellular pathophysiologic mechanism.Using a custom-made intravital lung microscopic imaging system in a murine model of sepsis-induced ALI, we achieved direct real-time visualisation of the pulmonary microcirculation and circulating cellsin vivo. We derived the functional capillary ratio (FCR) as a quantitative parameter for assessing the fraction of functional microvasculature in the pulmonary microcirculation and dead space.We identified that the FCR rapidly decreases in the early stage of sepsis-induced ALI. The intravital imaging revealed that this decrease resulted from the generation of dead space, which was induced by prolonged neutrophil entrapment within the capillaries. We further showed that the neutrophils had an extended sequestration time and an arrest-like dynamic behaviour, both of which triggered neutrophil aggregates inside the capillaries and arterioles. Finally, we found that Mac-1 (CD11b/CD18) was upregulated in the sequestered neutrophils and that a Mac-1 inhibitor restored the FCR and improved hypoxaemia.Using the intravital lung imaging system, we observed that Mac-1-upregulated neutrophil aggregates led to the generation of dead space in the pulmonary microcirculation that was recovered by a Mac-1 inhibitor in sepsis-induced ALI.

Sign in / Sign up

Export Citation Format

Share Document