Reverse-Thrust Ventilation in Hypercapnic Patients with Acute Respiratory Distress Syndrome

Rossi, Nicola De; Musch, Guido; Sangalli, Fabio; Verweij, Muriel; Patroniti, Nicolò; Artigas, Antonio

doi:10.1164/ajrccm.162.2.9908024

Cited by 9 publications

(3 citation statements)

References 30 publications

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“…Prone positioning has demonstrated improvement in hypoxia at the expense of increasing ICP and decreasing CPP (6,114). Tracheal gas insufflation may allow low tidal volumes with concomitant treatment of hypercarbia or maintenance of normocarbia (87,119). Extracorporeal membrane oxygenation has been used with success in trauma patients with ARDS, particularly demonstrating improved mortality when initiated early (18).…”

Section: Ventilator Management After Tbimentioning

confidence: 99%

Acute brain trauma, lung injury, and pneumonia: more than just altered mental status and decreased airway protection

Pittet

Kerby

et al. 2017

American Journal of Physiology-Lung Cellular and Molecular Phys

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Traumatic brain injury (TBI) is a major cause of mortality and morbidity worldwide. Even when patients survive the initial insult, there is significant morbidity and mortality secondary to subsequent pulmonary edema, acute lung injury (ALI), and nosocomial pneumonia. Whereas the relationship between TBI and secondary pulmonary complications is recognized, little is known about the mechanistic interplay of the two phenomena. Changes in mental status secondary to acute brain injury certainly impair airway- and lung-protective mechanisms. However, clinical and translational evidence suggests that more specific neuronal and cellular mechanisms contribute to impaired systemic and lung immunity that increases the risk of TBI-mediated lung injury and infection. To better understand the cellular mechanisms of that immune impairment, we review here the current clinical data that support TBI-induced impairment of systemic and lung immunity. Furthermore, we also review the animal models that attempt to reproduce human TBI. Additionally, we examine the possible role of damage-associated molecular patterns, the chlolinergic anti-inflammatory pathway, and sex dimorphism in post-TBI ALI. In the last part of the review, we discuss current treatments and future pharmacological therapies, including fever control, tracheostomy, and corticosteroids, aimed to prevent and treat pulmonary edema, ALI, and nosocomial pneumonia after TBI.

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Section: Ventilator Management After Tbimentioning

confidence: 99%

Acute brain trauma, lung injury, and pneumonia: more than just altered mental status and decreased airway protection

Pittet

Kerby

et al. 2017

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Several studies have shown that TGI can be used either to decrease PaCO 2 in the setting of hypercapnia or to maintain normocapnia while tidal volume is decreased [66]. In patients with severe head trauma and ALI, Martinez-Perez et al [67] showed that the application of phasic TGI (at mid-to-end expiration) allowed ventilation with lower tidal volumes and driving pressures while maintaining PaCO 2 constant without any deleterious effects on cerebral parameters.…”

Section: Alternative Ventilatory Techniquesmentioning

confidence: 99%

Acute Lung Injury in Patients with Severe Brain Injury: A Double Hit Model

2009

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The presence of pulmonary dysfunction after brain injury is well recognized. Acute lung injury (ALI) occurs in 20% of patients with isolated brain injury and is associated with a poor outcome. The "blast injury" theory, which proposes combined "hydrostatic" and "high permeability" mechanisms for the formation of neurogenic pulmonary edema, has been challenged recently by the observation that a systemic inflammatory response may play an integral role in the development of pulmonary dysfunction associated with brain injury. As a result of the primary cerebral injury, a systemic inflammatory reaction occurs, which induces an alteration in blood-brain barrier permeability and infiltration of activated neutrophils into the lung. This preclinical injury makes the lungs more susceptible to the mechanical stress of an injurious ventilatory strategy. Tight CO2 control is a therapeutic priority in patients with acute brain injury, but the use of high tidal volume ventilation may contribute to the development of ALI. Establishment of a therapeutic regimen that allows the combination of protective ventilation with the prevention of hypercapnia is, therefore, required. Moreover, in patients with brain injury, hypoxemia represents a secondary insult associated with a poor outcome. Optimal oxygenation may be achieved by using an adequate FiO2 and by application of positive end-expiratory pressure (PEEP). PEEP may, however, affect the cerebral circulation by hemodynamic and CO2-mediated mechanisms and the effects of PEEP on cerebral hemodynamics should be monitored in these patients and used to titrate its application.

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“…Durch transtracheale Katheter konnten wichtige physiologische und klinische Wirkungen des späteren NHF vorweggenommen werden. Dabei konnte eine Reduktion des Totraumes bei zusätzlichem Einsatz eines Flusses durch einen transtrachealen Katheter und eine Reduktion des PCO 2 gezeigt werden [3,4]. Folgeuntersuchungen ergaben, dass das Ausmaß der PCO 2 -Absenkung flowabhängig beeinflusst werden kann [5].…”

Section: Nhf: Pathophysiologische Konzepteunclassified

Nasaler Highflow (NHF): Eine neue Therapiealternative zur Behandlung der respiratorischen Insuffizienz

Bräunlich¹,

Nilius

2016

Pneumologie

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The therapy of choice in hypoxemic respiratory failure (type 1) is the application of supplemental oxygen at flow rates of 1 to 15 l/min via nasal prongs or mask. Non-invasive or invasive positive pressure ventilation will be initiated when the oxygen therapy effects are not sufficient or if hypercapnic respiratory failure (type 2) is the underlying problem. Recently, an alternative therapy option is available, from the pathophysiology it can be classified between oxygen therapy and positive pressure ventilation. The therapy called Nasal High Flow (NHF) is based on the nasal application of a heated and humidified air oxygen mixture with a flow range of up to 60 l/min. The precise pathophysiological principles of NHF are only partly understood, yet various aspects are well studied already: it is possible to deliver high oxygen concentrations, airway dryness can be avoided, dead space ventilation reduced and clearance of nasal dead space is achieved. Additionally, an end expiratory positive pressure is built up, which helps to prevent airway collapse, thus resulting in an improvement of respiratory efficiency and reduction of breathing work. Current studies demonstrate improvement in gas exchange and reduction of reintubation rate when applying the NHF treatment in acute respiratory failure. Thus the NHF therapy attracts attention in intensive care medicine. The application in other fields like chronic respiratory insufficiency is less well clarified. The objectives of this review are to present the pathophysiological effects and mechanisms of NHF, as far as understood, and to give an overview over the current state of relevant studies.

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Reverse-Thrust Ventilation in Hypercapnic Patients with Acute Respiratory Distress Syndrome

Cited by 9 publications

References 30 publications

Acute brain trauma, lung injury, and pneumonia: more than just altered mental status and decreased airway protection

Acute brain trauma, lung injury, and pneumonia: more than just altered mental status and decreased airway protection

Acute Lung Injury in Patients with Severe Brain Injury: A Double Hit Model

Nasaler Highflow (NHF): Eine neue Therapiealternative zur Behandlung der respiratorischen Insuffizienz

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