Diaphragm neurostimulation in mechanical ventilation: current status and future prospects.

Introduction: Diaphragm neurostimulation is a muscle stimulation technique that, through electrodes placed directly on or at the vicinity of the phrenic nerves, induces diaphragm contractions independently of the patient's cooperation. Recently, the technical development of temporary diaphragm neurostimulation devices has paved the way for a new era in the management of critically ill patients.

Areas Covered: In this review, we describe the latest technical developments in diaphragm neurostimulation and its physiological effects.

An Initial Investigation of Diaphragm Neurostimulation in Patients with Acute Respiratory Distress Syndrome.

Background: Lung protective ventilation aims at limiting lung stress and strain. By reducing the amount of pressure transmitted by the ventilator into the lungs, diaphragm neurostimulation offers a promising approach to minimize ventilator-induced lung injury. This study investigates the physiologic effects of diaphragm neurostimulation in acute respiratory distress syndrome (ARDS) patients.

Meta-analysis of serological biomarkers at hospital admission for the likelihood of developing delirium during hospitalization.

Importance: Identifying biomarkers that, at hospital admission, predict subsequent delirium will help to focus our clinical efforts on prevention and management.

Objective: The study aimed to investigate biomarkers at hospital admission that may be associated with delirium during hospitalization.

Data Sources: A librarian at the Fraser Health Authority Health Sciences Library performed searches from 28 June 2021 to 9 July 2021, using the following sources: Medline, EMBASE, Cochrane Database of Systematic Reviews, Cochrane Central Register of Controlled Trials, Cochrane Methodology Register, and the Database of Abstracts of Reviews and Effects.

Transvenous stimulation yields exposure-dependent protection from ventilator-induced diaphragm atrophy.

Mechanical ventilation (MV)-induced diaphragmatic atrophy can contribute to weaning difficulties. A temporary transvenous diaphragm neurostimulation (TTDN) device that elicits diaphragm contractions has previously been shown to mitigate atrophy during MV in a preclinical model; however, its effects on different myofiber types remain unknown. It is important to examine these effects, as each myofiber type plays a role in the range of diaphragmatic movements to ensure successful liberation from MV.

Phrenic nerve stimulation mitigates hippocampal and brainstem inflammation in an ARDS model.

In porcine healthy-lung and moderate acute respiratory distress syndrome (ARDS) models, groups that received phrenic nerve stimulation (PNS) with mechanical ventilation (MV) showed lower hippocampal apoptosis, and microglia and astrocyte percentages than MV alone. Explore whether PNS in combination with MV for 12 h leads to differences in hippocampal and brainstem tissue concentrations of inflammatory and synaptic markers compared to MV-only animals. Compare tissue concentrations of inflammatory markers (IL-1α, IL-1β, IL-6, IL-8, IL-10, IFN-γ, TNFα and GM-CSF), pre-synaptic markers (synapsin and synaptophysin) and post-synaptic markers (disc-large-homolog 4, N-methyl-D-aspartate receptors 2A and 2B) in the hippocampus and brainstem in three groups of mechanically ventilated pigs with injured lungs: MV only (MV), MV plus PNS every other breath (MV + PNS50%), and MV plus PNS every breath (MV + PNS100%).

Risk factors for ventilator-induced-lung injury develop three to five times faster after a single episode of lung injury.

Introduction: Mechanical ventilator breaths provided to deeply sedated patients have an abnormal volume distribution, encouraging alveolar collapse in dependent regions and promoting alveolar overdistention in non-dependent regions. Collapse and overdistention both start with the first breath and worsen over time, driving ventilator-induced lung injury (VILI). This is exacerbated when the lung is already injured or has increased heterogeneity.

Diaphragm Neurostimulation Mitigates Ventilation-Associated Brain Injury in a Preclinical Acute Respiratory Distress Syndrome Model.

Unlabelled: In a porcine healthy lung model, temporary transvenous diaphragm neurostimulation (TTDN) for 50 hours mitigated hippocampal apoptosis and inflammation associated with mechanical ventilation (MV).

Hypothesis: Explore whether TTDN in combination with MV for 12 hours mitigates hippocampal apoptosis and inflammation in an acute respiratory distress syndrome (ARDS) preclinical model.

Methods And Models: Compare hippocampal apoptosis, inflammatory markers, and serum markers of neurologic injury between never ventilated subjects and three groups of mechanically ventilated subjects with injured lungs: MV only (LI-MV), MV plus TTDN every other breath, and MV plus TTDN every breath.

Negative-pressure-assisted ventilation lowers driving pressure and mechanical power in an ARDS model.

Increased lung heterogeneity from regional alveolar collapse drives ventilator-induced lung injury in patients with acute respiratory distress syndrome (ARDS). New methods of preventing this injury require study. Our study objective was to determine whether the combination of temporary transvenous diaphragm neurostimulation (TTDN) with standard-of-care volume-control mode ventilation changes lung mechanics, reducing ventilator-induced lung injury risk in a preclinical ARDS model.

Transvenous Diaphragm Neurostimulation Mitigates Ventilation-associated Brain Injury.

Mechanical ventilation (MV) is associated with hippocampal apoptosis and inflammation, and it is important to study strategies to mitigate them. To explore whether temporary transvenous diaphragm neurostimulation (TTDN) in association with MV mitigates hippocampal apoptosis and inflammation after 50 hours of MV. Normal-lung porcine study comparing apoptotic index, inflammatory markers, and neurological-damage serum markers between never-ventilated subjects, subjects undergoing 50 hours of MV plus either TTDN every other breath or every breath, and subjects undergoing 50 hours of MV (MV group).

Diaphragm neurostimulation during mechanical ventilation reduces atelectasis and transpulmonary plateau pressure, preserving lung homogeneity and /.

Tidal volume delivered by mechanical ventilation to a sedated patient is distributed in a nonphysiological pattern, causing atelectasis (underinflation) and overdistension (overinflation). Activation of the diaphragm during controlled mechanical ventilation in these sedated patients may provide a method to reduce atelectasis and alveolar inhomogeneity, protecting the lungs from ventilator-induced lung injury while also protecting the diaphragm by preventing ventilator-induced diaphragm dysfunction. We studied the hypothesis that diaphragm contractions elicited by transvenous phrenic nerve stimulation, delivered in synchrony with volume-control ventilation, would reduce atelectasis and lung inhomogeneity in a healthy, normal lung pig model.

Systematic review of cognitive impairment and brain insult after mechanical ventilation.

We conducted a systematic review following the PRISMA protocol primarily to identify publications that assessed any links between mechanical ventilation (MV) and either cognitive impairment or brain insult, independent of underlying medical conditions. Secondary objectives were to identify possible gaps in the literature that can be used to inform future studies and move toward a better understanding of this complex problem. The preclinical literature suggests that MV is associated with neuroinflammation, cognitive impairment, and brain insult, reporting higher neuroinflammatory markers, greater evidence of brain injury markers, and lower cognitive scores in subjects that were ventilated longer, compared to those ventilated less, and to never-ventilated subjects.

Brain injury after 50 h of lung-protective mechanical ventilation in a preclinical model.

Mechanical ventilation is the cornerstone of the Intensive Care Unit. However, it has been associated with many negative consequences. Recently, ventilator-induced brain injury has been reported in rodents under injurious ventilation settings.

Diaphragm Activation in Ventilated Patients Using a Novel Transvenous Phrenic Nerve Pacing Catheter.

Objectives: Over 30% of critically ill patients on positive-pressure mechanical ventilation have difficulty weaning from the ventilator, many of whom acquire ventilator-induced diaphragm dysfunction. Temporary transvenous phrenic nerve pacing using a novel electrode-bearing catheter may provide a means to prevent diaphragm atrophy, to strengthen an atrophied diaphragm, and mitigate the harms of mechanical ventilation. We tested the initial safety, feasibility, and impact on ventilation of this novel approach.

Mitigation of Ventilator-induced Diaphragm Atrophy by Transvenous Phrenic Nerve Stimulation.

Rationale: Ventilator-induced diaphragm dysfunction is a significant contributor to weaning difficulty in ventilated critically ill patients. It has been hypothesized that electrically pacing the diaphragm during mechanical ventilation could reduce diaphragm dysfunction.

Objectives: We tested a novel, central line catheter-based, transvenous phrenic nerve pacing therapy for protecting the diaphragm in sedated and ventilated pigs.