Phrenic Nerve Stimulation Increases Human Diaphragm Fiber Force after Cardiothoracic Surgery

Ahn, Bumsoo; Beaver, Thomas M.; Martin, Tomas D.; Hess, Philip J.; Brumback, Babette; Ahmed, Shakeel; Smith, Barbara K.; Leeuwenburgh, Christiaan; Martin, A. Daniel; Ferreira, Leonardo

doi:10.1164/rccm.201405-0993le

Cited by 47 publications

(28 citation statements)

References 12 publications

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“…Among these, the preferential use of partially supported ventilatory modes, rather than controlled ventilation, may prevent diaphragm weakness by promoting its continuous activation [182,183]. Similarly, the use of temporary phrenic stimulation shows promise as a tool to mitigate the negative effects of MV, but remains to be explored in future studies [184,185,186,187]. …”

Section: Therapeutic Managementmentioning

confidence: 99%

Diaphragm Dysfunction: Diagnostic Approaches and Management Strategies

Dubé

Dres

2016

JCM

154

109

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The diaphragm is the main inspiratory muscle, and its dysfunction can lead to significant adverse clinical consequences. The aim of this review is to provide clinicians with an overview of the main causes of uni- and bi-lateral diaphragm dysfunction, explore the clinical and physiological consequences of the disease on lung function, exercise physiology and sleep and review the available diagnostic tools used in the evaluation of diaphragm function. A particular emphasis is placed on the clinical significance of diaphragm weakness in the intensive care unit setting and the use of ultrasound to evaluate diaphragmatic action.

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Section: Therapeutic Managementmentioning

confidence: 99%

Diaphragm Dysfunction: Diagnostic Approaches and Management Strategies

Dubé

Dres

2016

JCM

154

109

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show abstract

“…Interventions like intermittent spontaneous breathing or respiratory muscle training might be of benefit. Diaphragmatic contractions via phrenic nerve pacing have been successfully used in tetraplegic patients and during cardiothoracic surgery with documented increases in mitochondrial respiration . While short periods of intermittent spontaneous breathing had little effect in a rodent model, adding a resistive inspiratory load in order to train the inspiratory muscles has shown promising results for patients in small series and improved weaning outcome in a randomized trial …”

Section: Vidd Management: a Role For Ventilatory And Pharmacological mentioning

confidence: 99%

Dysfunction of respiratory muscles in critically ill patients on the intensive care unit

Berger

Bloechlinger

Haehling

et al. 2016

J cachexia sarcopenia muscle

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Muscular weakness and muscle wasting may often be observed in critically ill patients on intensive care units (ICUs) and may present as failure to wean from mechanical ventilation. Importantly, mounting data demonstrate that mechanical ventilation itself may induce progressive dysfunction of the main respiratory muscle, i.e. the diaphragm. The respective condition was termed ‘ventilator‐induced diaphragmatic dysfunction’ (VIDD) and should be distinguished from peripheral muscular weakness as observed in ‘ICU‐acquired weakness (ICU‐AW)’.Interestingly, VIDD and ICU‐AW may often be observed in critically ill patients with, e.g. severe sepsis or septic shock, and recent data demonstrate that the pathophysiology of these conditions may overlap. VIDD may mainly be characterized on a histopathological level as disuse muscular atrophy, and data demonstrate increased proteolysis and decreased protein synthesis as important underlying pathomechanisms. However, atrophy alone does not explain the observed loss of muscular force. When, e.g. isolated muscle strips are examined and force is normalized for cross‐sectional fibre area, the loss is disproportionally larger than would be expected by atrophy alone. Nevertheless, although the exact molecular pathways for the induction of proteolytic systems remain incompletely understood, data now suggest that VIDD may also be triggered by mechanisms including decreased diaphragmatic blood flow or increased oxidative stress. Here we provide a concise review on the available literature on respiratory muscle weakness and VIDD in the critically ill. Potential underlying pathomechanisms will be discussed before the background of current diagnostic options. Furthermore, we will elucidate and speculate on potential novel future therapeutic avenues.

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“…Some clinical studies showed that intermittent diaphragm stimulation during cardiothoracic surgery could exert benefits on diaphragmatic force generation and mitochondrial function [11,12]. On the other side, experimental studies showed that the mode of ventilation could influence the degree of diaphragmatic dysfunction.…”

Section: Introductionmentioning

confidence: 99%

Assisted mechanical ventilation promotes recovery of diaphragmatic thickness in critically ill patients: a prospective observational study

et al. 2020

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Background: Diaphragm atrophy and dysfunction are consequences of mechanical ventilation and are determinants of clinical outcomes. We hypothesize that partial preservation of diaphragm function, such as during assisted modes of ventilation, will restore diaphragm thickness. We also aim to correlate the changes in diaphragm thickness and function to outcomes and clinical factors. Methods: This is a prospective, multicentre, observational study. Patients mechanically ventilated for more than 48 h in controlled mode and eventually switched to assisted ventilation were enrolled. Diaphragm ultrasound and clinical data collection were performed every 48 h until discharge or death. A threshold of 10% was used to define thinning during controlled and recovery of thickness during assisted ventilation. Patients were also classified based on the level of diaphragm activity during assisted ventilation. We evaluated the association between changes in diaphragm thickness and activity and clinical outcomes and data, such as ventilation parameters. Results: Sixty-two patients ventilated in controlled mode and then switched to the assisted mode of ventilation were enrolled. Diaphragm thickness significantly decreased during controlled ventilation (1.84 ± 0.44 to 1.49 ± 0.37 mm, p < 0.001) and was partially restored during assisted ventilation (1.49 ± 0.37 to 1.75 ± 0.43 mm, p < 0.001). A diaphragm thinning of more than 10% was associated with longer duration of controlled ventilation (10 [5, 15] versus 5 [4, 8.5] days, p = 0.004) and higher PEEP levels (12.6 ± 4 versus 10.4 ± 4 cmH 2 O, p = 0.034). An increase in diaphragm thickness of more than 10% during assisted ventilation was not associated with any clinical outcome but with lower respiratory rate (16.7 ± 3.2 versus 19.2 ± 4 bpm, p = 0.019) and Rapid Shallow Breathing Index (37 ± 11 versus 44 ± 13, p = 0.029) and with higher Pressure Muscle Index (2 [0.5, 3] versus 0.4 [0, 1.9], p = 0.024). Change in diaphragm thickness was not related to diaphragm function expressed as diaphragm thickening fraction. Conclusion: Mode of ventilation affects diaphragm thickness, and preservation of diaphragmatic contraction, as during assisted modes, can partially reverse the muscle atrophy process. Avoiding a strenuous inspiratory work, as measured by Rapid Shallow Breathing Index and Pressure Muscle Index, may help diaphragm thickness restoration.

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Phrenic Nerve Stimulation Increases Human Diaphragm Fiber Force after Cardiothoracic Surgery

Cited by 47 publications

References 12 publications

Diaphragm Dysfunction: Diagnostic Approaches and Management Strategies

Diaphragm Dysfunction: Diagnostic Approaches and Management Strategies

Dysfunction of respiratory muscles in critically ill patients on the intensive care unit

Assisted mechanical ventilation promotes recovery of diaphragmatic thickness in critically ill patients: a prospective observational study

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