Is Weaning Failure Caused by Low-Frequency Fatigue of the Diaphragm?

Laghi, Franco; Cattapan, Steven E.; Jubran, Amal; Parthasarathy, Sairam; Warshawsky, Paul J.; Choi, Yoon Sub A.; Tobin, Martin J.

doi:10.1164/rccm.200210-1246oc

Cited by 302 publications

(219 citation statements)

References 63 publications

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“…Adult patients are often conscious or semiconscious when PI max is measured and their degree of mental alertness will directly affect their cooperation and ability to perform the test (35). The test is often applied in patients who are sufficiently awake to respond to commands, but their level of consciousness may prevent them from making truly maximal efforts (36). In the current study, sedation was stopped when children were deemed ready for extubation and patients were studied once this decision was made and within 4 hours of any attempted extubation (median 1 h).…”

Section: Discussionmentioning

confidence: 99%

Tension–Time Index as a Predictor of Extubation Outcome in Ventilated Children

Harikumar¹,

Egberongbe²,

Nadel³

et al. 2009

Am J Respir Crit Care Med

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Rationale: Indices that assess the load on the respiratory muscles, such as the tension-time index (TTI), may predict extubation outcome. Objectives: To evaluate the performance of a noninvasive assessment of TTI, the respiratory muscle tension time index (TTmus), by comparison to that of the diaphragm tension time index (TTdi) and other predictors of extubation outcome in ventilated children. Methods: Eighty children (median [range] age 2.1 yr [0.15-16]) admitted to pediatric intensive care units at King's College and St Mary's Hospitals who required mechanical ventilation for more than 24 hours were studied. Measurements and Main Results: TTmus, maximal inspiratory pressure, respiratory drive, respiratory system mechanics, and functional residual capacity using a helium dilution technique, the rapid shallow breathing and CROP indices (compliance, rate, oxygenation, and pressure) indexed for body weight were measured and standard clinical data recorded in all patients. TTdi was measured in 28 of the 80 children using balloon catheters. Eight children (three in the TTdi group) failed extubation. TTmus (0.199 vs. 0.09) and TTdi (0.157 vs. 0.07) were significantly higher in children who failed extubation. TTmus greater than 0.18 (n 5 80) and TTdi greater than 0.15 (n 5 28) had sensitivities and specificities of 100% in predicting extubation failure. The other predictors performed less well. Conclusions: Invasive and noninvasive measurements of TTI may provide accurate prediction of extubation outcome in mechanically ventilated children.Keywords: diaphragm; respiratory muscles; pediatric critical care; weaningPatients are extubated when assessed to be capable of sustaining spontaneous ventilation without respiratory support. Premature extubation leading to cardiorespiratory compromise necessitates reintubation and reinstitution of mechanical ventilation and increases mortality and morbidity (1), whereas prolonged ventilatory support exposes the child to increased risk of nosocomial infection and lung injury (2). Extubation failure has been reported to occur in 4 to 10% of children (3, 4), hence an accurate predictor of extubation outcome would be of significant clinical value (1).Univariate indices that examine a single aspect of physiological function often have poor predictive power probably because they do not fully reflect all the pathophysiological processes affecting extubation outcome (5). Accurate prediction is more likely using multivariate indices that integrate a number of physiological functions (6). Studies of multivariate indices in children, such as the rapid-shallow breathing index (RSB) (respiratory rate [RR] divided by tidal volume [VT]) (5) and the CROP index (compliance, RR, oxygenation, and inspiratory pressure [PI]), however, have been limited and yielded contradictory results. We (7) and others (8, 9) have shown that the predictive power of those indices in children is poor, whereas Baumeister and colleagues (10), demonstrated that the CROP index discriminated strongly between successful an...

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Section: Discussionmentioning

confidence: 99%

Tension–Time Index as a Predictor of Extubation Outcome in Ventilated Children

Harikumar¹,

Egberongbe²,

Nadel³

et al. 2009

Am J Respir Crit Care Med

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“…Nonetheless, several lines of indirect evidence support the belief that impaired inspiratory muscle function contributes to weaning difficulties. First, although debate exists, several studies reveal that inspiratory muscle endurance is decreased in patients during prolonged MV and that maximal inspiratory pressure generation is lower in patients that experience difficult weaning compared with patients that are successfully weaned (14,15,17,55). Furthermore, a recent study reveals that patients with diaphragmatic contractile dysfunction exhibit a high incidence of weaning failures compared with patients with normal diaphragm function (51).…”

Section: Contribution Of Vidd To Weaning Failurementioning

confidence: 99%

Ventilator-induced diaphragm dysfunction: cause and effect

Powers

Wiggs

Sollanek

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

143

156

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Powers SK, Wiggs MP, Sollanek KJ, Smuder AJ. Ventilator-induced diaphragm dysfunction: cause and effect. Am J Physiol Regul Integr Comp Physiol 305: R464 -R477, 2013. First published July 10, 2013 doi:10.1152/ajpregu.00231.2013 is used clinically to maintain gas exchange in patients that require assistance in maintaining adequate alveolar ventilation. Common indications for MV include respiratory failure, heart failure, drug overdose, and surgery. Although MV can be a life-saving intervention for patients suffering from respiratory failure, prolonged MV can promote diaphragmatic atrophy and contractile dysfunction, which is referred to as ventilator-induced diaphragm dysfunction (VIDD). This is significant because VIDD is thought to contribute to problems in weaning patients from the ventilator. Extended time on the ventilator increases health care costs and greatly increases patient morbidity and mortality. Research reveals that only 18 -24 h of MV is sufficient to develop VIDD in both laboratory animals and humans. Studies using animal models reveal that MV-induced diaphragmatic atrophy occurs due to increased diaphragmatic protein breakdown and decreased protein synthesis. Recent investigations have identified calpain, caspase-3, autophagy, and the ubiquitin-proteasome system as key proteases that participate in MV-induced diaphragmatic proteolysis. The challenge for the future is to define the MV-induced signaling pathways that promote the loss of diaphragm protein and depress diaphragm contractility. Indeed, forthcoming studies that delineate the signaling mechanisms responsible for VIDD will provide the knowledge necessary for the development of a pharmacological approach that can prevent VIDD and reduce the incidence of weaning problems. respiratory muscle; atrophy; mechanical ventilation; weaning; muscle wasting MECHANICAL VENTILATION (MV) is used clinically to achieve sufficient pulmonary gas exchange in patients unable to sustain adequate alveolar ventilation on their own. Common indications for MV include respiratory failure due to chronic obstructive pulmonary disease, status asthmaticus, and/or heart failure. In addition, MV is often an essential intervention in patients suffering from acute drug overdose, neuromuscular diseases, sepsis, and during surgery along with postsurgical recovery.The number of patients receiving prolonged MV in the United States exceeds more than 300,000 each year in the intensive care unit (ICU) (20). Although MV can be a lifesaving measure, prolonged MV results in the rapid development of diaphragmatic weakness due to both atrophy and contractile dysfunction. This detrimental impact of prolonged MV on the diaphragm has been termed ventilator-induced diaphragmatic dysfunction (VIDD) and VIDD is predicted to be a major contributor to problems in weaning patients from the ventilator (26, 114). Although previous reports describing the impact of prolonged MV on the diaphragm have appeared in the literature, advances in our understanding of the mechanisms responsible for VIDD h...

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“…21,23 Fatigue is defined further as either "low frequency" or "high frequency," according to the muscle fibers involved and the duration of degraded muscle performance. 24 In addition, the descriptor "incipient fatigue" has been used to describe situations in which voluntary respiratory muscle contractions are limited by central inhibition in the face of excessive work demands, but external electrical diaphragmatic stimulation is capable of eliciting stronger contractions. 25 In contrast, "overt fatigue" refers to the inability of external electrical stimulation to evoke stronger respiratory muscle contractions.…”

Section: Respiratory Muscle Fatiguementioning

confidence: 99%

“…26 High-frequency fatigue, as it involves fasttwitch fibers and forceful contractions, is believed to be caused by the accumulation of inorganic phosphate and the failure of electrical conduction to the contractile fibers in the muscle, as well as intramuscular acidosis. 24 Recovery from high-frequency fatigue generally occurs within 15 min. 24 In contrast, low-frequency fatigue is believed to be caused by muscle-fiber injury, recovery from which may take several days.…”

Section: Respiratory Muscle Fatiguementioning

confidence: 99%

Patient-Ventilator Interaction During Acute Lung Injury, and the Role of Spontaneous Breathing: Part 1: Respiratory Muscle Function During Critical Illness

Kallet

2011

Respir Care

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SummarySince the early 1970s there has been an ongoing debate regarding the wisdom of promoting unassisted spontaneous breathing throughout the course of critical illness in patients with severe respiratory failure. The basis of this debate has focused on the clinical relevance of opposite problems. Historically, the term "disuse atrophy" has described a situation wherein sustained inactivity of the respiratory muscles (ie, passive ventilation) results in deconditioning and weakness. More recently it has been referred to as "ventilator-induced diaphragmatic dysfunction." In contrast, "use atrophy" describes a situation where chronic high-tension inspiratory work causes structural damage to the diaphragm and weakness. Both laboratory and clinical studies demonstrated that relatively brief periods of complete respiratory muscle inactivity, as well as intense muscle loading, result in acute inflammation, loss of muscle mass, and weakness. Yet in critical illness other factors also affect respiratory muscle function, including prolonged use of neuromuscular blocking agents, administration of corticosteroids, and sepsis. This makes the attribution of acquired respiratory muscle weakness and ventilator-dependence to either ventilator-induced diaphragmatic dysfunction or loaded breathing extremely difficult. Regardless, the clinical implications of this research strongly suggest that passive mechanical ventilation should be avoided whenever possible. However, promotion of unassisted spontaneous breathing in the acute phase of critical illness also may carry a substantial risk of respiratory muscle injury and weakness. Use of mechanical ventilation modes in a manner that induces spontaneous breathing effort, while simultaneously reducing the work load on the respiratory muscles, is probably sufficient to minimize both problems. Key words: acute lung injury; acute respiratory distress syndrome; discoordinated breathing; disuse atrophy; respiratory muscle fatigue; ventilator-induced diaphragmatic dysfunction; use atrophy. [Respir Care 2011;56(2):181-189.

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Is Weaning Failure Caused by Low-Frequency Fatigue of the Diaphragm?

Cited by 302 publications

References 63 publications

Tension–Time Index as a Predictor of Extubation Outcome in Ventilated Children

Tension–Time Index as a Predictor of Extubation Outcome in Ventilated Children

Ventilator-induced diaphragm dysfunction: cause and effect

Patient-Ventilator Interaction During Acute Lung Injury, and the Role of Spontaneous Breathing: Part 1: Respiratory Muscle Function During Critical Illness

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