Lesión pulmonar autoinfligida por el paciente / Patient self inflicted lung injury / Lesão pulmonar autoinfligida pelo paciente

Resumen: La optimización del esfuerzo espontáneo en la ventilación mecánica tiene un lugar central en la Unidad de Cuidados Intensivos; aporta beneficios a los pacientes como la mejoría en el intercambio de gases, ayuda a recuperar la función del diafragma y el mantenimiento de los músculos periféricos. Por otro lado, también puede estar asociado al deterioro de la oxigenación y la lesión pulmonar. El incremento del impulso respiratorio neural aumenta el esfuerzo muscular inspiratorio, lo que condiciona presiones de distensión pulmonar lesivas, que en el contexto del síndrome de insuficiencia respiratoria aguda es de vital relevancia, ya que puede provocar el colapso y la sobredistensión regional alveolar de forma cíclica, con distribución heterogénea del estrés y tensión pulmonar. Existen tres mecanismos de lesión pulmonar por esfuerzo espontáneo: sobredistensión, aumento de la perfusión pulmonar y asincronía paciente-ventilador. La lesión pulmonar causa fuga capilar, edema pulmonar y alteración del intercambio de gases. Esto conduce a un aumento del impulso respiratorio y mayores volúmenes corrientes de las propias respiraciones espontáneas del paciente, que provocan fuga capilar y mayor daño pulmonar de forma similar a la lesión pulmonar inducida por ventilador.

Abstract: The optimization of spontaneous effort in mechanical ventilation has a central place in the intensive care unit; provides benefits to patients such as improved gas exchange, helps to regain function of the diaphragm and maintenance of peripheral muscles. On the other hand, it can also be associated with impaired oxygenation and lung injury. The increase in the neural respiratory drive increases the inspiratory muscular effort, conditioning damaging pulmonary distension pressures, which in the context of acute respiratory distress syndrome is of vital importance, since it can cause collapse and regional alveolar overdistention in a cyclical way. with heterogeneous distribution of pulmonary stress and strain. There are three mechanisms of lung injury due to spontaneous effort: overdistention, increased pulmonary perfusion, and patient-ventilator asynchrony. Lung injury causes capillary leakage, pulmonary edema, and impaired gas exchange. This leads to increased respiratory drive and higher tidal volumes of the patient's own spontaneous breaths, causing capillary leakage and increased lung damage like ventilator-induced lung injury.

Resumo: A otimização do esforço espontâneo na ventilação mecânica tem lugar central na unidade de terapia intensiva; Proporciona benefícios aos pacientes como melhora nas trocas gasosas, auxilia na recuperação da função do diafragma e na manutenção da musculatura periférica. Por outro lado, também pode estar associada ao deterioro da oxigenação e lesão pulmonar. O incremento do impulso respiratório neural aumenta o esforço muscular inspiratório, condicionando pressões de distensão pulmonar prejudiciais, o que no contexto da síndrome de insuficiência respiratória aguda é de vital relevância, pois pode causar colapso e hiperdistensão alveolar regional de forma cíclica, com distribuição heterogênea do estresse e tensão pulmonar. Existem três mecanismos de lesão pulmonar espontânea por esforço: hiperdistensão, aumento da perfusão pulmonar e assincronia paciente-ventilador. A lesão pulmonar causa vazamento capilar, edema pulmonar e troca gasosa prejudicada. Isso leva ao aumento do impulso respiratório e aos volumes correntes mais altos das próprias respirações espontâneas do paciente, causando vazamento capilar e danos pulmonares adicionais semelhantes aos danos pulmonares induzidos pelo ventilador.

Lesión pulmonar autoinflingida por el paciente en la Unidad de Cuidados Intensivos / Patient Self-Inflicted Lung Injury (P-SILI) in the Intensive Care Unit / Lesão pulmonar auto-infligida pelo paciente na Unidade de Cuidados Intensivos

Resumen: Hasta la fecha, no se ha demostrado superioridad de algún modo de ventilación mecánica invasiva en particular, la mayoría de los autores destacan la individualización de la programación y modalidad de la ventilación mecánica, teniendo en cuenta la presencia de asincronías y buscando el mejor confort del paciente, incluso la ventilación espontánea, aunque al parecer se asemeja a la manera fisiológica de la mecánica respiratoria, no está exenta de complicaciones. Tres mecanismos potenciales se proponen para el desarrollo de lesión pulmonar por esfuerzo respiratorio espontáneo: sobredistensión global y local, aumento de la perfusión pulmonar y la presencia de asincronías paciente-ventilador, derivadas en una lesión autoinfligida por el paciente o «P-SILI¼, por sus siglas en inglés Patient Self Inflicted Lung Injury. En los últimos 20 años se han desarrollado estrategias que permiten minimizar los riesgos asociados a la ventilación mecánica, la más importante de todas es mantener soporte ventilatorio guiado por metas, identificación del posible desarrollo del paciente y extubar al paciente lo más rápido posible, siempre y cuando sus condiciones lo permitan.

Abstract: To date, the superiority of any particular mode of invasive mechanical ventilation has not been demonstrated; most authors emphasize the individualization of the programming and modality of mechanical ventilation, taking into account the presence of asynchronies and seeking the best patient comfort; even spontaneous ventilation, although it seems to resemble the physiological manner of respiratory mechanics, is not free of complications. Three potential mechanisms are proposed for the development of lung injury by spontaneous respiratory effort: global and local overdistension, increased pulmonary perfusion and the presence of patient-ventilator asynchronies, resulting in a Patient Self-Inflicted Injury or «P-SILI¼. In the last twenty years, strategies have been developed to minimize the risks associated with mechanical ventilation, the most important of which is to maintain goal-directed ventilatory support, identify the possible development of the patient and extubate the patient as quickly as possible, as long as the patient's conditions allow it.

Resumo: Até o momento, nenhum modo específico de ventilação mecânica invasiva se mostrou superior, a maioria dos autores enfatiza a individualização da programação e modalidade de ventilação mecânica, levando em consideração a presença de assincronia e buscando o melhor conforto do paciente. Mesmo a ventilação espontânea, embora pareça assemelhar-se à maneira fisiológica da mecânica respiratória, não é isenta de complicações. Três mecanismos potenciais são propostos para o desenvolvimento de lesão pulmonar por esforço respiratório espontâneo: hiperdistensão global e local, aumento da perfusão pulmonar e presença de assincronia paciente-ventilador, derivada de uma lesão autoinfligida pelo paciente ou «P-SILI¼ por suas siglas em inglês patient self inflicted lung injury. Nos últimos vinte anos, foram desenvolvidas estratégias para minimizar os riscos associados à ventilação mecânica. O mais importante de tudo é manter o suporte ventilatório guiado por metas, identificar o possível desenvolvimento do paciente e extubar o paciente o mais rápido possível, enquanto suas condições permitirem.

Blunted Hypercapnic Respiratory Drive Response in Subjects With Late-Onset Pompe Disease.

BACKGROUND: Patients with late-onset Pompe disease develop progressive hypercapnic respiratory failure that can be disproportionate to the respiratory muscle compromise and/or thoracic restriction. Although recent studies have reported the presence of a blunted hypercapnic respiratory response in some subjects with neuromuscular disorders and chronic hypercapnia, no study has evaluated the integrity of the respiratory drive in subjects with late-onset Pompe disease. Thus, we endeavor to determine the CO2 rebreathing response in subjects with late-onset Pompe disease. METHODS: Respiratory muscle strength was assessed by measuring the maximum inspiratory pressure, and the maximum expiratory pressure. The maximum inspiratory pressure reflects the strength of the diaphragm and other inspiratory muscles, whereas the maximum expiratory pressure reflects the strength of the abdominal muscles and other expiratory muscles. We studied the hypercapnic drive response (measured as the ratio of the change in airway-occlusion pressure 0.1 s after the start of inspiration and end-tidal PCO2 in 13 subjects with late-onset Pompe disease and 51 healthy controls. RESULTS: Overall inspiratory muscle strength was within normal limits or slightly diminished in the late-onset Pompe disease group. Five subjects (38.5%) were chronically hypercapnic, and 9 (69.2%) had an increased breath-holding time. Compared with controls, the change in airway-occlusion pressure 0.1 s/change in end-tidal CO2 pressure slope (hypercapnic respiratory drive) was lower in the late-onset Pompe disease group (median 0.050 [interquartile range 0.027-0.118] vs 0.183 [0.153-0.233], P < .001). Nine subjects (69.2%) had a blunted change in airway-occlusion pressure 0.1 s/change in end-tidal carbon dioxide pressure slope. CONCLUSIONS: Subjects with late-onset Pompe disease had an impaired hypercapnic respiratory drive response. The clinical impact of this phenomenon in this subject subset deserves further investigation.

Evaluation of a new index of mechanical ventilation weaning: the timed inspiratory effort.

PURPOSE: The performance of most indices used to predict ventilator weaning outcomes remains below expectation. The purpose of this study was to evaluate a new weaning index, the timed inspiratory effort (TIE) index, which is based on the maximal inspiratory pressure and the occlusion time required to reach it. METHODS: This observational prospective study included patients undergoing mechanical ventilation. Patients ready to be weaned had their TIE index and 6 previously reported indices recorded. The primary end point was the overall predictive performance of the studied weaning indices (area under the receiver operating characteristic curves [AUCs]). The secondary end points were sensitivity, specificity, positive predictive value, and negative predictive value. P values <.05 were considered significant. RESULTS: From the 128 initially screened patients, the 103 patients selected for the study included 45 women and 58 men (mean age 60.8 ± 19.8 years). In all, 60 patients were weaned, 43 were not weaned, and 32 died during the study period. Tracheotomy was necessary in 61 patients. The mean duration of mechanical ventilation was 17.5 ± 17.3 days. The AUC of 3 weaning predictors (the TIE index, the integrative weaning index, and the frequency-to-tidal volume [f/Vt] ratio index) was higher than the other indices. The TIE index had the largest AUC. CONCLUSION: The TIE index performed better than the best weaning indices used in clinical practice.