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      Respiratory Drive in Critically Ill Patients. Pathophysiology and Clinical Implications

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          Abstract

          Respiratory drive, the intensity of the respiratory center's output, determines the effort exerted in each breath. The increasing awareness of the adverse effects of both strong and weak respiratory efforts during mechanical ventilation on patient outcome brings attention to the respiratory drive of the critically ill patient. Critical illness can affect patients' respiratory drive through multiple pathways, mainly operating through three feedback systems: cortical, metabolic, and chemical. The chemical feedback system, defined as the response of the respiratory center's output to changes in arterial blood gases and pH, is one of the most important determinants of respiratory drive. The purpose of this state-of-the-art review is to describe the determinants of respiratory drive in critically ill patients, review the tools available to assess respiratory drive at the bedside, and discuss the implications of altered respiratory drive during mechanical ventilation. An analysis that relates arterial carbon dioxide levels with brain's response to this stimulus will be presented, contrasting the brain's responses to the patient's ability to generate effective alveolar ventilation, both during unassisted breathing and with different modes of ventilatory assist. This analysis may facilitate comprehension of the pathophysiology of respiratory drive in critically ill patients. As we aim to avoid both over- and under-assistance with mechanical ventilation, considering the patients' respiratory drive at the bedside may improve clinical assessment and management of the patient and the ventilator.

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          Most cited references102

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          Evolution of Diaphragm Thickness during Mechanical Ventilation. Impact of Inspiratory Effort.

          Diaphragm atrophy and dysfunction have been reported in humans during mechanical ventilation, but the prevalence, causes, and functional impact of changes in diaphragm thickness during routine mechanical ventilation for critically ill patients are unknown.
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            Breathing matters

            Breathing is a well-described, vital and surprisingly complex behaviour, with behavioural and physiological outputs that are easy to directly measure. Key neural elements for generating breathing pattern are distinct, compact and form a network amenable to detailed interrogation, promising the imminent discovery of molecular, cellular, synaptic and network mechanisms that give rise to the behaviour. Coupled oscillatory microcircuits make up the rhythmic core of the breathing network. Primary among these is the preBötzinger Complex (preBötC), which is composed of excitatory rhythmogenic interneurons and excitatory and inhibitory pattern-forming interneurons that together produce the essential periodic drive for inspiration. The preBötC coordinates all phases of the breathing cycle, coordinates breathing with orofacial behaviours and strongly influences, and is influenced by, emotion and cognition. Here, we review progress towards cracking the inner workings of this vital core.
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              Diaphragm dysfunction assessed by ultrasonography: influence on weaning from mechanical ventilation.

              To determine the prevalence of diaphragmatic dysfunction diagnosed by M-mode ultrasonography (vertical excursion <10 mm or paradoxic movements) in medical intensive care unit patients and to assess the influence of diaphragmatic dysfunction on weaning outcome. Prospective, observational study. Twenty-eight-bed medical intensive care unit in a university-affiliated hospital. Eighty-eight consecutive patients in the medical intensive care unit who required mechanical ventilation over 48 hrs and met the criteria for a spontaneous breathing trial were assessed. Patients with a history of diaphragmatic or neuromuscular disease or evidence of pneumothorax or pneumomediastinum were excluded. During spontaneous breathing trial, each hemidiaphragm was evaluated by M-mode ultrasonography using the liver and spleen as windows with the patient supine. Rapid shallow breathing index was simultaneously calculated at the bedside. The prevalence of ultrasonographic diaphragmatic dysfunction among the eligible 82 patients was 29% (n = 24). Patients with diaphragmatic dysfunction had longer weaning time (401 [range, 226-612] hrs vs. 90 [range, 24-309] hrs, p < .01) and total ventilation time (576 [range, 374-850] hrs vs. 203 [range, 109-408] hrs, p < .01) than patients without diaphragmatic dysfunction. Patients with diaphragmatic dysfunction also had higher rates of primary (20 of 24 vs. 34 of 58, p < .01) and secondary (ten of 20 vs. ten of 46, p = .01) weaning failures than patients without diaphragmatic dysfunction. The area under the receiver operating characteristics curve of ultrasonographic criteria in predicting weaning failure was similar to that of rapid shallow breathing index. Using M-mode ultrasonography, diaphragmatic dysfunction was found in a substantial number of medical intensive care unit patients without histories of diaphragmatic disease. Patients with such diaphragmatic dysfunction showed frequent early and delayed weaning failures. Ultrasonography of the diaphragm may be useful in identifying patients at high risk of difficulty weaning.
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                Author and article information

                Journal
                American Journal of Respiratory and Critical Care Medicine
                Am J Respir Crit Care Med
                American Thoracic Society
                1073-449X
                1535-4970
                January 01 2020
                January 01 2020
                : 201
                : 1
                : 20-32
                Affiliations
                [1 ]Department of Intensive Care Medicine, University Hospital of Heraklion, Medical School University of Crete, Heraklion, Greece
                [2 ]Interdepartmental Division of Critical Care Medicine, University of Toronto, Toronto, Ontario, Canada
                [3 ]Keenan Research Center and Li Ka Shing Knowledge Institute, St. Michael’s Hospital, Toronto, Ontario, Canada
                [4 ]Department of Medicine, University Health Network, Toronto, Ontario, Canada; and
                [5 ]Toronto General Hospital Research Institute, Toronto, Ontario, Canada
                Article
                10.1164/rccm.201903-0596SO
                31437406
                d0af4237-3c83-443b-92b3-747c0f4841c5
                © 2020
                History

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