Ewan C Goligher1,2,3,4, Eddy Fan1,2,5,4, Margaret S Herridge1,2,4,6, Alistair Murray1,4, Stefannie Vorona1,4, Debbie Brace1,4, Nuttapol Rittayamai1,7, Ashley Lanys1,4,7, George Tomlinson2, Jeffrey M Singh1,2,4, Steffen-Sebastian Bolz3, Gordon D Rubenfeld1,2,5,8, Brian P Kavanagh1,3,9,10, Laurent J Brochard1,2,7, Niall D Ferguson1,2,3,5,4,6. 1. 1 Interdepartmental Division of Critical Care Medicine. 2. 2 Department of Medicine. 3. 3 Department of Physiology. 4. 4 Division of Respirology, Department of Medicine, University Health Network and Mount Sinai Hospital, Toronto, Ontario, Canada. 5. 5 Institute for Health Policy, Management and Evaluation, and. 6. 6 Toronto General Research Institute, Toronto, Ontario, Canada. 7. 7 Keenan Centre for Biomedical Research, St. Michael's Hospital, Toronto, Ontario, Canada. 8. 8 Department of Critical Care Medicine, Sunnybrook Health Sciences Centre, Toronto, Ontario, Canada; and. 9. 9 Department of Anesthesia, University of Toronto, Toronto, Ontario, Canada. 10. 10 Department of Critical Care Medicine, Hospital for Sick Children, Toronto, Ontario, Canada.
Abstract
RATIONALE: 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. OBJECTIVES: To describe the evolution of diaphragm thickness over time during mechanical ventilation, its impact on diaphragm function, and the influence of inspiratory effort on this phenomenon. METHODS: In three academic intensive care units, 107 patients were enrolled shortly after initiating ventilation along with 10 nonventilated intensive care unit patients (control subjects). Diaphragm thickness and contractile activity (quantified by the inspiratory thickening fraction) were measured daily by ultrasound. MEASUREMENTS AND MAIN RESULTS: Over the first week of ventilation, diaphragm thickness decreased by more than 10% in 47 (44%), was unchanged in 47 (44%), and increased by more than 10% in 13 (12%). Thickness did not vary over time following extubation or in nonventilated patients. Low diaphragm contractile activity was associated with rapid decreases in diaphragm thickness, whereas high contractile activity was associated with increases in diaphragm thickness (P = 0.002). Contractile activity decreased with increasing ventilator driving pressure (P = 0.01) and controlled ventilator modes (P = 0.02). Maximal thickening fraction (a measure of diaphragm function) was lower in patients with decreased or increased diaphragm thickness (n = 10) compared with patients with unchanged thickness (n = 10; P = 0.05 for comparison). CONCLUSIONS: Changes in diaphragm thickness are common during mechanical ventilation and may be associated with diaphragmatic weakness. Titrating ventilatory support to maintain normal levels of inspiratory effort may prevent changes in diaphragm configuration associated with mechanical ventilation.
RATIONALE: 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 illpatients are unknown. OBJECTIVES: To describe the evolution of diaphragm thickness over time during mechanical ventilation, its impact on diaphragm function, and the influence of inspiratory effort on this phenomenon. METHODS: In three academic intensive care units, 107 patients were enrolled shortly after initiating ventilation along with 10 nonventilated intensive care unit patients (control subjects). Diaphragm thickness and contractile activity (quantified by the inspiratory thickening fraction) were measured daily by ultrasound. MEASUREMENTS AND MAIN RESULTS: Over the first week of ventilation, diaphragm thickness decreased by more than 10% in 47 (44%), was unchanged in 47 (44%), and increased by more than 10% in 13 (12%). Thickness did not vary over time following extubation or in nonventilated patients. Low diaphragm contractile activity was associated with rapid decreases in diaphragm thickness, whereas high contractile activity was associated with increases in diaphragm thickness (P = 0.002). Contractile activity decreased with increasing ventilator driving pressure (P = 0.01) and controlled ventilator modes (P = 0.02). Maximal thickening fraction (a measure of diaphragm function) was lower in patients with decreased or increased diaphragm thickness (n = 10) compared with patients with unchanged thickness (n = 10; P = 0.05 for comparison). CONCLUSIONS: Changes in diaphragm thickness are common during mechanical ventilation and may be associated with diaphragmatic weakness. Titrating ventilatory support to maintain normal levels of inspiratory effort may prevent changes in diaphragm configuration associated with mechanical ventilation.
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