Lukas Brander
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Lukas Brander has a total of 15 co-authors. Here are the top co-authors by number of shared publications:
Arthur S Slutsky
Interdepartmental Division of Critical Care Medicine, University of Toronto, Department of Critical Care Medicine, St. Michael's Hospital, Toronto, Canada; Keenan Research Centre for Biomedical Science and Li Ka Shing Knowledge Institute of St. Michael's Hospital, Toronto, Canada
1 shared publicationChrister Sinderby
Interdepartmental Division of Critical Care Medicine, University of Toronto, Department of Critical Care Medicine, St. Michael's Hospital, Toronto, Canada; Keenan Research Centre for Biomedical Science and Li Ka Shing Knowledge Institute of St. Michael's Hospital, Toronto, Canada; Institute for Biomedical Engineering and Science Technology (iBEST) at Ryerson University and St. Michael's Hospital, Toronto, Canada
1 shared publication- Christer Sinderby
Department of Critical Care, KKeenan Centre for Biomedical Research and Li Ka, Canada
1 shared publication - David Berger
Department of Intensive Care Medicine, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland
1 shared publication - Göran Hedenstierna
Department of Medical Sciences Clinical Physiology Uppsala University Uppsala Sweden
1 shared publication Jennifer Beck
Department of Pediatrics, University of Toronto, Toronto, Canada; Keenan Research Centre for Biomedical Science and Li Ka Shing Knowledge Institute of St. Michael's Hospital, Toronto, Canada; Institute for Biomedical Engineering and Science Technology (iBEST) at Ryerson University and St. Michael's Hospital, Toronto, Canada
1 shared publication
Latest Publications
- 1 March 2017
- Published by Elsevier in Respiratory Physiology & Neurobiology
- Vol. 237, 57-67
Neural control of ventilation prevents both over-distension and de-recruitment of experimentally injured lungs
- 1 March 2017
- Published by Elsevier in Respiratory Physiology & Neurobiology
- Vol. 237, 57-67
Neural control of ventilation prevents both over-distension and de-recruitment of experimentally injured lungs
- Open Access
- 12 September 2014
- Published by Springer Nature in Critical Care
- Vol. 18 (5) , 499
Heart–lung interactions during neurally adjusted ventilatory assist
Assist in unison to the patient’s inspiratory neural effort and feedback-controlled limitation of lung distension with neurally adjusted ventilatory assist (NAVA) may reduce the negative effects of mechanical ventilation on right ventricular function. Heart–lung interaction was evaluated in 10 intubated patients with impaired cardiac function using esophageal balloons, pulmonary artery catheters and echocardiography. Adequate NAVA level identified by a titration procedure to breathing pattern (NAVAal), 50% NAVAal, and 200% NAVAal and adequate pressure support (PSVal, defined clinically), 50% PSVal, and 150% PSVal were implemented at constant positive end-expiratory pressure for 20 minutes each. NAVAal was 3.1 ± 1.1cmH2O/μV and PSVal was 17 ± 2 cmH20. For all NAVA levels negative esophageal pressure deflections were observed during inspiration whereas this pattern was reversed during PSVal and PSVhigh. As compared to expiration, inspiratory right ventricular outflow tract velocity time integral (surrogating stroke volume) was 103 ± 4%, 109 ± 5%, and 100 ± 4% for NAVAlow, NAVAal, and NAVAhigh and 101 ± 3%, 89 ± 6%, and 83 ± 9% for PSVlow, PSVal, and PSVhigh, respectively (p < 0.001 level-mode interaction, ANOVA). Right ventricular systolic isovolumetric pressure increased from 11.0 ± 4.6 mmHg at PSVlow to 14.0 ± 4.6 mmHg at PSVhigh but remained unchanged (11.5 ± 4.7 mmHg (NAVAlow) and 10.8 ± 4.2 mmHg (NAVAhigh), level-mode interaction p = 0.005). Both indicate progressive right ventricular outflow impedance with increasing pressure support ventilation (PSV), but no change with increasing NAVA level. Right ventricular performance is less impaired during NAVA compared to PSV as used in this study. Proposed mechanisms are preservation of cyclic intrathoracic pressure changes characteristic of spontaneous breathing and limitation of right-ventricular outflow impedance during inspiration, regardless of the NAVA level. Clinicaltrials.gov Identifier: NCT00647361, registered 19 March 2008
- 12 September 2014
- Published by Springer Nature in Critical Care
- Vol. 18 (5) , 499
Open AccessHeart–lung interactions during neurally adjusted ventilatory assist
Assist in unison to the patient’s inspiratory neural effort and feedback-controlled limitation of lung distension with neurally adjusted ventilatory assist (NAVA) may reduce the negative effects of mechanical ventilation on right ventricular function. Heart–lung interaction was evaluated in 10 intubated patients with impaired cardiac function using esophageal balloons, pulmonary artery catheters and echocardiography. Adequate NAVA level identified by a titration procedure to breathing pattern (NAVAal), 50% NAVAal, and 200% NAVAal and adequate pressure support (PSVal, defined clinically), 50% PSVal, and 150% PSVal were implemented at constant positive end-expiratory pressure for 20 minutes each. NAVAal was 3.1 ± 1.1cmH2O/μV and PSVal was 17 ± 2 cmH20. For all NAVA levels negative esophageal pressure deflections were observed during inspiration whereas this pattern was reversed during PSVal and PSVhigh. As compared to expiration, inspiratory right ventricular outflow tract velocity time integral (surrogating stroke volume) was 103 ± 4%, 109 ± 5%, and 100 ± 4% for NAVAlow, NAVAal, and NAVAhigh and 101 ± 3%, 89 ± 6%, and 83 ± 9% for PSVlow, PSVal, and PSVhigh, respectively (p < 0.001 level-mode interaction, ANOVA). Right ventricular systolic isovolumetric pressure increased from 11.0 ± 4.6 mmHg at PSVlow to 14.0 ± 4.6 mmHg at PSVhigh but remained unchanged (11.5 ± 4.7 mmHg (NAVAlow) and 10.8 ± 4.2 mmHg (NAVAhigh), level-mode interaction p = 0.005). Both indicate progressive right ventricular outflow impedance with increasing pressure support ventilation (PSV), but no change with increasing NAVA level. Right ventricular performance is less impaired during NAVA compared to PSV as used in this study. Proposed mechanisms are preservation of cyclic intrathoracic pressure changes characteristic of spontaneous breathing and limitation of right-ventricular outflow impedance during inspiration, regardless of the NAVA level. Clinicaltrials.gov Identifier: NCT00647361, registered 19 March 2008
- Open Access
- 1 January 2013
- Published by Elsevier in Annals of Intensive Care
- Vol. 3 (1) , 6
Cumulative lactate and hospital mortality in ICU patients
- 1 January 2013
- Published by Elsevier in Annals of Intensive Care
- Vol. 3 (1) , 6
Open AccessCumulative lactate and hospital mortality in ICU patients