LBLukas Brander

Lukas Brander

*This is an algorithmically generated author record based on publicly available information.

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 publication
  • Christer 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

  • Neural control of ventilation prevents both over-distension and de-recruitment of experimentally injured lungs

    by Lukas Brander, Onnen Moerer, Göran Hedenstierna, Jennifer Beck, Jukka Takala, Arthur S Slutsky, Christer Sinderby


  • Open Access

    Heart–lung interactions during neurally adjusted ventilatory assist

    by David Berger, Stefan Bloechlinger, Jukka Takala, Christer Sinderby, Lukas Brander

    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

    Cumulative lactate and hospital mortality in ICU patients

    by Paul A van Beest, Lukas Brander, Sebastiaan Pa Jansen, Johannes H Rommes, Michaël A Kuiper, Peter E Spronk