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Haemodynamics and vasopressor support during prolonged targeted temperature management for 48 hours after out-of-hospital cardiac arrest: a post hoc substudy of a randomised clinical trial

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DOI

  • Johannes Grand, Department of Cardiology, Rigshospitalet
  • ,
  • Christian Hassager, Department of Cardiology, Rigshospitalet
  • ,
  • Markus B Skrifvars, University of Helsinki and Helsinki University Hospital
  • ,
  • Marjaana Tiainen, University of Helsinki and Helsinki University Hospital
  • ,
  • Anders M Grejs
  • Anni Nørgaard Jeppesen
  • Christophe Henri Valdemar Duez
  • ,
  • Bodil S Rasmussen, Aalborg Universitets Hospital
  • ,
  • Timo Laitio, Turku University Hospital, turku, Finland.
  • ,
  • Jens Nee, Department of Internal Medicine, Nephrology and Intensive Care, Charité-Universitätsmedizin Berlin, Berlin, Germany.
  • ,
  • FabioSilvio Taccone, Department of Gastroenterology, Erasme Hospital (ULB), Brussels, Belgium.
  • ,
  • Eldar Søreide, University of Bergen, Stavanger University Hospital, Stavanger
  • ,
  • Hans Kirkegaard

BACKGROUND: Comatose patients admitted after out-of-hospital cardiac arrest frequently experience haemodynamic instability and anoxic brain injury. Targeted temperature management is used for neuroprotection; however, targeted temperature management also affects patients' haemodynamic status. This study assessed the haemodynamic status of out-of-hospital cardiac arrest survivors during prolonged (48 hours) targeted temperature management at 33°C.

METHODS: Analysis of haemodynamic and vasopressor data from 311 patients included in a randomised, clinical trial conducted in 10 European hospitals (the TTH48 trial). Patients were randomly allocated to targeted temperature management at 33°C for 24 (TTM24) or 48 (TTM48) hours. Vasopressor and haemodynamic data were reported hourly for 72 hours after admission. Vasopressor load was calculated as norepinephrine (µg/kg/min) plus dopamine(µg/kg/min/100) plus epinephrine (µg/kg/min).

RESULTS: After 24 hours, mean arterial pressure (mean±SD) was 74±9 versus 75±9 mmHg (P=0.19), heart rate was 57±16 and 55±14 beats/min (P=0.18), vasopressor load was 0.06 (0.03-0.15) versus 0.08 (0.03-0.15) µg/kg/min (P=0.22) for the TTM24 and TTM48 groups, respectively. From 24 to 48 hours, there was no difference in mean arterial pressure (Pgroup=0.32) or lactate (Pgroup=0.20), while heart rate was significantly lower (average difference 5 (95% confidence interval 2-8) beats/min, Pgroup<0.0001) and vasopressor load was significantly higher in the TTM48 group (Pgroup=0.005). In a univariate Cox regression model, high vasopressor load was associated with mortality in univariate analysis (hazard ratio 1.59 (1.05-2.42) P=0.03), but not in multivariate analysis (hazard ratio 0.77 (0.46-1.29) P=0.33).

CONCLUSIONS: In this study, prolonged targeted temperature management at 33°C for 48 hours was associated with higher vasopressor requirement but no sign of any detrimental haemodynamic effects.

OriginalsprogEngelsk
TidsskriftEuropean Heart Journal: Acute Cardiovascular Care
Vol/bind10
Nummer2
Sider (fra-til)132-141
Antal sider10
ISSN2048-8726
DOI
StatusUdgivet - feb. 2021

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