Cardiac arrest – prognostic biomarkers and aspects of shock
(2014) In Lund University Faculty of Medicine Doctoral Dissertation Series 2014:140.- Abstract
- Background:
Some improvement has been seen in survival after cardiac arrest but the outcome is still poor and 50-70% of patients do not survive despite successful return of spontaneous circulation (ROSC). The cause of death is multifactorial. The majority of patients die from brain injury, but up to 35% die as a result of circulatory failure.
Purpose:
First, to investigate the release profiles of an array of biomarkers in patients treated with mild induced hypothermia after cardiac arrest and study their correlation to the post-cardiac arrest syndrome (PCAS) and long-term outcome; Second, to investigate the effect of two different target temperatures (33°C and 36°C) on hemodynamics and vasopressor... (More) - Background:
Some improvement has been seen in survival after cardiac arrest but the outcome is still poor and 50-70% of patients do not survive despite successful return of spontaneous circulation (ROSC). The cause of death is multifactorial. The majority of patients die from brain injury, but up to 35% die as a result of circulatory failure.
Purpose:
First, to investigate the release profiles of an array of biomarkers in patients treated with mild induced hypothermia after cardiac arrest and study their correlation to the post-cardiac arrest syndrome (PCAS) and long-term outcome; Second, to investigate the effect of two different target temperatures (33°C and 36°C) on hemodynamics and vasopressor requirement in cardiac arrest patients and; Third, to investigate the association of target temperature with outcome in patients with shock in admission.
Methods:
The biomarkers were collected serially at 8 time points during the first 72 hours following cardiac arrest in 84 still comatose post-resuscitation cardiac arrest patients treated with mild induced hypothermia. We analysed markers of inflammation; procalcitonin (PCT) and c-reactive protein (CRP), oxidation; peroxiredoxin 4 (prx4), cardiac stress; MR-proANP, cardiac injury; Troponin T (TnT), brain injury; Neuron specific enlolase (NSE), and the stress hormone; CT-proAVP (copeptin). Outcome was assessed at 6 months with the cerebral performance category scale (CPC) where CPC 1-2 was considered a good outcome. The cardiovascular sequential organ failure assessment score (SOFA-score) and the time to ROSC were used as surrogate markers for the PCAS. Three different definitions of infection were used to assess occurrence of infection.
The effect of a target temperature of 33°C or 36°C on hemodynamics was investigated in all patients with available vasopressor data (n=920) in the ‘Targeted temperature management at 33°C versus 36°C after cardiac arrest’ trial and in patients with shock on admission (n=139). Primary outcome was mortality. Secondary outcomes were vasopressor requirements as assessed by the cardiovascular SOFA-score, serum lactate concentrations, mean arterial pressure, and heart rate.
Results:
PCT, CT-proAVP and MR-proANP were all significantly higher in patients with poor outcome and correlated to surrogate markers of the PCAS. No specific cut-off levels were identified. PCT release was not associated to infection. Combinations of biomarkers may be a promising concept to improve prognostication. A targeted temperature of 33°C was associated with increased vasopressor requirements and increased lactate levels in both our investigated cohorts. A low MAP during the intervention (0-36 hours) was associated with poor outcome after adjustment for baseline characteristics.
Conclusion:
Biomarkers from other sources than the brain are associated to the PCAS and may be promising biomarkers to prognosticate outcome, alone or in combination. Targeted temperature management at 33°C is associated with increased vasopressor requirements and severity of shock and does not improve outcome as compared to 36°C. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/4812666
- author
- Annborn, Martin LU
- supervisor
-
- Hans Friberg LU
- David Erlinge LU
- Niklas Nielsen LU
- opponent
-
- Prof. Cariou, Alain, Paris Descarets University, Paris, France
- organization
- publishing date
- 2014
- type
- Thesis
- publication status
- published
- subject
- keywords
- Cardiac arrest, shock, outcome, prognostication, post cardiac arrest syndrome, hypothermia
- in
- Lund University Faculty of Medicine Doctoral Dissertation Series
- volume
- 2014:140
- pages
- 91 pages
- publisher
- Anaesthesiology and Intensive Care
- defense location
- Segerfalkssalen, BMC, Sölvegatan 17, Lund.
- defense date
- 2014-12-11 09:00:00
- ISSN
- 1652-8220
- ISBN
- 978-91-7619-069-2
- language
- English
- LU publication?
- yes
- id
- cb829585-5632-4d3e-aac1-f38309a8ef99 (old id 4812666)
- date added to LUP
- 2016-04-01 13:40:58
- date last changed
- 2019-05-22 05:03:17
@phdthesis{cb829585-5632-4d3e-aac1-f38309a8ef99, abstract = {{Background: <br/><br> Some improvement has been seen in survival after cardiac arrest but the outcome is still poor and 50-70% of patients do not survive despite successful return of spontaneous circulation (ROSC). The cause of death is multifactorial. The majority of patients die from brain injury, but up to 35% die as a result of circulatory failure.<br/><br> <br/><br> Purpose: <br/><br> First, to investigate the release profiles of an array of biomarkers in patients treated with mild induced hypothermia after cardiac arrest and study their correlation to the post-cardiac arrest syndrome (PCAS) and long-term outcome; Second, to investigate the effect of two different target temperatures (33°C and 36°C) on hemodynamics and vasopressor requirement in cardiac arrest patients and; Third, to investigate the association of target temperature with outcome in patients with shock in admission.<br/><br> <br/><br> Methods: <br/><br> The biomarkers were collected serially at 8 time points during the first 72 hours following cardiac arrest in 84 still comatose post-resuscitation cardiac arrest patients treated with mild induced hypothermia. We analysed markers of inflammation; procalcitonin (PCT) and c-reactive protein (CRP), oxidation; peroxiredoxin 4 (prx4), cardiac stress; MR-proANP, cardiac injury; Troponin T (TnT), brain injury; Neuron specific enlolase (NSE), and the stress hormone; CT-proAVP (copeptin). Outcome was assessed at 6 months with the cerebral performance category scale (CPC) where CPC 1-2 was considered a good outcome. The cardiovascular sequential organ failure assessment score (SOFA-score) and the time to ROSC were used as surrogate markers for the PCAS. Three different definitions of infection were used to assess occurrence of infection.<br/><br> The effect of a target temperature of 33°C or 36°C on hemodynamics was investigated in all patients with available vasopressor data (n=920) in the ‘Targeted temperature management at 33°C versus 36°C after cardiac arrest’ trial and in patients with shock on admission (n=139). Primary outcome was mortality. Secondary outcomes were vasopressor requirements as assessed by the cardiovascular SOFA-score, serum lactate concentrations, mean arterial pressure, and heart rate.<br/><br> <br/><br> Results: <br/><br> PCT, CT-proAVP and MR-proANP were all significantly higher in patients with poor outcome and correlated to surrogate markers of the PCAS. No specific cut-off levels were identified. PCT release was not associated to infection. Combinations of biomarkers may be a promising concept to improve prognostication. A targeted temperature of 33°C was associated with increased vasopressor requirements and increased lactate levels in both our investigated cohorts. A low MAP during the intervention (0-36 hours) was associated with poor outcome after adjustment for baseline characteristics.<br/><br> <br/><br> Conclusion: <br/><br> Biomarkers from other sources than the brain are associated to the PCAS and may be promising biomarkers to prognosticate outcome, alone or in combination. Targeted temperature management at 33°C is associated with increased vasopressor requirements and severity of shock and does not improve outcome as compared to 36°C.}}, author = {{Annborn, Martin}}, isbn = {{978-91-7619-069-2}}, issn = {{1652-8220}}, keywords = {{Cardiac arrest; shock; outcome; prognostication; post cardiac arrest syndrome; hypothermia}}, language = {{eng}}, publisher = {{Anaesthesiology and Intensive Care}}, school = {{Lund University}}, series = {{Lund University Faculty of Medicine Doctoral Dissertation Series}}, title = {{Cardiac arrest – prognostic biomarkers and aspects of shock}}, url = {{https://lup.lub.lu.se/search/files/3530700/4813665.pdf}}, volume = {{2014:140}}, year = {{2014}}, }