scholarly journals 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

2020 ◽  
pp. 204887262093430
Author(s):  
Johannes Grand ◽  
Christian Hassager ◽  
Markus B Skrifvars ◽  
Marjaana Tiainen ◽  
Anders M Grejs ◽  
...  

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.

2019 ◽  
Vol 50 ◽  
pp. 234-241 ◽  
Author(s):  
Johannes Grand ◽  
Christian Hassager ◽  
Matilde Winther-Jensen ◽  
Malin Rundgren ◽  
Hans Friberg ◽  
...  

Platelets ◽  
2017 ◽  
Vol 29 (5) ◽  
pp. 504-511 ◽  
Author(s):  
Anni Nørgaard Jeppesen ◽  
Anne-Mette Hvas ◽  
Anders Morten Grejs ◽  
Christophe Duez ◽  
Susanne Ilkjær ◽  
...  

2019 ◽  
Vol 9 (4_suppl) ◽  
pp. S122-S130 ◽  
Author(s):  
Johannes Grand ◽  
Gisela Lilja ◽  
Jesper Kjaergaard ◽  
John Bro-Jeppesen ◽  
Hans Friberg ◽  
...  

Objectives: During targeted temperature management after out-of-hospital cardiac arrest infusion of vasoactive drugs is often needed to ensure cerebral perfusion pressure. This study investigated mean arterial pressure after out-of-hospital cardiac arrest and the association with brain injury and long-term cognitive function. Methods: Post-hoc analysis of patients surviving at least 48 hours in the biobank substudy of the targeted temperature management trial with available blood pressure data. Patients were stratified in three groups according to mean arterial pressure during targeted temperature management (4–28 hours after admission; <70 mmHg, 70–80 mmHg, >80 mmHg). A biomarker of brain injury, neuron-specific enolase, was measured and impaired cognitive function was defined as a mini-mental state examination score below 27 in 6-month survivors. Results: Of the 657 patients included in the present analysis, 154 (23%) had mean arterial pressure less than 70 mmHg, 288 (44%) had mean arterial pressure between 70 and 80 mmHg and 215 (33%) had mean arterial pressure greater than 80 mmHg. There were no statistically significant differences in survival ( P=0.35) or neuron-specific enolase levels ( P=0.12) between the groups. The level of target temperature did not statistically significantly interact with mean arterial pressure regarding neuron-specific enolase ( Pinteraction_MAP*TTM=0.58). In the subgroup of survivors with impaired cognitive function ( n=132) (35%) mean arterial pressure during targeted temperature management was significantly higher ( Pgroup=0.03). Conclusions: In a large cohort of comatose out-of-hospital cardiac arrest patients, low mean arterial pressure during targeted temperature management was not associated with higher neuron-specific enolase regardless of the level of target temperature (33°C or 36°C for 24 hours). In survivors with impaired cognitive function, mean arterial pressure during targeted temperature management was significantly higher.


Author(s):  
Thomas Hvid Jensen ◽  
Peter Juhl-Olsen ◽  
Bent Roni Ranghøj Nielsen ◽  
Johan Heiberg ◽  
Christophe Henri Valdemar Duez ◽  
...  

Abstract Background Transthoracic echocardiographic (TTE) indices of myocardial function among survivors of out-of-hospital cardiac arrest (OHCA) have been related to neurological outcome; however, results are inconsistent. We hypothesized that changes in average peak systolic mitral annular velocity (s’) from 24 h (h) to 72 h following start of targeted temperature management (TTM) predict six-month neurological outcome in comatose OHCA survivors. Methods We investigated the association between peak systolic velocity of the mitral plane (s’) and six-month neurological outcome in a population of 99 patients from a randomised controlled trial comparing TTM at 33 ± 1 °C for 24 h (h) (n = 47) vs. 48 h (n = 52) following OHCA (TTH48-trial). TTE was conducted at 24 h, 48 h, and 72 h after reaching target temperature. The primary outcome was 180 days neurological outcome assessed by Cerebral Performance Category score (CPC180) and the primary TTE outcome measure was s’. Secondary outcome measures were left ventricular ejection fraction (LVEF), global longitudinal strain (GLS), e’, E/e’ and tricuspid annular plane systolic excursion (TAPSE). Results Across all three scan time points s’ was not associated with neurological outcome (ORs: 24 h: 1.0 (95%CI: 0.7–1.4, p = 0.98), 48 h: 1.13 (95%CI: 0.9–1.4, p = 0.34), 72 h: 1.04 (95%CI: 0.8–1.4, p = 0.76)). LVEF, GLS, E/e’, and TAPSE recorded on serial TTEs following OHCA were neither associated with nor did they predict CPC180. Estimated median e’ at 48 h following TTM was 5.74 cm/s (95%CI: 5.27–6.22) in patients with good outcome (CPC180 1–2) vs. 4.95 cm/s (95%CI: 4.37–5.54) in patients with poor outcome (CPC180 3–5) (p = 0.04). Conclusions s’ assessed on serial TTEs in comatose survivors of OHCA treated with TTM was not associated with CPC180. Our findings suggest that serial TTEs in the early post-resuscitation phase during TTM do not aid the prognostication of neurological outcome following OHCA. Trial registration NCT02066753. Registered 14 February 2014 – Retrospectively registered,


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