4.6 Article

Hemodynamics and Vasopressor Support During Targeted Temperature Management at 33°C Versus 36°C After Out-of-Hospital Cardiac Arrest A Post Hoc Study of the Target Temperature Management Trial

期刊

CRITICAL CARE MEDICINE
卷 43, 期 2, 页码 318-327

出版社

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/CCM.0000000000000691

关键词

cardiac arrest; hennodynamics; hypothermia; mortality; vasopressor

资金

  1. Swedish Heart-Lung Foundation
  2. Arbetsmarknadens Forsakringsaktiebolag Insurance foundation
  3. Swedish Research Council
  4. Region Skane (Sweden)
  5. National Health Service (Sweden)
  6. Thelma Zoegas Foundation
  7. Krapperup Foundation
  8. Thure Carlsson Foundation
  9. Hans-Gabriel and Alice Trolle-Wachtmeister Foundation for Medical Research
  10. Skane University Hospital
  11. TrygFonden (Denmark)
  12. European Clinical Research Infrastructures Network
  13. EU Interreg programme IV A
  14. Trygfonden
  15. National Institute for Social Care and Health Research (NISCHR) Academic Health Science Collaboration (AHSC) Clinical Research Fellowship [0.4WTE]
  16. Swedish Heart and Lung foundation
  17. Regional fund within the Swedish Health Care system
  18. Governmental fund within the Swedish Health Care system
  19. European Union Interreg IVA

向作者/读者索取更多资源

Objective: To investigate the hemodynamic profile associated with different target temperatures and to assess the prognostic implication of inotropic/vasopressor support and mean arterial pressure after out-of-hospital cardiac arrest. There is a lack of information how different target temperatures may affect hennodynamics. Design: Post hoc analysis of a prospective randomized study. Setting: Thirthy-six ICUs in 10 countries. Patients: Nine hundred twenty patients (97%) with available vasopressor data out of 950 patients from-the Target Temperature Management trial randomly assigned patients to a targeted temperature management at 33 degrees C or 36 degrees C: Interventions: None. Measurements and Main Results: Mean arterial pressure, heart rate, and lactate were registered at prespecified time points. The population was stratified according to cardiovascular Sequential Organ Failure Assessment = 4 defining the high vasopressor group and cardiovascular Sequential Organ Failure. Assessment less than or equal to 3 defining the low vasopressor group. The targeted temperature management 33 (TTM33) group had a hemodynamic profile with lower heart rate (-7.0 min(-1) [95% confidence limit, 8.7, 5.1]; [P-group < 0.0001), similar mean arterial pressure (-1.1 mm Hg [95% confidence limit, 2.3, 0.2]; P-group = 0.10), and increased lactate (0.6 mmol/L [95% confidence limit, 0.3, 0.8]; p(group) < 0.0001) compared with the targeted temperature management 36 (11M36) group. A cardiovascular Sequential Organ Failure Assessment score = 4 was recorded in 54% versus 45%, p = 0.03 in the TTM33 and the TTM36 group, respectively. The high vasopressor group carried a 53% mortality rate when compared with a 34% in the low vasopressor group, Plog-rank, less than 0.0001, with an adjusted hazard ratio of 1.38 (95% CI, 1.11 1.71; p = 0.004). There was no interaction between vasopressor group and allocated target temperature group (p = 0.40). An inverse relationship between mean arterial pressure and mortality was identified (p = 0.0008). Conclusions: Targeted temperature management at 33 degrees C was associated with hemodynamic alterations with decreased heart rate, elevated levels of lactate, and need for increased vasopressor support compared with targeted temperature management at 36 degrees C. Low mean arterial pressure and need for high doses of vasopressors were associated with increased mortality independent of allocated targeted temperature management.

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