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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*

Bro-Jeppesen, John MD, PhD1; Annborn, Martin MD2; Hassager, Christian MD, DMSc1; Wise, Matt P. MD, DPhil3; Pelosi, Paolo MD4; Nielsen, Niklas MD, PhD5; Erlinge, David MD, PhD6; Wanscher, Michael MD, PhD7; Friberg, Hans MD, PhD2; Kjaergaard, Jesper MD, PhD, DMSc1 on behalf of the TTM Investigators

doi: 10.1097/CCM.0000000000000691
Clinical Investigations
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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 hemodynamics.

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°C or 36°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]; pgroup < 0.0001), similar mean arterial pressure (–1.1 mm Hg [95% confidence limit, –2.3, 0.2]; pgroup = 0.10), and increased lactate (0.6 mmol/L [95% confidence limit, 0.3, 0.8]; pgroup < 0.0001) compared with the targeted temperature management 36 (TTM36) 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°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°C. Low mean arterial pressure and need for high doses of vasopressors were associated with increased mortality independent of allocated targeted temperature management.

1Department of Cardiology, The Heart Centre, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.

2Department of Anesthesia and Intensive Care, Lund University, Skåne University Hospital, Lund, Sweden.

3Adult Clinical Care, University Hospital of Wales, Cardiff, United Kingdom.

4Department of Surgical Sciences and Integrated Diagnostics, University of Genoa, Anesthesia and Intensive Care, IRCCS San Martino IST, Genoa, Italy.

5Department of Anesthesia and Intensive Care, Lund University, Helsingborg Hospital, Helsingborg, Sweden.

6Department of Cardiology, Lund University, Skåne University Hospital, Lund, Sweden.

7Department of Cardiothoracic Anaesthesia, The Heart Centre, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.

* See also p. 483.

Unique identifier: NCT01020916 (http://clinicaltrials.gov/ct2/show/NCT01020916).

Supported, in part, by independent research grants from the Swedish Heart-Lung Foundation, Arbetsmarknadens Försäkringsaktiebolag Insurance foundation, Swedish Research Council, Region Skåne (Sweden), National Health Service (Sweden), Thelma Zoegas Foundation, Krapperup Foundation, Thure Carlsson Foundation, Hans-Gabriel and Alice Trolle-Wachtmeister Foundation for Medical Research, Skåne University Hospital, TrygFonden (Denmark), European Clinical Research Infrastructures Network, and EU Interreg programme IV A.

The institution of Dr. Bro-Jeppesen received grant support from Trygfonden. Dr. Hassager lectured for Astra Zeneca. Dr. Wise received grant support from the National Institute for Social Care and Health Research (NISCHR) Academic Health Science Collaboration (AHSC) Clinical Research Fellowship (research fellowship funding 0.4WTE for research); served as board member for the Bard Advisory Board (hypothermia) and the Merck Advisory Board (Nutrition); is employed by the NISCHR AHSC Research Fellowship; lectured for Fisher & Paykel (educational meeting); received royalties from Wiley Publishing (book chapters for textbook); received support for travel from International Symposium on Intensive Care and Emergency Medicine, Eli Lilly, British Thoracic Society, and Intensive Care Society; and received other support from CareFusion (loan of EIT equipment for research) and Sage Products (gift of oral care products for research). Dr. Nielsen received speaker’s honorarium from Bard International. His institution received grant support from the Swedish Heart and Lung foundation, Arbetsmarknadens Försäkringsaktiebolag Insurance Foundation, Swedish Research Council, and from Regional and Governmental funds within the Swedish Health Care system. Dr. Friberg lectured for Bard Medical Natus. His institution received grant support from the European Union Interreg IVA. Dr. Kjaergaard received grant support from TrygFonden. The remaining authors have disclosed that they do not have any potential conflicts of interest.

For information regarding this article, E-mail:jbj@dadlnet.dk

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