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Association of arterial blood pressure and vasopressor load with septic shock mortality: a post hoc analysis of a multicenter trial

Martin W Dünser1*, Esko Ruokonen2, Ville Pettilä3, Hanno Ulmer4, Christian Torgersen5, Christian A Schmittinger5, Stephan Jakob1 and Jukka Takala1

Author Affiliations

1 Department of Intensive Care Medicine, Inselspital, Freiburgstrasse, 3010 Bern, Switzerland

2 Department of Intensive Care, Kuopio University Hospital and Kuopio University, 70211 Kuopio, Finland

3 Australian and New Zealand Intensive Care Research Centre, Department of EPM, Monash University, 89 Commercial Road, Melbourne 3004, Victoria, Australia

4 Department of Medical Statistics, Informatics and Health Economics, Innsbruck Medical University, Schöpfstrasse, 6020 Innsbruck, Austria

5 Department of Anaesthesiology and Critical Care Medicine, Innsbruck Medical University, Anichstrasse 35, 6020 Innsbruck, Austria

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Critical Care 2009, 13:R181  doi:10.1186/cc8167

See related commentary by Jones et al.,

Published: 16 November 2009



It is unclear to which level mean arterial blood pressure (MAP) should be increased during septic shock in order to improve outcome. In this study we investigated the association between MAP values of 70 mmHg or higher, vasopressor load, 28-day mortality and disease-related events in septic shock.


This is a post hoc analysis of data of the control group of a multicenter trial and includes 290 septic shock patients in whom a mean MAP ≥ 70 mmHg could be maintained during shock. Demographic and clinical data, MAP, vasopressor requirements during the shock period, disease-related events and 28-day mortality were documented. Logistic regression models adjusted for the geographic region of the study center, age, presence of chronic arterial hypertension, simplified acute physiology score (SAPS) II and the mean vasopressor load during the shock period was calculated to investigate the association between MAP or MAP quartiles ≥ 70 mmHg and mortality or the frequency and occurrence of disease-related events.


There was no association between MAP or MAP quartiles and mortality or the occurrence of disease-related events. These associations were not influenced by age or pre-existent arterial hypertension (all P > 0.05). The mean vasopressor load was associated with mortality (relative risk (RR), 1.83; confidence interval (CI) 95%, 1.4-2.38; P < 0.001), the number of disease-related events (P < 0.001) and the occurrence of acute circulatory failure (RR, 1.64; CI 95%, 1.28-2.11; P < 0.001), metabolic acidosis (RR, 1.79; CI 95%, 1.38-2.32; P < 0.001), renal failure (RR, 1.49; CI 95%, 1.17-1.89; P = 0.001) and thrombocytopenia (RR, 1.33; CI 95%, 1.06-1.68; P = 0.01).


MAP levels of 70 mmHg or higher do not appear to be associated with improved survival in septic shock. Elevating MAP >70 mmHg by augmenting vasopressor dosages may increase mortality. Future trials are needed to identify the lowest acceptable MAP level to ensure tissue perfusion and avoid unnecessary high catecholamine infusions.