Increasing mean arterial pressure in patients with septic shock: Effects on oxygen variables and renal function*

Bourgoin, A; Léone, Marc; Delmas, Anne; Garnier, F.; Albanèse, Jacques; Martin, Claude

doi:10.1097/01.ccm.0000157788.20591.23

Cited by 309 publications

(167 citation statements)

References 33 publications

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“…In fact, there is no evidence that higher values of blood pressure are of benefit in septic patients. This conclusion is supported by some recently published clinical studies, which have not shown improvement in renal function, splanchnic perfusion or oxygen variables when mean arterial pressure was increased with noradrenalin from 65 to 85 mmHg in volume-resuscitated patients [27,28].…”

Section: Discussionsupporting

confidence: 73%

Effect of blood pressure on plasma volume loss in the rat under increased permeability

2007

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This is an author produced version of a paper published in Intensive care medicine. This paper has been peerreviewed but does not include the final publisher proofcorrections or journal pagination.Citation for the published paper: Dubniks M, Persson J, Grände PO. "Effect of blood pressure on plasma volume loss in the rat under increased permeability" Intensive care medicine, 2007, Vol: 33, Issue: 12, pp. 2192 http://dx.doi.org/10.1007/s00134-007-0756-2Access to the published version may require journal subscription. Published with permission from: Springer Verlag Design: Prospective randomised laboratory study.Subject: Forty-five adult male Sprague-Dawley rats.Interventions: Permeability was increased via an anaphylactic reaction by injection of 0.5 ml dextran 70. One hour later, volume expansion with 15 ml/kg of 5% albumin was given for 15 min.Plasma volume was measured just before and 2.5 hours after the albumin infusion ( 125 I-albumin tracer technique). The study included a control group, a noradrenalin group and a metoprolol/clonidine group (n=10 in each group). The vasoactive treatment started after albumin infusion and continued throughout the experiment. Plasma volume was also measured in a separate group without albumin infusion, to evaluate the effect of noradrenalin-induced increase in blood pressure under hypovolemia (n=9). CVP was measured to estimate the venous pressure effect of noradrenalin (n=6). Results:The remaining increase in plasma volume 2.5 h after infusion of 15 ml/kg of albumin was 11.8 ± 3.6 ml/kg in the control group compared with 0.5 ± 6.3 ml/kg in the noradrenalin group (p < 0.001) and with 12.5 ± 4.9 ml/kg in the metoprolol/clonidine group (ns). The reduction in plasma volume by noradrenalin infusion was much smaller in the group not given albumin, or 3.5 ± 3.0 ml/kg. Conclusion:Noradrenalin infusion increases the loss of plasma volume during a state of increased permeability which, according to the 2-pore theory of transvascular fluid exchange, may be explained by increased hydrostatic capillary pressure. The loss was less pronounced in hypovolemia.3

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Section: Discussionsupporting

confidence: 73%

Effect of blood pressure on plasma volume loss in the rat under increased permeability

2007

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“…In a single-center trial [26], dose titration of norepinephrine from 65 to 75 and 85 mm Hg raised cardiac index (from 4.7 ± 0.5 to 5.5 ± 0.6 L/min/m 2 ) but did not change urinary flow, arterial lactate levels, oxygen delivery and consumption, gastric mucosal Pco 2 , RBC velocity, or skin capillary flow. Another single-center [27] trial compared, in norepinephrine-treated septic shock, dose titration to maintain MAP at 65 mm Hg versus achieving 85 mm Hg. In this trial, targeting high MAP increased cardiac index from 4.8 (3.8-6.0) to 5.8 (4.3-6.9) L/min/m 2 but did not change renal function, arterial lactate levels, or oxygen consumption.…”

mentioning

confidence: 99%

Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016

et al. 2017

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Objective: To provide an update to "Surviving Sepsis Campaign Guidelines for Management of Sepsis and Septic Shock: 2012". Design:A consensus committee of 55 international experts representing 25 international organizations was convened. Nominal groups were assembled at key international meetings (for those committee members attending the conference). A formal conflict-of-interest (COI) policy was developed at the onset of the process and enforced throughout. A stand-alone meeting was held for all panel members in December 2015. Teleconferences and electronic-based discussion among subgroups and among the entire committee served as an integral part of the development. Methods:The panel consisted of five sections: hemodynamics, infection, adjunctive therapies, metabolic, and ventilation. Population, intervention, comparison, and outcomes (PICO) questions were reviewed and updated as needed, and evidence profiles were generated. Each subgroup generated a list of questions, searched for best available evidence, and then followed the principles of the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) system to assess the quality of evidence from high to very low, and to formulate recommendations as strong or weak, or best practice statement when applicable.

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“…Because a MAP level of 65 mmHg is a survival factor in critically ill patients [88], especially during sepsis [89][90][91], this value is usually considered as the lowest acceptable level required for maintaining renal perfusion during AKI [92]. A diastolic arterial pressure <50-55 mmHg is associated with an increased AKI occurrence during septic shock [93,94]. Because the threshold for renal autoregulation may be higher in the elderly and patients with a cardiovascular history, the requirement of maintaining MAP above a 65-mmHg threshold is frequently questioned for these patients.…”

Section: (Grade 2+) Strong Agreementmentioning

confidence: 99%

Acute kidney injury in the perioperative period and in intensive care units (excluding renal replacement therapies)

Ichai

Vinsonneau

Souweine

et al. 2016

Anaesthesia Critical Care & Pain Medicine

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Acute kidney injury (AKI) is a syndrome that has progressed a great deal over the last 20 years. The decrease in urine output and the increase in classical renal biomarkers, such as blood urea nitrogen and serum creatinine, have largely been used as surrogate markers for decreased glomerular filtration rate (GFR), which defines AKI. However, using such markers of GFR as criteria for diagnosing AKI has several limits including the difficult diagnosis of non-organic AKI, also called "functional renal insufficiency" or "pre-renal insufficiency". This situation is characterized by an oliguria and an increase in creatininemia as a consequence of a reduction in renal blood flow related to systemic haemodynamic abnormalities. In this situation, "renal insufficiency" seems rather inappropriate as kidney function is not impaired. On the contrary, the kidney delivers an appropriate response aiming to recover optimal systemic physiological haemodynamic conditions. Considering the kidney as insufficient is erroneous because this suggests that it does not work correctly, whereas the opposite is occurring, because the kidney is healthy even in a threatening situation. With current definitions of AKI, normalization of volaemia is needed before defining AKI in order to avoid this pitfall.

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Increasing mean arterial pressure in patients with septic shock: Effects on oxygen variables and renal function*

Abstract: Increasing mean arterial pressure from 65 to 85 mm Hg with norepinephrine neither affects metabolic variables nor improves renal function.

Cited by 309 publications

References 33 publications

Effect of blood pressure on plasma volume loss in the rat under increased permeability

Effect of blood pressure on plasma volume loss in the rat under increased permeability

Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016

Acute kidney injury in the perioperative period and in intensive care units (excluding renal replacement therapies)

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