Goals of Resuscitation from Circulatory Shock

2004 ◽  
pp. 94-104 ◽  
Author(s):  
M.R. Pinsky
Keyword(s):  
Circulatory Shock

scholarly journals H2S in acute lung injury: a therapeutic dead end(?)

2020 ◽  
Vol 8 (S1) ◽  
Author(s):  
Tamara Merz ◽  
Nicole Denoix ◽  
Martin Wepler ◽  
Holger Gäßler ◽  
David A. C. Messerer ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Circulatory Shock ◽  
Therapeutic Window ◽  
Pharmacokinetics And Pharmacodynamics ◽  
Clinical Reality ◽  
Dead End

AbstractThis review addresses the plausibility of hydrogen sulfide (H2S) therapy for acute lung injury (ALI) and circulatory shock, by contrasting the promising preclinical results to the present clinical reality. The review discusses how the narrow therapeutic window and width, and potentially toxic effects, the route, dosing, and timing of administration all have to be balanced out very carefully. The development of standardized methods to determine in vitro and in vivo H2S concentrations, and the pharmacokinetics and pharmacodynamics of H2S-releasing compounds is a necessity to facilitate the safety of H2S-based therapies. We suggest the potential of exploiting already clinically approved compounds, which are known or unknown H2S donors, as a surrogate strategy.

Endothelial Dysfunction in Shock States

Physiology ◽  
1993 ◽  
Vol 8 (4) ◽  
pp. 145-148 ◽  
Author(s):  
AGB Kovach ◽  
AM Lefer
Keyword(s):  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
Tissue Injury ◽  
Circulatory Shock ◽  
Relaxing Factor ◽  
Vascular Beds ◽  
Endothelium Derived Relaxing Factor

Circulatory shock results in dysfunction of the endothelium in various vascular beds. This dysfunction is characterized by marked impairment in the vasculature's ability to relax to endothelium-dependent vasodilators. This loss of endothelium-derived relaxing factor, or nitric oxide, leads to profound tissue injury.

scholarly journals Noradrenaline versus Dopamine in the Treatment of Circulatory Shock

2010 ◽  
Vol 11 (4) ◽  
pp. 272-274
Author(s):  
Hozefa Ebrahim ◽  
Tomasz Torlinski
Keyword(s):  
Circulatory Shock

scholarly journals Target arterial PO2 according to the underlying pathology: a mini-review of the available data in mechanically ventilated patients

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Julien Demiselle ◽  
Enrico Calzia ◽  
Clair Hartmann ◽  
David Alexander Christian Messerer ◽  
Pierre Asfar ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Large Scale ◽  
Retrospective Studies ◽  
Prolonged Exposure ◽  
Oxygen Toxicity ◽  
Circulatory Shock ◽  
Mechanically Ventilated ◽  
Ischaemia Reperfusion ◽  
Arterial Po2 ◽  
Underlying Pathology

AbstractThere is an ongoing discussion whether hyperoxia, i.e. ventilation with high inspiratory O2 concentrations (FIO2), and the consecutive hyperoxaemia, i.e. supraphysiological arterial O2 tensions (PaO2), have a place during the acute management of circulatory shock. This concept is based on experimental evidence that hyperoxaemia may contribute to the compensation of the imbalance between O2 supply and requirements. However, despite still being common practice, its use is limited due to possible oxygen toxicity resulting from the increased formation of reactive oxygen species (ROS) limits, especially under conditions of ischaemia/reperfusion. Several studies have reported that there is a U-shaped relation between PaO2 and mortality/morbidity in ICU patients. Interestingly, these mostly retrospective studies found that the lowest mortality coincided with PaO2 ~ 150 mmHg during the first 24 h of ICU stay, i.e. supraphysiological PaO2 levels. Most of the recent large-scale retrospective analyses studied general ICU populations, but there are major differences according to the underlying pathology studied as well as whether medical or surgical patients are concerned. Therefore, as far as possible from the data reported, we focus on the need of mechanical ventilation as well as the distinction between the absence or presence of circulatory shock. There seems to be no ideal target PaO2 except for avoiding prolonged exposure (> 24 h) to either hypoxaemia (PaO2 < 55–60 mmHg) or supraphysiological (PaO2 > 100 mmHg). Moreover, the need for mechanical ventilation, absence or presence of circulatory shock and/or the aetiology of tissue dysoxia, i.e. whether it is mainly due to impaired macro- and/or microcirculatory O2 transport and/or disturbed cellular O2 utilization, may determine whether any degree of hyperoxaemia causes deleterious side effects.

Mechanism of circulatory shock induced by monoclonal antibody against neutrophils

1994 ◽  
Vol 1 ◽  
pp. 212
Author(s):  
I. Shiraishi ◽  
EF. Sato ◽  
M. Nishikawa ◽  
F. Sendo ◽  
M. Inoue
Keyword(s):  
Monoclonal Antibody ◽  
Circulatory Shock

Circulatory shock in pregnant sheep

1972 ◽  
Vol 112 (8) ◽  
pp. 1084-1094 ◽  
Author(s):  
P. Bech-Jansen ◽  
C.R. Brinkman ◽  
G.H. Johnson ◽  
N.S. Assali
Keyword(s):  
Circulatory Shock ◽  
Pregnant Sheep

THE ROLE OF INFLAMMATORY CELLS IN THE DEVELOPMENT OF CIRCULATORY SHOCK ELICITED BY THE REPERFUSION INJURY OF THE SMALL INTESTINE.

Shock ◽  
1994 ◽  
Vol 2 (Supplement) ◽  
pp. 28
Author(s):  
J. Hamar ◽  
G. Illyés ◽  
G. Gösi ◽  
L. Vimláti ◽  
I. B. Rácz ◽  
...  
Keyword(s):  
Small Intestine ◽  
Reperfusion Injury ◽  
Inflammatory Cells ◽  
Circulatory Shock
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