Literature DB >> 11096549

Cardiovascular Dysfunction in Sepsis and Septic Shock.

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Abstract

The optimal therapy for the treatment of sepsis and septic shock remains controversial. Many protocols are followed, using different strategies for initial resuscitation, cardiovascular monitoring, hemodynamic intervention, and eradication of infection. Overall, an aggressive approach to the management of cardiovascular dysfunction in septic shock is warranted. Initially, large volume fluid resuscitation is instituted. Our first choice of resuscitation fluid is 0.9% normal saline. Invasive hemodynamic monitoring using a flotation pulmonary artery catheter as well as invasive arterial blood pressure monitoring is a necessity in the hemodynamic management of septic shock. If the patient remains hypotensive (mean arterial pressure < 65 mm Hg) after adequate volume resuscitation has been established (pulmonary capillary wedge pressure 12 to 15 mm Hg), then vasopressor agents must be instituted. Our first choice is usually dopamine. In patients who remain hypotensive after maximal doses of dopamine are reached, norepinephrine is added. If these agents generate excessive tachycardia or if tachyarrhythmias develop, phenylephrine can be substituted or added. Inotropic agents are useful if the patient demonstrates hypotension with a low cardiac output state. Dobutamine is the agent of choice. We initiate broad-spectrum empiric antibiotics at presentation, modifying the exact regimen based on 1) site of infection; 2) prevailing organisms and antibiotic resistance patterns in the patient's environment; and 3) other specific risk factors (immunosuppression, chronic disease, exposure and vaccination history, invasive medical devices). When appropriate, aggressive surgical debridement is pursued. Currently, there are no clinical data to support the use of antagonists for sepsis mediators, although various clinical trials remain underway. Steroids are contraindicated except for adrenal replacement therapy.

Entities:  

Year:  2000        PMID: 11096549     DOI: 10.1007/s11936-000-0040-z

Source DB:  PubMed          Journal:  Curr Treat Options Cardiovasc Med        ISSN: 1092-8464


  13 in total

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Authors:  A Kumar; V Thota; L Dee; J Olson; E Uretz; J E Parrillo
Journal:  J Exp Med       Date:  1996-03-01       Impact factor: 14.307

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  5 in total

1.  Bacterial RNA induces myocyte cellular dysfunction through the activation of PKR.

Authors:  Farag Bleiblo; Paul Michael; Danielle Brabant; Chilakamarti V Ramana; Tc Tai; Mazen Saleh; Joseph E Parrillo; Anand Kumar; Aseem Kumar
Journal:  J Thorac Dis       Date:  2012-04-01       Impact factor: 2.895

2.  Chronic kidney disease and risk of death from infection.

Authors:  Henry E Wang; Christopher Gamboa; David G Warnock; Paul Muntner
Journal:  Am J Nephrol       Date:  2011-08-22       Impact factor: 3.754

3.  Bigendothelin-1 (1-21) fragment during early sepsis modulates tau, p38-MAPK phosphorylation and nitric oxide synthase activation.

Authors:  Sachin Brahmbhatt; Akanksha Gupta; Avadhesh C Sharma
Journal:  Mol Cell Biochem       Date:  2005-03       Impact factor: 3.396

Review 4.  Proinflammatory Cytokines Mediate GPCR Dysfunction.

Authors:  Maradumane L Mohan; Neelakantan T Vasudevan; Sathyamangla V Naga Prasad
Journal:  J Cardiovasc Pharmacol       Date:  2017-08       Impact factor: 3.105

Review 5.  Clinical review: splanchnic ischaemia.

Authors:  Stephan M Jakob
Journal:  Crit Care       Date:  2002-04-08       Impact factor: 9.097

  5 in total

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