Sierra-Unzueta A

Language: Spanish
References: 8
Page: 412-414
PDF size: 55.90 Kb.

ABSTRACT

In 1987 Moncada and Ignarro introduced nitric oxide (NO) and described it as one of the factors causing hypotension and disruptions in perfusion distribution observed during shock. NO is able to produce systemic vasodilation, vascular hyporesponsiveness to vasopressor agents, reduced oxygen extraction from tissues, decreased muscle contractility, increased epithelial and vascular permeability, and sequential dysfunction of vital organs. Therefore, is to a great extent responsible for the refractory vascular failure observed in septic shock and the progression to multiple organ failure. As a result of the above, a hypothesis stating that the selective inhibition of nitric oxide synthases (iNOS) could be beneficial during septic shock was proposed. However, to date no clinical trial has proven this hypothesis.One of the most difficult aspects during resuscitation after shock is to assure an optimum effective tidal volume. A study published by Michar, Y. et al. in 2000 tried to determine the optimal variable to assure target tidal volume. Finally, a study by Rivers et al. on an early aggressive approach to patients with septic shock and severe sepsis was reported.

REFERENCES

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6. Betbesé AJ, Net A, Mancebo J, Vallverdú I. Papel del óxido nítrico inhalado en la función cardiopulmonary. En: Net A, Vallverdú I, eds. Función cardioascular en el paciente grave. Barcelona: Masson; 2005. pp. 73-91.

7. LeDoux D, Astiz ME, Carpati ChM, et al. Effects of perfusion pressure on tissue perfusion in septic shock. Crit Care Med 2000;28:2729-2732.

8. Rivers E, Nguyen B, Havstaq S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001;345:1368- 1377.