New horizons (Baltimore, Md.)
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Patients undergoing prolonged, complex oncological surgery are at increased risk of developing the adult respiratory distress syndrome (ARDS) and other organ failures. Our hypothesis is that maintaining adequate tissue perfusion and oxygenation may prevent tissue hypoxia and acidosis in pulmonary, peripheral, and splanchnic microcirculations. Experimental evidence suggests that the hypoxic, acidotic endothelium stimulates the release of cytokines, kinins, and other mediators. ⋯ Nitroglycerin and fluids were used to maintain tissue perfusion and prevent tissue hypoxia as reflected by transcutaneous oxygen tension values. In 155 high-risk patients, none developed ARDS. We conclude that maintenance of tissue perfusion and oxygenation in high-risk surgical patients decreases the incidence of ARDS.
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Near-infrared spectroscopy (NIRS) is a relatively new tool that allows continuous noninvasive monitoring of in vivo oxygenation in selected tissues such as muscle and brain. Since hemoglobin, myoglobin, and cytochrome c oxidase are the only biological compounds to exhibit variable absorption of near-infrared (NIR) light in response to changes in oxygen availability, NIRS can determine changes in tissue oxygenation. ⋯ As a comprehensive monitor of regional oxygen metabolism, NIRS has been applied in certain clinical and research settings. Despite technical limitations and the lack of definite "gold standards" to allow validation of results, NIRS remains a promising technology with applications in both the critical care environment and the research laboratory studying mechanisms of oxygen metabolism.
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Burn resuscitation has been performed predominantly by means of the Parkland formula for the past 25 years. Normalization of heart rate, blood pressure, and production of 1 mL/kg/hr of urine were proposed as suitable guides to resuscitation. Recently, it has become apparent that the standard circulatory criteria of fluid replacement adequacy are too inaccurate to produce optimal hemodynamic end points. ⋯ Elderly burn patients were resuscitated at lower end points than younger individuals because of volume intolerance. Inability to be aggressively resuscitated results in twice the mortality in burn-injured elderly patients. These experiences indicate that burn resuscitation as currently practiced with existing formulas produces inadequate circulatory responses, and both survival and organ function can be improved by maximizing circulatory end points.
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During shock resuscitation, a combination of fluids, vasopressors, vasodilators, and inotropes is administered in order to achieve a cardiac output or overall oxygen delivery as per guidelines of individual clinicians. The measurement of ventricular end-diastolic pressure allows a clinician to describe a therapeutic goal of optimum cardiac output response to changes in end-diastolic pressure. This concept has formed the backbone of resuscitative strategies in many forms of shock. ⋯ It is now clear that a significant gradient between pulmonary capillary pressure and PAOP may be present in inflammatory disorders which are not present in noninflammatory states, and that pulmonary capillary pressure may be measured at the bedside of critically ill patients. Bedside measurement of pulmonary capillary pressure may allow for added precision in our therapeutic goals in resuscitation from inflammatory shock. If further studies confirm the reliability and reproducibility of bedside measurement, pulmonary capillary pressure may become an invaluable part of the hemodynamic profile in the critically ill patient in shock.
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The endothelial cell (EC) was once though to be a passive bystander in the inflammatory response to shock and injury. We now know, however, that these cells play a central role in the coordination of the response to injury. Hypovolemic shock following traumatic injury initiates two primary mechanisms of cellular damage. ⋯ In the settings of ischemia/reperfusion and acute inflammation, the EC takes on a proinflammatory phenotype and as such becomes prothrombotic, demonstrates enhanced vascular permeability, and becomes chemoattractant, facilitating leukocyte adhesion, activation, and migration. In this article, we explore each of the four EC functions in detail along with the alterations that occur when the proinflammatory phenotype becomes manifest. In addition, we elucidate novel therapeutic strategies that have arisen from this research.