Critical care : the official journal of the Critical Care Forum
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An association between abnormal gastrointestinal perfusion and critical illness has been suggested for a number of years. Much of the data to support this idea comes from studies using gastric tonometry. ⋯ Furthermore, current understanding of the physiology of gastrointestinal perfusion in health and disease is incomplete. This review considers critically the striking clinical data and basic physiological investigations that support a key role for gastrointestinal hypoperfusion in initiating and/or perpetuating critical disease.
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An advanced understanding of acid-base physiology is as central to the practice of critical care medicine, as are an understanding of cardiac and pulmonary physiology. Intensivists spend much of their time managing problems related to fluids, electrolytes, and blood pH. Recent advances in the understanding of acid-base physiology have occurred as the result of the application of basic physical-chemical principles of aqueous solutions to blood plasma. ⋯ These variables are carbon dioxide, relative electrolyte concentrations, and total weak acid concentrations. All changes in blood pH, in health and in disease, occur through changes in these three variables. Clinical implications for these findings are also discussed.
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A moribund and debilitated patient arrives in an emergency department and is placed on life support systems. Subsequently it is determined that she has a 'living will' proscribing aggressive measures should her condition be judged 'terminal' by her physicians. ⋯ The patient's surrogates are unable to agree on whether she would desire continuation of mechanical ventilation if there was a real chance of improvement or if she would want to have her living will enforced as soon it's terms were revealed. The problem of the potential ambiguity of a living will is explored.
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Comparative Study
Heat stress is associated with decreased lactic acidemia in rat sepsis.
Elevated plasma lactate has been shown to correlate with mortality in patients with septic shock. Heat stress prior to sepsis has resulted in reduction in acute lung injury and mortality. We investigated whether heat stress resulted in decreased plasma lactate concentration and protected the lung by decreasing the inflammatory response to sepsis. ⋯ Prior heat stress ameliorates lactic acidemia in rat sepsis. Heat stress did not attenuate the pulmonary inflammatory process. The mechanism of heat-induced protection from lactic acidemia in sepsis needs to be further explored.