New horizons (Baltimore, Md.)
-
Artificial ventilation using intermittent positive airway pressure is the mainstay support of patients in respiratory failure. By maintaining alveolar ventilation and alveolar stability, positive airway pressure can sustain respiratory gas exchange between the lungs and circulation, thereby supporting pulmonary homeostasis in patients who would otherwise be unable to maintain oxygen transfer and CO2 elimination. However, positive-pressure ventilation (PPV) also results in complex cardiovascular interactions. ⋯ However, when considered in this manner, such interactions can be understood more easily. In most patients it is usually clear which process is dominant, permitting adjustments in overall therapy in order to optimize care. This review identifies these interactions and demonstrates which are dominant in specific clinical scenarios.
-
Multiple organ failure is the most common cause of death in critically ill patients in the United States. Acute respiratory failure is the most important single component of this clinical scenario, with a mortality risk > 50%. Key pathophysiologic events occur in the pulmonary microvasculature at the interface between circulating elements and the external environment. ⋯ We are now approaching the threshold for utilization of several new and specific approaches. While no single pharmacologic therapy is likely to be curative for this complex problem, it is probable that certain approaches will be of clinical benefit in the near future. This review is designed to provide a basis for understanding this evolution.
-
Organ interactions are increasingly recognized as key determinants of the pathogenesis and potential for resolution of tissue injury during critical illness. A paradigm for a systems model that takes into account the modulatory effects of organ interactions and incorporates the expanding number of molecular and cellular pro-inflammatory networks is still lacking. Unifying hypotheses for multiple organ dysfunction during the systemic inflammatory response syndrome have been slow to emerge. ⋯ These regulatory elements include: a) control of systemic endotoxemia, bacteremia, and vasoactive by-products of sepsis and trauma by the gut-liver axis of inflammation, mononuclear phagocytic clearance, and Fc and complement receptor-mediated events; b) production and export of endogenous cytokine and eicosanoid mediators by Kupffer cells, especially in relation to changes in the prevailing hepatic oxygen supply; c) metabolic inactivation and detoxification of such mediators via cell-to-cell interactions at the Kupffer cell-hepatocyte interface; and d) cytokine-driven synthesis of acute-phase proteins that critically modulate metabolism and inflammation. Our goal is to summarize and integrate recent information that sheds light on mechanisms by which hepatic function modulates host defense homeostasis, thereby influencing pulmonary function in the adult respiratory distress syndrome. Liver-lung interactions are presented as a heuristic paradigm of organ interactions that dynamically modulate systemic immunophysiologic responses during critical illness.