In critically ill patients, emergency tracheal intubation is associated with a significant frequency of major complications. In this study, complications were not increased when intubations were accomplished without the supervision of an attending physician as long as the intubation was carried out or supervised by an individual skilled in airway management. Mortality associated with emergent tracheal intubation is highest in patients who are hemodynamically unstable and receiving vasopressor therapy before intubation.

The maximal exercise capacity of patients with chronic heart failure is frequently reduced. To investigate whether this exercise intolerance is caused by inadequate nutritive flow to skeletal muscle, we compared cardiac outputs, leg blood flow, and leg metabolism during maximal bicycle exercise in seven patients with normal maximal oxygen uptake (V02) (>20 ml/min/kg; group A), eight patients with heart failure and moderately reduced maximal V02 (15 to 18 ml/min/kg; group B), and eight patients with heart failure and markedly reduced maximal V02 (<14 ml/min/kg; group C). As the severity of exercise intolerance increased from group A to group C there was a progressive decline in cardiac output and leg blood flow at any given workload accompanied by a progressive decline in maximal cardiac output (liters/min) (A, 12.4 + 1.0; B, 8.7 ± 0.9; C, 5.5 ± 0.7), maximal leg flow (liters/min) (A, 4.0 0.3; B, 2.6 + 0.4; C, 1.4 + 0.2), and maximal leg V02 (ml/min) (A, 564 + 49; B, 403 + 41; C, 213 ± 35 ml/min). All patients terminated exercise because of severe leg fatigue. At termination of exercise, all three groups exhibited similar marked levels of leg 02 extraction (%) (A, 80 ± 2; B, 83 + 3; C, 89 + 1) and high femoral-arterial lactate gradients (mg/dl) (A, 15.4 + 2.6; B, 18.3 ± 3.5; C, 19.2 ± 3.6), suggesting that exercise was limited when a critical level of muscle underperfusion was reached. These data suggest that the reduced maximal exercise capacity of patients with chronic heart failure is primarily due to impaired nutritive flow to skeletal muscle and resultant muscular fatigue. Circulation 69, No. 6, 1079No. 6, -1087No. 6, , 1984. THE MAXIMAL exercise capacity of patients with chronic heart failure is frequently reduced.'-1 It has recently been suggested that this exercise intolerance is primarily caused by inadequate blood flow to working skeletal muscle,3'4 since patients with heart failure have reduced cardiac outputs, early increases in lactate concentration, and augmented limb 02 extraction during exercise.3 6 However, it has yet to be directly demonstrated that perfusion of working skeletal muscle is impaired during upright maximal exercise in such patients.Accordingly, this study was undertaken to determine whether blood flow in skeletal muscle is reduced during maximal exercise in patients with chronic heart

Mechanical ventilation of lungs is capable of activating the innate immune system and inducing sterile inflammatory response. The proinflammatory cytokine IL-1β is among the definitive markers for accurately identifying ventilator-induced lung inflammation. However, mechanisms of IL-1β release during mechanical ventilation are unknown. Here we show that cyclic stretch activates the NLRP3 inflammasomes and induces the release of IL-1β in mouse alveolar macrophages via caspase-1- and TLR4-dependent mechanisms. We also observed that NADPH oxidase subunit gp91phox was dispensable for stretch-induced cytokine production whereas mitochondrial generation of reactive oxygen species was required for stretch-induced NLRP3 inflammasome activation and IL-1β release. Further, mechanical ventilation activated the NLRP3 inflammasomes in mouse alveolar macrophages and increased the production of IL-1β in vivo. IL-1β neutralization significantly reduced mechanical ventilation-induced inflammatory lung injury. These findings suggest that the alveolar macrophage NLRP3 inflammasome may sense lung alveolar stretch to induce the release of IL-1β, and hence may contribute to the mechanism of lung inflammatory injuryduring mechanical ventilation.

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Abstract-We investigated the role of caveolae in the mechanism of increased pulmonary vascular permeability and edema formation induced by the activation of polymorphonuclear neutrophils (PMNs). We observed that the increase in lung vascular permeability induced by the activation of PMNs required caveolin-1, the caveolae scaffold protein.

Mechanically flexible arrays of alkaline electrochemical cells fabricated using stencil printing onto fibrous substrates are shown to provide the necessary performance characteristics for driving ink-jet printed circuits. Due to the dimensions and material set currently required for reliable low-temperature print processing of electronic devices, a battery potential greater than that sourced by single cells is typically needed. The developed battery is a series interconnected array of 10 low resistance Zn-MnO2 alkaline cells, giving an open circuit potential of 14 V. This flexible battery is used to power an ink-jet printed 5-stage complementary ring oscillator based on organic semiconductors.

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Hemodynamic and metabolic metrics during resuscitation with lipid surpassed those with epinephrine, which were no better than those seen in the saline control group. Further studies are required to optimize the clinical management of systemic local anesthetic toxicity.