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critical care dependsWithin an effective command and control system to coordinate regional response, surge capacity in critical care depends on three crucial elements: (1) “stuff,” medical equipment and supplies; (2) “staff,” appropriately trained health professionals to competently care for critically ill and injured patients; and (3) “space,” the physical location suitable for safe provision of critical care. Although a rather simplistic conceptual approach, one can confidently state that a system that fails to meet any one of these requirements will not be able to cope with a large surge. Medical response to disasters, including the critical care response, is dependent on a number of non-clinical medical institution services (eg, logistics and procurement, environmental services, food services) and external services (eg, transportation, consistent functional utilities, commerce infrastructure). For expediency, this article will focus on critical care-specific capabilities.

Stuff

Mechanical ventilators are unique to the critical care environment, and they are essential equipment for the management of respiratory failure. There are no realistic substitutes for ventilators. Proposals to train hundreds of volunteers to provide manual ventilation to patients during a pandemic are naive and fraught with serious logistical and scientific shortfalls, such as the lack of staff or volunteers during bioevents as well as the risk of secondary transmission to the caregivers who must remain at the bedside and the adverse consequences of prolonged manual ventilation.

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Electron beam CTCoronary artery calcification has been shown to play an important role in the development of atherosclerosis and is strongly associated with the total plaque burden proved in previous histopathologic studies. The use of electron beam CT (EBCT) for accurate quantitative measurements has led to an increased interest in understanding the clinical importance of coronary calcium. The coronary calcium score (CCS) determined by EBCT could provide useful prognostic information regarding subsequent coronary events in high-risk subjects with no clinical coronary artery disease (CAD), as well as in patients with the presence of CAD.> EBCT has also been demonstrated to be a useful technique for assessing the progression or regression of CAD in response to treatment of cardiovascular risk factors.

Endothelial dysfunction is thought to be an early sign of vascular endothelium injury and is the first critical step in the pathogenesis of atherosclerosis. Endothelial function plays a key role in determining the clinical manifestations of established atherosclerotic lesions and was proved predictive of further cardiovascular events.’ However, no previous study has shown the relationship between the extent of coronary artery calcification and endothelial function. Therefore, in this study we test the hypothesis that enhanced CCSs determined by EBCT would be associated with endothelial dysfunction assessed by brachial ultrasonography. In addition, although conflicting results were shown about the relationship between C-reactive protein (CRP) and coronary calcification in asymptomatic patients, in this study the associations of CRP and monocyte che-moattractant protein-1 (MCP-1) with coronary calcification and endothelial function were also evaluated in patients with suspected CAD.

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muscular dystrophyPatients with quadriplegia, muscular dystrophy, and other forms of neuromuscular disease demonstrate significant abnormalities in chest wall and lung mechanics which are attributed to ventilatory muscle weakness. These abnormalities place these patients at significant risk to develop life-threatening respiratory complications. Previous investigators have described a reduction in chest wall compliance in patients with neuromuscular weakness. This finding is attributed to an inability to fully expand the chest which leads to stiffening of the joints and tissues of the rib cage. Patients with chest wall muscle weakness also have reduced lung compliance. This is explained by atelectasis or an increase in the surface tension of the alveolar lining layer resulting from breathing at low lung volume.

A reduction in lung and chest wall compliance is also seen with kyphoscoliosis. Sinha and Bergofsky demonstrated that hyperinflation with intermittent positive pressure breathing (IPPB) for five minutes at 22 cm HsO pressure increased dynamic lung compliance up to 70 percent above baseline values and the effect lasted for as long as three hours. Thus, by increasing lung compliance, the work of breathing decreases, and respiratory failure may theoretically be averted.

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VC and QFIn the present study, we found that QF is reduced in patients with IPF, and this weakness correlates with exercise limitation as well as lung function impairment in those patients. Among these variables, VC and QF were particularly significant contributing factors according to the stepwise analysis. To our knowledge, this is the first report clarifying the relationship between peripheral muscle performance and exercise capacity in patients with IPF.

Some factors and mechanisms that determine exercise capacity in ILD have been reported, although those in IPF have not been extensively studied. A decrease in exercise capacity has been reported even in ILD patients who have normal resting pulmonary function results. Thus, directly measuring exercise capacity of patients with ILD is important in evaluating impairment. Factors reported to correlate with exercise limitation in patients with ILD include VC, FEV1, TLC, Dlco, and, possibly, Pa02. Mechanism of exercise limitation in patients with ILD has also been explored. Marciniuk et al described expiratory flow limitation in all patients who stopped exercise due to dyspnea. In the remaining patients who discontinued exercise because of leg fatigue, no flow limitation was evi-dent. Harris-Eze et al reported that patients with ild were able to increase both peak ventilation and exercise performance with supplemental oxygen. This finding suggests a hypothesis that arterial hypoxemia, not ventilatory limitation, limits exercise. As another contributing factor, ventilation-perfusion mismatching, may contribute to exercise limita-tion. Diffusion limitation and circulatory limitation can also affect exercise tolerance of patients with ILD. Hansen and Wasserman reported that Dlco was the best correlate of Vo2max in ILD. It is also suggested that higher respiratory drive during exercise can be attributed to increased afferent reflexes originating from the lung or chest wall, which might thereby limit exercise tolerance. To become familiar with ordering procedure online you may go to the page using the link – canadian health care mall publications on wordpress.

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sleep apneaThis study shows that a large majority of patients with sleep apnea and associated hypoxemia have cognitive impairment. In addition, this study demonstrates that patients with sleep apnea and associated hypoxemia have poorer cognitive functioning than such patients without hypoxemia. The hypoxemic patients with sleep apnea had a significantly greater number of performance scores in the impaired range than patients without hypoxemia. Finally, the degree of hypoxemia during the awake and sleeping states was significantly correlated with the degree of cognitive impairment in patients with sleep apnea.

Hypoxemia during both wakefulness and sleep may cause a disruption in the biochemical and hemodynamic state of the central nervous system. Hypoxemia markedly affects central neurotransmitter function and brain adenosine levels in animals. Hypoxemia and hypercapnia also significantly increase cerebral blood flow in humans. Given such disruptions in the central nervous system, it is not surprising that previous investigators have found an association of hypoxemia with cognitive dysfunction in humans at high altitudes and in patients with severe COPD.

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disordered breathingTable 2 gives the total time in apnea as a percentage of total sleep time, the number of episodes of apnea per hour of sleep, and the decrements in Sa02 during apnea for each patient before, during, and after treatment. Table 3 gives the same information for episodes of disordered breathing. All patients continued to have apneic episodes during and following treatment. There were no significant differences among the group means before, during, and after treatment for either apneic or disordered breathing episodes. Examination of Tables 2 and 3 reveals that there was no consistent pattern of responses to medroxyprogesterone over all variables among the different patients.

The total times spent in apnea and disordered breathing episodes, expressed as percentages of total sleep time, are shown in Figure 1. There were no significant differences in mean percentage of time in apnea before (20.8±3.5 percent [±SE]), during (18.6 ±4.3 percent), and after (16.9 ±4.5 percent) medroxyprogesterone. Likewise, there were no differences in the mean percentages of disordered breathing time before (17.0±6.1 percent), during (17.4±5.3 percent), or after (21.6 ±6.8 percent) the drug. The mean durations of apneic and disordered breathing episodes for all patients are shown in Figure 2. There were no significant changes associated with administration of medroxyprogesterone. The distribution for the number of apneic episodes by duration is given in Figure 3. Again, there was no difference in mean values resulting from treatment.

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BloodAfter excluding 31 patients who did not authorize their medical records to be reviewed for research, 816 simultaneous bGlu and pGlu measurements were found for 197 patients. The mean age of these patients was 56 years (SD, 15.8 years), 95.4% were white, and 51.8% were women. The blood samples had been obtained on four occasions when patients were receiving continuous IV insulin treatment.

On 18 occasions, the bGlu level was reported as 400 mg/dL. In these cases, the mean pGlu level was 423 mg/dL (SD, 110 mg/dL; range, 300 to 900 mg/dL). On 767 occasions, the mean bGlu level was 159 mg/dL (SD, 56.4 mg/dL), and the mean pGlu level was 151 mg/dL (SD, 54.3 mg/dL; p < 0.001). The mean difference between measurements made using the two techniques was 7.9 mg/dL (SD, 17.6 mg/dL), and the limits of agreement were + 43.1 and -27.2 (Fig 1). The pGlu level was elevated on 589 occasions and was nonelevated on 178 occasions, when the pGlu level was between 50 and 400 mg/dL. The mean differences in pGlu and bGlu levels were not statistically significant between the elevated and nonelevated bGlu groups (p = 0.331). In the elevated pGlu group, the mean difference between measurements made using the two techniques was 7.6 mg/dL (SD, 17.1 mg/dL), and the limits of agreement were + 41.8 and -26.6, In the nonelevated pGlu group, the mean difference between measurements made using the two techniques was 9.0 mg/dL (SD, 19.1 mg/dL), and the limits of agreement were + 47.3 and -29.2.

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