Background The patient monitor (PM) is one of the most commonly used medical devices in hospitals... more Background The patient monitor (PM) is one of the most commonly used medical devices in hospitals worldwide. PMs are used to monitor patients’ vital signs in a wide variety of patient care settings, especially in critical care settings, such as intensive care units. An interesting observation is that the design of PMs has not significantly changed over the past 2 decades, with the layout and structure of PMs more or less unchanged, with incremental changes in design being made rather than transformational changes. Thus, we believe it well-timed to review the design of novel PM interfaces, with particular reference to usability and human factors. Objective This paper aims to review innovations in PM design proposed by researchers and explore how clinicians responded to these design changes. Methods A literature search of relevant databases, following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, identified 16 related studies. A detailed descriptio...
Chronic infection of the lungs with Pseudomonas aeruginosa complicates many long-term lung diseas... more Chronic infection of the lungs with Pseudomonas aeruginosa complicates many long-term lung diseases including cystic fibrosis, bronchiectasis, chronic obstructive lung disease, and mechanical ventilation. In acute inflammatory lung diseases, increased nitric oxide synthase (NOS-2) expression leads to excess nitric oxide (NO) production, resulting in the production of reactive nitrogen intermediates, which contribute to tissue damage. In contrast, the contribution of NO to pulmonary damage in chronic Pseudomonas infection of the lung has not been directly examined and is unclear. Although NOS-2 expression is increased in this condition, NO production is not abnormally elevated. It was hypothesized that chronic infection of the airways does not cause increased NO production but, in contrast, leads to inappropriately low NO concentrations that are pro-inflammatory. A rodent model of chronic airway infection was used to examine the effects on lung damage of augmenting or inhibiting NO production after airway infection with P. aeruginosa was well established. Three days post-infection, L-arginine, which augments NO production, or L-NAME, an inhibitor of NO production, was administered in drinking water. Lung damage was assessed 12 days later. L-arginine treatment reduced tissue damage, inhibited neutrophil recruitment, and reduced the pro-inflammatory cytokine interleukin (IL)-1beta. Treatment with L-NAME caused loss of alveolar walls, greater vascular damage, and increased levels of the pro-inflammatory cytokine IL-6. Thus, in chronic airway infection, inhibition of NO production worsened lung damage, whereas augmenting NO ameliorated this damage. This is the first demonstration that augmenting endogenous NO production in chronic infective lung disease caused by P. aeruginosa is anti-inflammatory. Given that infection with this organism complicates many chronic lung diseases, most notoriously cystic fibrosis, these findings have important clinical implications.
Deliberate induction of hypercapnic acidosis protects against lung injury after ischemia-reperfus... more Deliberate induction of hypercapnic acidosis protects against lung injury after ischemia-reperfusion, endotoxin-induced, and ventilation-induced lung injury. The efficacy of hypercapnic acidosis in bacterial lung infection, a common cause of acute respiratory distress syndrome, is not known. Furthermore, its effect may differ depending on the presence or absence of antibiotic therapy. We investigated whether hypercapnic acidosis-induced by adding CO2 to inspired gas-would protect against acute lung injury induced by pulmonary Escherichia coli instillation in an in vivo model in the presence and absence of effective antibiotic therapy. Prospective randomized animal study. University research laboratory. Adult male Wistar-Kyoto rats. The animals were anesthetized and ventilated. In series 1, rats were administered intravenous ceftriaxone (100 mg x kg) and randomized to normocapnia (Normocapnia-ABx; Fico2 0.00, n = 10) or hypercapnia (Hypercapnia-ABx; Fico2 0.05, n = 10) groups. E. coli (8.4 x 10 colony forming units) was instilled intratracheally. Series 2 animals did not receive antibiotics. They were randomized to normocapnia (Normocapnia, n = 10) or hypercapnia (Hypercapnia, n = 10) groups, and intratracheal E. coli was administered. All animals were ventilated for 6 hrs. In series 1, there were no differences between Hypercapnia-ABx and Normocapnia-ABx groups with regard to: (a-a)o2 gradient (mean +/- sem; 215 +/- 13 vs. 252 +/- 22 mm Hg), Pao2, bronchoalveolar lavage neutrophil count, static lung compliance, or histologic injury. Lung bacterial yield was not different between the groups. In series 2, in the absence of antibiotic therapy, there were no differences between Hypercapnia and Normocapnia groups in: (a-a)o2 gradient (mean +/- sem, 345 +/- 25 vs. 332 +/- 23 mm Hg), systemic Pao2, bronchoalveolar lavage neutrophil count, or static lung compliance. Lung bacterial yield was not altered by hypercapnia in either series 1 or 2. We conclude that hypercapnic acidosis did not alter the magnitude of the lung injury induced by intratracheal E. coli instillation in the presence or absence of antibiotics.
Hypercapnia is a central component of current protective ventilatory strategies. This review aims... more Hypercapnia is a central component of current protective ventilatory strategies. This review aims to present and interpret data from recent clinical and experimental studies relating to hypercapnia and its role in protective ventilatory strategies. Increasing clinical evidence supports the use of permissive hypercapnia, particularly in acute lung injury/acute respiratory distress syndrome, status asthmaticus, and neonatal respiratory failure. However, there are no clinical data examining the contribution of hypercapnia per se to protective ventilatory strategies. Recent experimental studies provide further support for the concept of therapeutic hypercapnia, whereby deliberately elevated PaCO2 may attenuate lung and systemic organ injury. CO2 administration attenuates experimental acute lung injury because of adverse ventilatory strategies, mesenteric ischemia reperfusion, and pulmonary endotoxin instillation. Hypercapnic acidosis attenuates key effectors of the inflammatory response and reduces lung neutrophil infiltration. At the genomic level, hypercapnic acidosis attenuates the activation of nuclear factor-kappaB, a key regulator of the expression of multiple genes involved in the inflammatory response. The physiologic effects of hypercapnia, both beneficial and potentially deleterious, are increasingly well understood. In addition, reports suggest that humans can tolerate extreme levels of hypercapnia for relatively prolonged periods without adverse effects. The potential for hypercapnia to contribute to the beneficial effects of protective lung ventilatory strategies is clear from experimental studies. However, the optimal ventilatory strategy and the precise contribution of hypercapnia to this strategy remain unclear. A clearer understanding of its effects and mechanisms of action is central to determining the safety and therapeutic utility of hypercapnia in protective lung ventilatory strategies.
Background The patient monitor (PM) is one of the most commonly used medical devices in hospitals... more Background The patient monitor (PM) is one of the most commonly used medical devices in hospitals worldwide. PMs are used to monitor patients’ vital signs in a wide variety of patient care settings, especially in critical care settings, such as intensive care units. An interesting observation is that the design of PMs has not significantly changed over the past 2 decades, with the layout and structure of PMs more or less unchanged, with incremental changes in design being made rather than transformational changes. Thus, we believe it well-timed to review the design of novel PM interfaces, with particular reference to usability and human factors. Objective This paper aims to review innovations in PM design proposed by researchers and explore how clinicians responded to these design changes. Methods A literature search of relevant databases, following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, identified 16 related studies. A detailed descriptio...
Chronic infection of the lungs with Pseudomonas aeruginosa complicates many long-term lung diseas... more Chronic infection of the lungs with Pseudomonas aeruginosa complicates many long-term lung diseases including cystic fibrosis, bronchiectasis, chronic obstructive lung disease, and mechanical ventilation. In acute inflammatory lung diseases, increased nitric oxide synthase (NOS-2) expression leads to excess nitric oxide (NO) production, resulting in the production of reactive nitrogen intermediates, which contribute to tissue damage. In contrast, the contribution of NO to pulmonary damage in chronic Pseudomonas infection of the lung has not been directly examined and is unclear. Although NOS-2 expression is increased in this condition, NO production is not abnormally elevated. It was hypothesized that chronic infection of the airways does not cause increased NO production but, in contrast, leads to inappropriately low NO concentrations that are pro-inflammatory. A rodent model of chronic airway infection was used to examine the effects on lung damage of augmenting or inhibiting NO production after airway infection with P. aeruginosa was well established. Three days post-infection, L-arginine, which augments NO production, or L-NAME, an inhibitor of NO production, was administered in drinking water. Lung damage was assessed 12 days later. L-arginine treatment reduced tissue damage, inhibited neutrophil recruitment, and reduced the pro-inflammatory cytokine interleukin (IL)-1beta. Treatment with L-NAME caused loss of alveolar walls, greater vascular damage, and increased levels of the pro-inflammatory cytokine IL-6. Thus, in chronic airway infection, inhibition of NO production worsened lung damage, whereas augmenting NO ameliorated this damage. This is the first demonstration that augmenting endogenous NO production in chronic infective lung disease caused by P. aeruginosa is anti-inflammatory. Given that infection with this organism complicates many chronic lung diseases, most notoriously cystic fibrosis, these findings have important clinical implications.
Deliberate induction of hypercapnic acidosis protects against lung injury after ischemia-reperfus... more Deliberate induction of hypercapnic acidosis protects against lung injury after ischemia-reperfusion, endotoxin-induced, and ventilation-induced lung injury. The efficacy of hypercapnic acidosis in bacterial lung infection, a common cause of acute respiratory distress syndrome, is not known. Furthermore, its effect may differ depending on the presence or absence of antibiotic therapy. We investigated whether hypercapnic acidosis-induced by adding CO2 to inspired gas-would protect against acute lung injury induced by pulmonary Escherichia coli instillation in an in vivo model in the presence and absence of effective antibiotic therapy. Prospective randomized animal study. University research laboratory. Adult male Wistar-Kyoto rats. The animals were anesthetized and ventilated. In series 1, rats were administered intravenous ceftriaxone (100 mg x kg) and randomized to normocapnia (Normocapnia-ABx; Fico2 0.00, n = 10) or hypercapnia (Hypercapnia-ABx; Fico2 0.05, n = 10) groups. E. coli (8.4 x 10 colony forming units) was instilled intratracheally. Series 2 animals did not receive antibiotics. They were randomized to normocapnia (Normocapnia, n = 10) or hypercapnia (Hypercapnia, n = 10) groups, and intratracheal E. coli was administered. All animals were ventilated for 6 hrs. In series 1, there were no differences between Hypercapnia-ABx and Normocapnia-ABx groups with regard to: (a-a)o2 gradient (mean +/- sem; 215 +/- 13 vs. 252 +/- 22 mm Hg), Pao2, bronchoalveolar lavage neutrophil count, static lung compliance, or histologic injury. Lung bacterial yield was not different between the groups. In series 2, in the absence of antibiotic therapy, there were no differences between Hypercapnia and Normocapnia groups in: (a-a)o2 gradient (mean +/- sem, 345 +/- 25 vs. 332 +/- 23 mm Hg), systemic Pao2, bronchoalveolar lavage neutrophil count, or static lung compliance. Lung bacterial yield was not altered by hypercapnia in either series 1 or 2. We conclude that hypercapnic acidosis did not alter the magnitude of the lung injury induced by intratracheal E. coli instillation in the presence or absence of antibiotics.
Hypercapnia is a central component of current protective ventilatory strategies. This review aims... more Hypercapnia is a central component of current protective ventilatory strategies. This review aims to present and interpret data from recent clinical and experimental studies relating to hypercapnia and its role in protective ventilatory strategies. Increasing clinical evidence supports the use of permissive hypercapnia, particularly in acute lung injury/acute respiratory distress syndrome, status asthmaticus, and neonatal respiratory failure. However, there are no clinical data examining the contribution of hypercapnia per se to protective ventilatory strategies. Recent experimental studies provide further support for the concept of therapeutic hypercapnia, whereby deliberately elevated PaCO2 may attenuate lung and systemic organ injury. CO2 administration attenuates experimental acute lung injury because of adverse ventilatory strategies, mesenteric ischemia reperfusion, and pulmonary endotoxin instillation. Hypercapnic acidosis attenuates key effectors of the inflammatory response and reduces lung neutrophil infiltration. At the genomic level, hypercapnic acidosis attenuates the activation of nuclear factor-kappaB, a key regulator of the expression of multiple genes involved in the inflammatory response. The physiologic effects of hypercapnia, both beneficial and potentially deleterious, are increasingly well understood. In addition, reports suggest that humans can tolerate extreme levels of hypercapnia for relatively prolonged periods without adverse effects. The potential for hypercapnia to contribute to the beneficial effects of protective lung ventilatory strategies is clear from experimental studies. However, the optimal ventilatory strategy and the precise contribution of hypercapnia to this strategy remain unclear. A clearer understanding of its effects and mechanisms of action is central to determining the safety and therapeutic utility of hypercapnia in protective lung ventilatory strategies.
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