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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The obstetric patient poses exceptional challenges in the intensive care unit. Knowledge of the physiologic changes of pregnancy and specific pregnancy-related disorders is necessary for optimal management. Intensive care unit diagnoses may include preeclampsia, including the HELLP syndrome, pulmonary embolic disease, amniotic fluid embolism, status asthmaticus, respiratory infection, the acute respiratory distress syndrome, and sepsis. The management of mechanical ventilation is based on principles of avoiding lung injury, and hypercapnia may be tolerated even during the pregnancy. When the clinician is faced with the extraordinary instance of cardiopulmonary arrest, perimortem cesarean delivery must be considered to improve the potential for maternal and fetal survival.
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PMID:Critical care of the obstetric patient. 1694 43

Experimental models of sepsis-induced pulmonary alterations are important for the study of pathogenesis and for potential intervention therapies. The objective of the present study was to characterize lung dysfunction (low PaO2 and high PaCO2, and increased cellular infiltration, protein extravasation, and malondialdehyde (MDA) production assessed in bronchoalveolar lavage) in a sepsis model consisting of intraperitoneal (ip) injection of Escherichia coli and the protective effects of pentoxifylline (PTX). Male Wistar rats (weighing between 270 and 350 g) were injected ip with 10(7) or 10(9) CFU/100 g body weight or saline and samples were collected 2, 6, 12, and 24 h later (N = 5 each group). PaO2, PaCO2 and pH were measured in blood, and cellular influx, protein extravasation and MDA concentration were measured in bronchoalveolar lavage. In a second set of experiments either PTX or saline was administered 1 h prior to E. coli ip injection (N = 5 each group) and the animals were observed for 6 h. Injection of 10(7) or 10(9) CFU/100 g body weight of E. coli induced acidosis, hypoxemia, and hypercapnia. An increased (P < 0.05) cell influx was observed in bronchoalveolar lavage, with a predominance of neutrophils. Total protein and MDA concentrations were also higher (P < 0.05) in the septic groups compared to control. A higher tumor necrosis factor-alpha (P < 0.05) concentration was also found in these animals. Changes in all parameters were more pronounced with the higher bacterial inoculum. PTX administered prior to sepsis reduced (P < 0.05) most functional alterations. These data show that an E. coli ip inoculum is a good model for the induction of lung dysfunction in sepsis, and suitable for studies of therapeutic interventions.
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PMID:Effect of pentoxifylline on lung inflammation and gas exchange in a sepsis-induced acute lung injury model. 1714 58

1. Acute lung injury (ALI) as a result of sepsis is a major cause of mortality. Certain anaesthetic agents have been reported to suppress pro-inflammatory cytokines and inducible nitric oxide (NO) synthase (iNOS) activities. We investigated the effects of pentobarbital on ALI and organ functions after the administration of endotoxin. 2. Intravenous (i.v.) pentobarbital (20 or 40 mg/kg) was administered 5 min after lipopolysaccharide (LPS; 10 or 30 mg/kg via i.v. infusion). To avoid hypoxia and/or hypercapnia following anaesthesia, we installed a special chamber connected to a rodent ventilator to provide ventilation with 95% oxygen content and 5% nitrogen. The animal was kept at eucapnic conditions (arterial PCO2 at an average of 38 +/- 2 mmHg). 3. We monitored the arterial pressure (AP) and heart rate (HR). Acute lung injury was evaluated by lung weight changes, protein concentration in bronchoalveolar lavage, and Evans blue leakage. Plasma nitrate/nitrite, methyl guanidine and biochemical factors were determined. Pathological and immunofluorescent examinations were performed to observe the lung changes and to determine the activities of pro-inflammatory cytokines, nitrotyrosine and iNOS. 4. Lipopolysaccharide caused dose-dependent systemic hypotension with an increase in the extent of ALI. The lung pathology included oedema and inflammatory cell infiltration. Accompanying the ALI, LPS elevated plasma nitrate/nitrite, methyl guanidine, blood urea nitrogen, lactic dehydrogenase, creatinine phosphokinase, glutamic transaminase and amylase. The lung tissue content of tumour necrosis factor-alpha, interleukin-lbeta, iNOS and nitrotyrosine was increased following LPS administration. These changes were abrogated by pentobarbital anaesthesia. 5. Our results indicated that pentobarbital anaesthesia significantly augmented the LPS-induced systemic hypotension. However, it attenuated the LPS-induced ALI and organ dysfunctions. This agent also improved the survival rate following LPS at high and low doses. This mechanism may be related to the inhibitory effects on the increases in the production or activity of NO, free radicals, pro-inflammatory cytokines, nitrotyrosine and iNOS.
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PMID:Endotoxin-induced acute lung injury and organ dysfunction are attenuated by pentobarbital anaesthesia. 1743 19

Intramucosal acidosis, that it is to say, an increased intramucosal-arterial PCO2 difference, is a common finding in clinical and experimental sepsis. Nevertheless, the physiologic significance of increases in tissue PCO2 is controversial, since CO2 can be generated by both aerobic and anaerobic biochemical processes. PCO2 can rise after buffering of protons produced in the hydrolysis of high-energy phosphate compounds by bicarbonate, or after the anaerobic production of acids, like lactate. In this case, it could represent tissue dysoxia. Alternatively, an increase in tissue PCO2 could denote hypoperfusion and diminished removal of the CO2 produced during the oxidation of pyruvate. In this last situation, aerobic metabolism might be preserved. In the present review, we discuss the physiologic mechanisms that determine tissue and venous hypercarbia during the three classic forms of hypoxia: stagnant, hypoxic and anemic hypoxia. The results of experimental studies suggest that tissue minus arterial and venoarterial PCO2 gradients primarily reflect alterations in tissue perfusion. These conclusions are further confirmed by a mathematical model of CO2 transport. In sepsis, however, tissue hypercarbia might develop despite normal or high cardiac output. This phenomenon has been initially interpreted as secondary to alterations in energetic metabolism, the so-called cytopathic hypoxia. Yet, new evidences show that the underlying mechanism to tissue hypercarbia in sepsis might be due to severe microcirculatory derangements. In summary, experimental results support the hypothesis that increases in tissue and venous CO2 are insensitive markers of tissue dysoxia, and merely reflect vascular hypoperfusion.
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PMID:Mechanisms of tissue hypercarbia in sepsis. 1798 34

The symptoms and signs of heart failure can occur in the setting of an increased cardiac output and has been termed 'high output heart failure'. An elevated cardiac output with clinical heart failure is associated with several diseases including chronic anaemia, systemic arterio-venous fistulae, sepsis, hypercapnia and hyperthyroidism. The underlying primary physiological problem is of reduced systemic vascular resistance either due to arterio-venous shunting or peripheral vasodilatation. Both scenarios can lead to a fall in systemic arterial blood pressure and neurohormonal activation leading to overt clinical heart failure. In contrast to low output heart failure, clinical trial data in this area are lacking. The use of conventional therapies for heart failure, such as angiotensin converting enzyme inhibitors, angiotensin receptor blockers and certain beta-blockers with vasodilatory properties, is likely to further reduce systemic vascular resistance resulting in deterioration. The condition, although uncommon, is often associated with a potentially correctable aetiology. In the absence of a remediable cause, therapeutic options are very limited but include dietary restriction of salt and water combined with judicious use of diuretics. Vasodilators and beta-adrenoceptor positive inotropes are not recommended.
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PMID:High output heart failure. 1899 Jul 20

This study was performed to provide simplified quantitative evidence of the impact of hemoglobin concentration on blood CO(2) binding and transport capacity. Linear regression equations were obtained for gas analyses data obtained from 85 surgical patients with sepsis and various degrees of illness. Venoarterial CO(2) concentration differences were calculated by a complex procedure, and then simplified equations were derived to highlight the impact of hemoglobin concentration on blood CO(2) binding and the Haldane effect. The results showed that, although in normal conditions the impact of hemoglobin concentration is less evident, it becomes relevant in extreme conditions, also protecting against venous and tissue hypercapnia and acidosis.
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PMID:Significance of hemoglobin concentration in determining blood CO2 binding capacity in critical illness. 2041 69

Carbon dioxide is a waste product of aerobic cellular respiration in all aerobic life forms. PaCO2 represents the balance between the carbon dioxide produced and that eliminated. Hypocapnia remains a common - and generally underappreciated - component of many disease states, including early asthma, high-altitude pulmonary edema, and acute lung injury. Induction of hypocapnia remains a common, if controversial, practice in both adults and children with acute brain injury. In contrast, hypercapnia has traditionally been avoided in order to keep parameters normal. More recently, advances in our understanding of the role of excessive tidal volume has prompted clinicians to use ventilation strategies that result in hypercapnia. Consequently, hypercapnia has become increasingly prevalent in the critically ill patient. Hypercapnia may play a beneficial role in the pathogenesis of inflammation and tissue injury, but may hinder the host response to sepsis and reduce repair. In contrast, hypocapnia may be a pathogenic entity in the setting of critical illness. The present paper reviews the current clinical status of low and high PaCO2 in the critically ill patient, discusses the insights gained to date from studies of carbon dioxide, identifies key concerns regarding hypocapnia and hypercapnia, and considers the potential clinical implications for the management of patients with acute lung injury.
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PMID:Bench-to-bedside review: carbon dioxide. 2049 20

In the neonatal population, pleural effusion and particularly tension pneumothorax can be a deadly situation. Pneumothorax occurs more often in the neonatal period that any other time of life. Tension pneumothorax can result in very high pressures within the pleural space, collapsing the lung on the involved side and resulting in immediate hypoxia, hypercapnia and subsequent circulatory collapse. For these reasons, the ability to recognize, understand and treat these pathologies is essential for neonatal health and a good outcome. Neonates have many factors that can contribute to. these problems. These include respiratory distress syndrome, mechanical ventilation, sepsis, pneumonia, aspiration of meconium, congentital malformation, hydrothorax, congenital or acquired chylothorax. The diagnosis can be made by clinical examination, transillumination (pneumothorax) and chest x-ray. Besides, lung ultrasound constitutes a visual medicine and provides a transparent approach to the acutely ill patient, newborn included, guiding diagnosis, management and care. Newborns with moderate to severe symptoms and those receiving positive pressure ventilation require tube thoracostomy. If a tension pneumothorax is suspected, emergency needle decompression in the second intercostal space in the midclavicular line is required. In this article, we describe the management of tube thoracostomy using trocar tubes or pigtail catheters. Besides, we pay attention to the use of pain control for neonates undergoing painful procedures such as chest tube insertion.
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PMID:[Management of pleural drainage]. 2109 89

Myxoedema coma is a rare and extreme presentation of hypothyroidism. It has a poor prognosis due to multisystem decompensation, and demands prompt but careful management in a high-dependency / intensive care setting. Early recognition of hypercapnia, hyponatraemia, and sepsis are especially important. Treatment should begin on suspicion of the diagnosis and can be life-saving. Intravenous thyroid hormone replacement is required at first, with steroid cover, although the optimum dose regimen remains unclear.
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PMID:Myxoedema coma. 2165 18

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are associated with impaired gas exchange, severe inflammation and alveolar damage including cell death. Patients with ALI or ARDS typically experience respiratory failure and thus require mechanical ventilation for support, which itself can aggravate lung injury. Recent developments in this field have revealed several therapeutic strategies that improve gas exchange, increase survival and minimize the deleterious effects of mechanical ventilation. Among those strategies is the reduction in tidal volume and allowing hypercapnia to develop during ventilation, or actively inducing hypercapnia. Here, we provide an overview of hypercapnia and the hypercapnic acidosis that typically follows, as well as the therapeutic effects of hypercapnia and acidosis in clinical studies and experimental models of ALI. Specifically, we review the effects of hypercapnia and acidosis on the attenuation of pulmonary inflammation, reduction of apoptosis in alveolar epithelial cells, improvement in sepsis-induced ALI and the therapeutic effects on other organ systems, as well as the potentially harmful effects of these strategies. The clinical implications of hypercapnia and hypercapnic acidosis are still not entirely clear. However, future research should focus on the intracellular signaling pathways that mediate ALI development, potentially focusing on the role of reactive biological species in ALI pathogenesis. Future research can also elucidate how such pathways may be targeted by hypercapnia and hypercapnic acidosis to attenuate lung injury.
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PMID:Effects of hypercapnia and hypercapnic acidosis on attenuation of ventilator-associated lung injury. 2170 55


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