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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The single breath test for carbon dioxide (SBT-CO2) is the plot of expired FCO2 or CO2% against expired volume. It can be monitored during anaesthesia and in the intensive care unit with modest additions to generally available equipment. This paper describes some aspects of a computer program for presenting SBT-CO2 during controlled ventilation, in particular, the corrections to the primary data necessary for scientific accuracy. Examples are given of how the use of SBT-CO2 has increased our understanding of factors which influence the arterial-end-tidal PCO2 difference (PaCO2-PE,CO2). PaCO2-PE, CO2 is, in a given individual, usually dependent on tidal volume and frequency. Changes in lung volume and manoeuvres such as opening the pleura also affect gas exchange. Monitoring CO2 elimination gives a measure of metabolic rate if ventilation and pulmonary perfusion are maintained. This facilitates ventilatory therapy in situations where CO2 production is greatly increased, e.g. sepsis and tetanus. On the other hand, if metabolism and ventilation are unchanged, a reduction in CO2 elimination implies reduced pulmonary perfusion. This can be seen during increased right-left shunting, such as in surgery in patients with congenital heart disease.
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PMID:On-line expiratory CO2 monitoring. 309 79

Little is known of the endorphins' role in sepsis-induced respiratory distress and naloxone's effect as a treatment of it. Thirteen piglets were infused with live Escherichia coli at a rate of 2 to 10 X 10(8) colony-forming units per hour for six hours or until death and were divided into two groups: the septic control group (n = 8), and the naloxone-treated group (n = 5), which received 8 mg/kg/h of naloxone by continuous infusion. Hemodynamic parameters, the intrapulmonary shunt fraction (QS/QT), physiologic dead space (VD/VT), minute ventilation, and blood gas levels were measured. Lung lymph flow was obtained by cannulating the right lymphatic duct. The extravascular lung water weight was also measured. The results showed a significant reduction of QS/QT, VD/VT, and arterial carbon dioxide pressure at one hour and a significant increase of arterial carbon dioxide pressure and minute ventilation at 1, 3, and 4 hours in the naloxone-treated group, compared with the untreated septic group. None of the piglets in the naloxone-treated group developed ventilatory depression, while 75% of those in the untreated septic group did. Among the latter piglets, three died of apnea within one hour. These beneficial effects of naloxone are likely related to its action on the central and peripheral respiratory regulatory mechanisms. A transient protection of the cardiac output and relatively decreased extravascular lung water with naloxone treatment may also, in part, improve the ventilation-perfusion maldistribution and secondarily reduce QS/QT and VD/VT. We conclude that endorphins play a role in septic ventilatory depression and that naloxone is effective in ameliorating it.
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PMID:Prevention of septic ventilatory depression with naloxone. 311 29

Lipid X (2,3-diacylglucosamine-1-phosphate) is a novel monosaccharide precursor of lipid A that has some of the physiologic activities of endotoxin but little toxicity. To determine whether lipid X would interfere with the toxic effects of endotoxin, we pretreated sheep with either 100 or 200 micrograms of lipid X per kg of body weight and then challenged them with a potentially fatal dose of Escherichia coli endotoxin (20 micrograms/kg). Twenty-one sheep underwent pulmonary artery catheterization and were monitored for changes in pulmonary artery pressure, temperature, pH, partial O2 pressure, partial CO2 pressure, blood pressure, and cell counts over 7 h. Overall mortality for control animals was 37% versus 5.3% for pretreated animals. None of the 13 animals pretreated with 100 micrograms of lipid X per kg died. These differences in survival were significant (P less than 0.05). Animals pretreated with 100 micrograms of lipid X per kg had significantly lower pulmonary artery pressure during both phases 1 and 2 of endotoxin-induced pulmonary artery hypertension. A higher dose of lipid X, 200 micrograms/kg, produced pulmonary hypertension. Perhaps because lipid X is a subunit of lipid A, lipid X shows a partial pyrogenic effect while also decreasing the pyrogenic activity of complete lipopolysaccharide (LPS). Lipid X did not prevent endotoxin-induced neutropenia or moderate hypotension in response to LPS. Lipid X is a potential prototype compound for a new type of chemotherapy directed at blocking the harmful effects of LPS during bacterial septicemia.
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PMID:Lipid X ameliorates pulmonary hypertension and protects sheep from death due to endotoxin. 330 7

Dysgonic fermenter 2 (DF-2) is a fastidious, gram-negative organism well recognized as a cause of fulminant septicemia in patients without spleens or patients with alcoholic cirrhosis. In vitro antibiotic susceptibility testing of eight strains with a Schaedler broth dilution technique revealed DF-2 to be susceptible to all of the antibiotics tested except aztreonam. Previous reports that DF-2 is aminoglycoside resistant were based on disk diffusion or agar dilution assays that may be less reliable given the slow growth of the organism and its requirement for CO2 incubation. Penicillin is commonly used as prophylaxis after dog bites and has excellent activity against DF-2.
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PMID:Susceptibility of dysgonic fermenter 2 to antimicrobial agents in vitro. 334 15

Hypercapnia is a poorly investigated problem in the management of postoperative complications. In order to define the clinical implication of postoperative hypercapnia, hospital records of fifty patients, who had hypercapnia (PaCO2 greater than or equal to 45 torr) within 30 days after major laparotomy, were analyzed retrospectively. Patients with chronic pulmonary disease, prolonged apnea, additional thoracotomy and inadequate setting of ventilator were excluded. Results were as follows. 1. Thirty-two patients were hypercapnic before the 3rd postoperative day. These patients had various causes for hypercapnia, and clinical course and outcome were dependent on the underlying clinical problem. 2. Eighteen patients showed hypercapnia after the 4th postoperative day. In these patients, invasive infection was a common problem and 17 out of 18 patients died mainly of sepsis. 3. Sites of septic focus were mostly in the abdominal area (i.e., intraperitoneal, retroperitoneal and intrahepatic), and in most cases, hypercapnia preceded the establishment of diagnosis of septic focus or the recognition of other organ dysfunction. CO2 retention in the septic patients was due to the increased dead space ventilation by ventilation-perfusion maldistribution. Therefore, hypercapnia found after the 4th day following laparotomy seems to indicate potential intraabdominal sepsis and prompts the necessity for effective drainage.
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PMID:[Hypercapnia following major laparotomy--retrospective analysis of 50 cases]. 336 24

Twenty mechanically ventilated patients with acute renal failure were studied on 31 occasions to determine their energy expenditure (EE) during a 2 h period before a hemodialysis. Oxygen consumption and CO2 elimination were measured continuously with a mass spectrometer system. EE (1660 +/- 48 kcal day-1) was close to the total caloric intake (1682 +/- 83 kcal day-1) and represented 1.19 +/- 0.03 times the predicted resting energy expenditure (PREE) with large inter-individual variations (0.7-1.7 PREE). EE/PREE was higher when sepsis was present (1.31 +/- 0.03 versus 1.14 +/- 0.02; p less than 0.05). Glucose oxidation rate (4.35 mg kg-1 min-1) exceeded glucose intake (2.6 mg kg-1 min-1). Respiratory quotient was 1.02 +/- 0.01. Nitrogen loss was 17.3 +/- 1.7 g day-1 and nitrogen balance -11.9 +/- 1.9 g day-1. In conclusion, EE values were scattered but never exceeded 1.7 times the PREE. Sepsis increased EE. With a nutritional support covering EE, nitrogen balance remained markedly negative and a preferential utilisation of glucose and lipogenesis occurred.
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PMID:Energy expenditure in the acute renal failure patient mechanically ventilated. 366 74

The management of severe adult respiratory distress syndrome in critically injured patients requires the frequent measurement of arterial blood gases for adjustment of cardiovascular and ventilatory support. Since these require blood withdrawal and laboratory determinations, a noninvasive method of assessment of arterial gas tensions would permit more frequent assessment of the patient as well as permitting rapid changes in the patient's ventilatory status to be detected earlier in the clinical course. The role of transcutaneous O2 and CO2 tension in providing these measurements was evaluated in 92 studies in 38 critically ill patients with ARDS due to trauma and/or sepsis. All patients were normodynamic or hyperdynamic at the time of study (cardiac index 2.5 to 7.6 L/min/m2) and were intubated and on increased inspired oxygen fractions (FIO2 = 30 to 100%) delivered by mechanical ventilation, had a range of body temperature from 35.0 to 39.5 degrees C and pH from 7.29 to 7.57 The data from a transcutaneous O2 and CO2 sensor applied to the skin of the anterior thorax were analyzed by multiple regression analysis of variances. Prediction of the arterial oxygen tension (PaO2) from 52 to 253 torr was possible from regression-corrected measurements of the transcutaneous O2 (TcO2): [PaO2 = 1.1 (TcO2) - 0.28 (FIO2) + 45.5]. The arterial carbon dioxide tension (PaCO2) from 26 to 57 torr was predicted from the transcutaneous CO2 (TcCO2):[PaCO2 = 0.76 (TcCO2) + 0.06 (FIO2) + 0.035 (TcO2) + 4.1]. With these corrections, a noninvasive Respiratory Index was computed for assessing ARDS severity, and dynamic changes in arterial gases could be followed in response to postural changes, ventilatory alterations, or cardiovascular perturbations. These data suggest that a reasonable estimate of the arterial blood gases can be obtained from a regression-corrected measurement of the transcutaneous O2 and CO2 tensions in critically injured normodynamic or hyperdynamic ARDS patients.
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PMID:Prediction of arterial blood gases by transcutaneous O2 and CO2 in critically ill hyperdynamic trauma patients. 368 36

The effect of gram-negative sepsis on the kinetics and oxidation of very low-density lipoprotein (VLDL) fatty acids was assessed in conscious dogs in the normal state and 24 h after infusion of live Escherichia coli. VLDL, labeled with [2-3H]glycerol and [1-14C]palmitic acid, was used to trace VLDL kinetics and oxidation, and [1-13C]palmitic acid bound to albumin was infused simultaneously to quantify kinetics and oxidation of free fatty acid (FFA) in plasma. Sepsis caused a fivefold increase in the rate of VLDL production (RaVLDL). In the control dogs, the direct oxidation of VLDL-fatty acids was not an important contributor to their overall energy metabolism, but in dogs with sepsis, 17% of the total rate of CO2 production could be accounted for by VLDL-fatty acid oxidation. When glucose was infused into dogs with insulin and glucagon levels clamped at basal levels (by means of infusion of somatostatin and replacement of the hormones), RaVLDL increased significantly in the control dogs, but it did not increase further in dogs with sepsis. We conclude that the increase in triglyceride concentration in fasting dogs with gram-negative sepsis is the result of an increase in VLDL production and that the fatty acids in VLDL can serve as an important source of energy in sepsis.
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PMID:Effect of sepsis on VLDL kinetics: responses in basal state and during glucose infusion. 389 May 59

The pathogenesis of small intestinal mucosal damage in septic shock was explored in experiments on 15 cats given live E coli i.v. Villous (absorptive site) blood flow was studied by the carbon monoxide uptake technique using isolated small intestinal segments. In eight of the cats, segments were perfused intraluminally with oxygenated or nitrogenated saline. The main part of the small intestine was unperfused and served as control. Nine cats (60%) developed mucosal damage. They had significantly lower arterial blood pressure at the end of septicemia (56 +/- 6) than cats without mucosal damage (76 +/- 3 mmHg). Total intestinal blood flow was similar before or during septicemia. Villous blood flow before septicemia was 3.7 +/- 0.5 ml/min X 100 g intestine and 5.1 +/- 1.0 (n.s.) in the two groups, respectively, and remained unchanged. Intraluminal perfusion with oxygenated but not with nitrogenated saline prevented the development of mucosal damage. It was concluded that the small intestinal mucosal damage is due to hypoxia in spite of unchanged villous blood supply.
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PMID:Small intestinal mucosal lesions in feline septic shock: a study on the pathogenesis. 409 46

Hemodynamic and respiratory effects of a continuous 5-h intravenous infusion of live Escherichia coli were studied in rats. Control animals were infused with saline. Rats infused with 1.8 +/- 0.4 X 10(10) bacteria/h did not survive a 5-h infusion. These animals developed early hypotension and reduced cardiac output (CO) measured by thermal dilution technique. Rats infused with 8.0 +/- 0.4 X 10(9) bacteria/h survived a 5-h infusion with hypotension and reduced CO occurring later in the course of bacteremia. Heart rate was markedly elevated in both septic groups. Arterial blood gas measurements revealed that partial pressure of O2 was not affected by bacteremia, but partial pressure of CO2 was significantly decreased. Arterial pH remained within the normal range indicating respiratory compensation of a metabolic acidosis. Since hypotension and reduced CO were accompanied by a fall in right atrial pressure (RAP) during bacteremia, a third septic group was studied to evaluate cardiac performance during volume loading. After 3-5 h of bacteremia, a 40% reduction in CO was associated with a significant drop in arterial pressure and RAP. Despite volume loading, ventricular stroke work and arterial pressure were significantly reduced compared with control animals. The results indicate that severe gram-negative bacteremia produces myocardial depression in the rat. This model can be useful for further studies of cardiac dysfunction during sepsis.
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PMID:Cardiopulmonary response of the rat to gram-negative bacteremia. 636 87


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