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R Schlichtig

Publications and source records attributed to R Schlichtig.

17 recordsLinked to original sources
PubMed1994

Distinguishing between aerobic and anaerobic appearance of dissolved CO2 in intestine during low flow.

Increased intestinal mucosal PCO2 is used to detect the condition of inadequate O2 delivery, i.e., "dysoxia." However, mucosal PCO2 (PmCO2) can arise from oxidative phosphorylation, in which case it would detect metabolism that persists as blood stagnates, and/or from HCO3- neutralization by anaerobically produced metabolic acid, in which event it could represent dysoxia. We measured portal venous PCO2 (PVCO2) directly and PmCO2 indirectly with saline-filled CO2-permeable Silastic balloon tonometers in the intestinal lumen during progressive lethal cardiac tamponade in six pentobarbital-anesthetized dogs. PVCO2 and PmCO2 were relatively constant, differing by approximately 10 Torr until an O2 delivery (DO2) of approximately 1.3 ml.kg-1.min-1 was reached, below which PVCO2 and PmCO2 diverged strikingly, achieving a final difference of 78.7 +/- 35.81 (SD) Torr. To determine whether PCO2 arose from aerobic or anaerobic metabolism, we used the Dill nomogram to predict venous oxyhemoglobin (HbO2v) saturation (%HbO2v) from PVCO2. Portal venous %HbO2 predicted by the Dill nomogram agreed well with measured portal venous %HbO2 during all but the final values, indicating primarily aerobic appearance of PCO2 in venous blood, suggesting that portions of intestine that remained perfused at very low flow produced dissolved CO2 mainly by oxidative phosphorylation. As PmCO2 increased below critical DO2, however, predicted mucosal %HbO2v became strikingly negative, achieving a final value of -192 +/- 106.1%, indicating anaerobic dissolved CO2 production in mucosa. We conclude that PCO2 measured in intestinal lumen can be used to detect dysoxia.

Aerobiosis↗
PubMed1994

Adult respiratory distress syndrome associated with epidural fentanyl infusion.

OBJECTIVE: To determine the cause of unexplained postoperative adult respiratory distress syndrome (ARDS). DESIGN: Case-control study of postoperative ARDS. SETTING: Intensive care unit (ICU) of a Veterans Affairs hospital. PATIENTS: Six postoperative patients recovering from uncomplicated vascular or cardiothoracic surgery developed unexplained ARDS. Controls were 17 patients having similar procedures without the development of ARDS. INTERVENTION: Infusion of fentanyl with a tamper-proof device. MEASUREMENTS AND MAIN RESULTS: Development of ARDS. ARDS began 1 to 4 days after surgery, was characterized by maximum alveolar-arterial oxygen gradient that ranged from 232 to 544 torr (30.9 to 72.5 kPa), and was associated with death of two patients. We observed no association with patient location before ARDS onset, nonanalgesic medication administered, staff assignment, or mode of respiratory therapy. All six patients who developed unexplained ARDS had received epidural fentanyl compared with none of 17 control patients without ARDS (p = .0002). We instituted a tamper-proof mode of parenteral fentanyl administration, and subsequently observed one case of ARDS in 26 consecutive surgical patients (p = .000014). CONCLUSIONS: Based on these findings, as well as a prior history of fentanyl theft at our institution, we conclude that tampering with fentanyl infusate was responsible for the ARDS epidemic that we observed.

Aged↗
PubMed1992

Hepatic dysoxia commences during O2 supply dependence.

Hepatic O2 consumption (VO2) remains relatively constant (O2 supply independent) as O2 delivery (DO2) progressively decreases, until a critical DO2 (DO2c) is reached below which hepatic VO2 also decreases (O2 supply dependence). Whether this decrease in VO2 represents an adaptive reduction in O2 demand or a manifestation of tissue dysoxia, i.e., O2 supply that is inadequate to support O2 demand, is unknown. We tested the hypothesis that the decrease in hepatic VO2 during O2 supply dependence represents dysoxia by evaluating hepatic mitochondrial NAD redox state during O2 supply independence and dependence induced by progressive hemorrhage in six pentobarbital-anesthetized dogs. Hepatic mitochondrial NAD redox state was estimated by measuring hepatic venous beta-hydroxybutyrate-to-acetoacetate ratio (beta OHB/AcAc). The value of DO2c was 5.02 +/- 1.64 (SD) ml.100 g-1.min-1. The beta-hydroxybutyrate-to-acetoacetate ratio was constant until a DO2 value (3.03 +/- 1.08 ml.100 g-1.min-1) was reached (P = 0.05 vs. DO2c) and then increased linearly. Peak liver lactate extraction ratio was 15.2 +/- 14.1%, occurring at a DO2 of 5.48 +/- 2.54 ml.100 g-1.min-1 (P = NS vs. DO2c). Our data support the hypothesis that the decrease in VO2 during O2 supply dependence represents tissue dysoxia.

3-Hydroxybutyric Acid↗
PubMed1991

Flow redistribution during progressive hemorrhage is a determinant of critical O2 delivery.

O2 consumption (VO2) of anesthetized whole mammals is independent of O2 delivery (DO2) until DO2 declines to a critical value (DO2c). Below this value, VO2 becomes O2 supply dependent. We assessed the influence of whole body DO2 redistribution among organs with respect to the commencement of O2 supply dependency. We measured DO2, VO2, and DO2c of whole body, liver, intestine, kidney, and remaining carcass in eight mongrel dogs during graded progressive hemorrhage. Whole body DO2 was redistributed such that the organ-to-whole body DO2 ratio declined for liver and kidney and increased for carcass. We then created a mathematical model wherein each organ-to-whole body DO2 ratio remained approximately constant at all values of whole body DO2 and assigned organ VO2 to predicted organ DO2 by interpolation and extrapolation of observed VO2-DO2 plots. The model predicted that O2 supply dependency without redistribution would have commenced at a higher value of whole body DO2 for whole body (8.11 +/- 0.89 vs. 6.98 +/- 1.16 ml.kg-1.min-1, P less than 0.05) and carcass (6.83 +/- 1.16 vs. 5.06 +/- 1.15 ml.kg-1.min-1, P less than 0.01) and at a lower value of whole body DO2 for liver (6.33 +/- 1.86 vs. 7.59 +/- 1.95, ml.kg-1.min-1, P less than 0.02) and kidney (1.25 +/- 0.64 vs. 4.54 +/- 1.29 ml.kg-1.min-1, P less than 0.01). We conclude that redistribution of whole body DO2 among organs facilitates whole body O2 regulation.

Animals↗
PubMed1991

Renal O2 consumption during progressive hemorrhage.

Most mammalian tissues regulate O2 utilization such that O2 consumption (VO2) is relatively constant at O2 delivery (DO2) higher than a critical value (DO2c). We studied the relationship between VO2 and DO2 of kidney and whole body during graded progressive exsanguination. The relationship between whole body VO2 and DO2 was biphasic, and whole body VO2 decreased by 5.6 +/- 14.4% (P = NS) from the initial value to the value nearest whole body DO2c. Kidney DO2 decreased in direct proportion to whole body DO2 such that the average R2 value describing the linear regression of kidney DO2 vs. whole body DO2 was 0.94 +/- 0.02. The relationship between kidney, like whole body, VO2 and DO2 appeared biphasic; however, kidney VO2 decreased by 63.3 +/- 10.4% (P less than 0.0001) from the initial value to the value nearest kidney DO2c. Renal O2 extraction ratio was relatively constant over a wide range of kidney DO2, whereas whole body O2 extraction ratio increased progressively at all whole body DO2 values as whole body DO2 decreased. However, final values of O2 extraction ratio were indistinguishable for whole body (0.86 +/- 0.1) and kidney (0.86 +/- 0.06) (P = NS). We conclude that the pattern of kidney and whole body VO2 response to decreasing DO2 differs during hemorrhage, particularly in the range of DO2 normally associated with tissue wellness.

Animals↗
PubMed1991

Auto-PEEP during CPR. An "occult" cause of electromechanical dissociation?

A 64-year-old man with severe COPD developed refractory nonperfusing sinus rhythm after intubation and positive-pressure ventilation. Fifteen minutes after resuscitative efforts were halted, the patient was noted to have spontaneous respirations and blood pressure, suggesting that dynamic hyperinflation was responsible for the observed electromechanical dissociation (EMD). We recommend a brief trial of apnea for patients with COPD and EMD when conventional measures are unsuccessful.

Heart Block↗
PubMed1990

Regional oxygen delivery in oxygen supply-dependent states.

Assessment of the adequacy of systemic O2 delivery (DO2) is central in the evaluation of critically ill patients, but estimates of systemic DO2 do not assess the effectiveness of regional DO2 to all vascular beds whose functions may require different degrees of blood flow depending on their metabolic and functional demands. The oxygen supply-consumption curve includes a supply-independent portion, which represents the reserve capacity of the body to maintain oxygen consumption (VO2) despite inadequate increases in DO2, and a supply-dependent portion, which represents the physiologic adaptation that occurs once DO2 is unable to meet the metabolic demands of the body. Experiments in dogs revealed that when systemic DO2 was progressively reduced, blood flow was maintained in the vital organs (heart and brain) and redistributed away from the kidneys and liver, enhancing the ability of the whole organism to use oxygen efficiently. Disease states and iatrogenic conditions that alter this vasoregulatory process may directly impair organ system function.

Animals↗
PubMed1990

Nutritional support of the mechanically ventilated patient.

Mechanically ventilated patients generally depend on artificial means for nutritional supplementation. In this article we review the magnitude, pathophysiology, and clinical significance of proteolysis, and evidence that nutritional repletion is beneficial. Methods for assessing nutritional status and response to nutritional intervention are briefly discussed, as well as basic principles of anabolic and anticatabolic therapy.

Enteral Nutrition↗
PubMed1986

Tolerance of unusually low mixed venous oxygen saturation. Adaptations in the chronic low cardiac output syndrome.

Introduction of a reliable method for continuous monitoring of mixed venous oxygen saturation has focused attention on the therapeutic and prognostic implications of this value. It is generally agreed that mixed venous oxygen saturation in the 40 to 60 percent range is associated with substantial patient morbidity and mortality if not rapidly corrected. However, several patients with chronic low cardiac output syndrome who have had mixed venous oxygen saturation of less than 40 percent for prolonged periods of time and who have not had decompensation were observed. Three representative patients with these findings are described and mechanisms put forth that may account for the observed relations between mixed venous oxygen saturation and mortality in these and other patients.

Adaptation, Physiological↗