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Biomedical subjects

T J Morgan

Publications and source records attributed to T J Morgan.

At least 37 records · Page 2Linked to original sources

Transient mesenteric ischaemic episodes tracked by continuous jejunal PCO2 monitoring during liquid feeding.

OBJECTIVE: To test the effect of liquid feeds on the responses to splanchnic ischaemia of a continuous rapid response PCO2 sensor inserted in the jejunum. DESIGN: Prospective experimental animal study in a university research laboratory. SUBJECTS: Adult male Wistar rats. INTERVENTIONS: Adult male Wistar rats (285-425 g) were anaesthetised with sodium pentobarbitone 60 mg/kg i.p. and ventilated with 100% oxygen and isoflurane via tracheostomy to a PaCO2 of 30-40 mmHg. A sensor was inserted into the mid-jejunum to record PCO2 every second. Distal aortic pressure was transduced. Four control rats received no feeds whilst in another four rats liquid feed was infused into the proximal jejunum at 3 ml/h. In each rat five episodes of splanchnic ischaemia were induced by 2-min elevations of an aortic sling to a mean distal aortic pressure of 30 mmHg. MEASUREMENTS AND MAIN RESULTS: PCO2 elevations were always detectable, usually less than a minute from the onset of splanchnic ischaemia in both fed and unfed rats, with no difference in mean times to detectable response. In the fed rats there was a small but significant increase in the time to peak sensor response (196+/-16 vs. 180+/-12 s) and a trend towards an elevated mean baseline luminal PCO2 (67+/-9 vs. 55+/-4 mmHg). CONCLUSIONS: Brief episodes of splanchnic ischaemia were tracked successfully by a rapid response jejunal continuous PCO2 sensor during the infusion of a proprietary liquid feed preparation despite minor changes in PCO2 response characteristics and a possible elevation in baseline luminal PCO2.

Analysis of Variance↗

Testing the effectiveness of cognitive-behavioral treatment for substance abuse in a community setting: within treatment and posttreatment findings.

This study evaluated the short-term effectiveness of cognitive-behavioral treatment (CBT) for substance abuse delivered in a community setting. At entry into outpatient community substance abuse treatment, participants (N = 252) were randomly assigned to 3 conditions: high-standardization CBT, low-standardization CBT, and treatment as usual. Treatment consisted of 12 weekly individual therapy sessions. There was a significant decrease in substance use from baseline, with participants reporting being abstinent on 90% of within-treatment days and 85% of days during the 6 months posttreatment. However, there were no significant differences in outcomes across conditions. Findings do not support the hypothesis that disseminating CBT to community settings will improve outcomes and suggest that standard substance abuse counseling may be more effective than previously thought.

Adult↗

Monitoring tissue oxygenation during resuscitation of major burns.

BACKGROUND: Because subcutaneous and splanchnic oxygenation indices are sensitive indicators of evolving hemorrhagic shock and adequacy of resuscitation, we postulated that these indices might have an equivalent role in the monitoring of severely burned patients. This observational study was undertaken to examine changes in tissue oxygenation indices during burn resuscitation. METHODS: Seven patients with major burns (54 +/- 21% total body surface area) were studied during the first 36 hours of fluid resuscitation. Silastic tubing was placed in the subcutaneous tissue just beneath both normal skin and deep partial thickness burn. Fiberoptic sensors inserted into the tubing measured subcutaneous oxygen and carbon dioxide tensions in the burnt skin (PO2scb and PCO2scb) and normal skin (PO2scn and PCO2scn) continuously. Gastric intramucosal pH (pHi) and the mucosal CO2 (PCO2m) gap were calculated using gastric tonometers. Mean arterial pressure, arterial pH, lactate, and pHi measurements were obtained for 36 hours. RESULTS: There were no significant differences in mean arterial pressure, arterial pH, or lactate concentrations throughout the study period, whereas indices of tissue oxygenation showed deterioration: pHi decreased from 7.2 +/- 0.1 to 6.7 +/- 0.3 (p = 0.06), the PCO2m gap increased from 12 +/- 17 to 108 +/- 123 mm Hg (p < 0.01), PO2scn decreased from 112 +/- 18 to 50 +/- 11 mm Hg (p < 0.01), PO2scb decreased from 62 +/- 23 to 29 +/- 16 mm Hg (p < 0.01), PCO2scn increased from 42 +/- 4 to 46 +/- 10 mm Hg (p = 0.2), and PCO2scb increased from 42 +/- 10 to 52 +/- 5 mm Hg (p = 0.05). CONCLUSION: Despite adequate global indices of tissue perfusion after 36 hours of resuscitation, tissue monitoring indicated significant deterioration in the splanchnic circulation and in the normal and burnt skin.

Adult↗

Reduced red cell 2,3-diphosphoglycerate concentrations in critical illness without decreased in vivo P50.

We investigated whether red cell 2,3-diphosphoglycerate (2,3-DPG) concentrations are reduced in critical illness, whether acidaemia, hypophosphataemia or anaemia influence 2,3-DPG, and whether there is any net effect on in vivo P50. Twenty healthy, non-smoking, male volunteers were compared with 20 male intensive care patients with APACHE 2 scores >20 on the preceding day. Those transfused in this time were excluded. Venous red cell 2,3-DPG concentrations were measured in both groups. In the patient group, routine multichannel biochemical profile and arterial blood gas analysis were also performed and in vivo P50 calculated. The mean 2,3-DPG concentration was significantly lower in the patient group than in the controls (4.2+/-1.3 mmol/l vs 4.9+/-0.5 mmol/l, P=0.016). The patients were well oxygenated (lowest arterial PO2=75 mm Hg) and showed a tendency to acidaemia (median pH 7.37, range 7.06 to 7.48) and anaemia (median haemoglobin concentration 113 g/l, range 89 to 154 g/l). By linear regression of patient data, pH had a significant effect on 2,3-DPG concentrations (r=0.6, P=0.011). Haemoglobin and phosphate concentrations did not, but there were few abnormal phosphate values. There was no correlation between 2,3-DPG concentrations and in vivo P50 (r2 < or = 0.08). We conclude that 2,3-DPG concentrations were reduced in a broad group of critically ill patients. Although this would normally reduce the P50, the reduction was primarily linked with acidaemia, which increases the P50. Overall, there was no net effect on the P50 and thus no affinity-related decrease in tissue oxygenation.

2,3-Diphosphoglycerate↗

Manual-guided cognitive-behavioral therapy training: a promising method for disseminating empirically supported substance abuse treatments to the practice community.

A gap exists between empirically supported substance abuse treatments and those used in community settings. This study examined the feasibility of training substance abuse counselors to deliver cognitive-behavioral treatment (CBT) using treatment manuals. Participants were 29 counselors. Counselors were randomly assigned to receive CBT training or to a control group. Counselor attitudes were assessed pre- and posttraining. In addition, CBT therapy sessions were videotaped and rated for adherence and skillfulness. CBT counselors reported high levels of satisfaction with the training, intention to use CBT interventions, and confidence in their ability to do so. Ratings indicated that 90% of counselors were judged as having attained at least adequate levels of CBT skillfulness. Findings demonstrate the feasibility of using psychotherapy technology tools as a means of disseminating science-based treatments to the substance abuse practice community.

Adult↗

Subcutaneous oxygen tensions provide similar information to ileal luminal CO2 tensions in an animal model of haemorrhagic shock.

OBJECTIVES: The cutaneous and splanchnic circulations undergo early vasoconstriction in shock. Methodological problems and insufficient information on subcutaneous carbon dioxide partial pressures limit the usefulness of previous studies on splanchnic and subcutaneous gas tensions in shock. Little comparative data exist on the responses of these tissues to shock and resuscitation. We therefore compared continuous subcutaneous PO2 (PO2sc) and PCO2 (PCO2sc) with simultaneous continuous gut luminal PCO2 (PCO2gi) in an animal model of haemorrhagic shock and resuscitation. DESIGN: Prospective observational study. SETTING: Intensive care laboratory in a teaching hospital. SUBJECTS: Five anaesthetised rats. INTERVENTIONS: Electrochemical-fiberoptic gas sensors inserted into Silastic tubing placed in the subcutaneous tissue and in the ileal lumen measured PCO2sc, PO2sc and PCO2gi continuously in five anaesthetised rats. After steady state conditions, hypotension [mean arterial blood pressure (MAP) 40 mmHg] was induced by controlled haemorrhage. The rats were allowed to remain hypotensive for 15 min and then resuscitated with shed blood and crystalloids. Arterial plasma lactate concentrations were measured at defined periods during the study. MEASUREMENTS AND MAIN RESULTS: Hypovolaemia resulted in a significant decrease in PO2sc (P < 0.01) and a significant increase in PCO2gi and PCO2sc (P < 0.05). These values returned to baseline with resuscitation. PO2sc appeared to respond to haemorrhage earlier than PCO2gi and PCO2sc (P = 0.02). PO2sc was inversely correlated with PCO2gi (r2 0.7, P < 0.001). There were no significant changes in arterial plasma lactate concentrations. CONCLUSIONS: In our rat model, subcutaneous oxygen tension provided similar information to ileal luminal PCO2 and was more rapidly responsive than subcutaneous carbon dioxide tensions and arterial lactate during evolving haemorrhagic shock and resuscitation.

Animals↗

Blood in the gastrointestinal tract delays and blunts the PCO2 response to transient mucosal ischaemia.

OBJECTIVE: To determine whether the presence of blood in the gastrointestinal tract impairs the detection of splanchnic mucosal ischaemia by reducing the rate and magnitude of rise in gut luminal PCO2. DESIGN: Prospective observational study. SETTING: University Research Laboratory. SUBJECTS: Four adult male Wistar rats with four controls from a concurrent study. INTERVENTIONS: Four adult male Wistar rats were anaesthetised with sodium pentobarbitone and ventilated with oxygen and isoflurane to an initial PaCO2 of 30-40 torr. Electrochemical-fiberoptic gas sensors inserted into silastic tubing placed in the ileal lumen measured luminal PCO2 at 1-s intervals. Distal aortic pressure was monitored continuously. Six 2-min episodes of aortic hypotension were induced in each rat to a mean pressure of 30 mmHg by intermittent elevation of a silk sling placed around the proximal aorta. Before the last three episodes in each rat 0.75-1.0 ml blood was injected into the ileal lumen via a 25-gauge needle. Four control rats from a concurrent experiment were treated in an identical fashion except that the rats were subjected to five ischaemic episodes, and there was no intraluminal injection of blood, although a 20-gauge cannula was placed in the proximal ileal lumen. MEASUREMENTS AND MAIN RESULTS: The presence of blood in the lumen significantly decreased the ischaemic deltaPCO2 response from 33 +/- 8 to 15 +/- 4 torr (P < 0.001) and also significantly increased the peak response time from 188 +/- 12 to 227 +/- 24 s (P < 0.001). The corresponding measurements in the concurrent controls differed only from the values after blood injection in the experimental group. CONCLUSIONS: In this animal model the presence of intraluminal blood significantly delayed the rate and the amplitude of luminal PCO2 increases in response to transient ischaemia. This raises questions about the validity of luminal CO2 measurements as an indicator of splanchnic ischaemia in the presence of gastrointestinal haemorrhage.

Analysis of Variance↗

Accuracy of base excess--an in vitro evaluation of the Van Slyke equation.

OBJECTIVES: To evaluate the precision, bias and CO2 invariance of base excess as determined by the Van Slyke equation over a wide P(CO2) range at normal and low hemoglobin concentrations. DESIGN: Prospective in vitro study. SETTING: University research laboratory. SUBJECTS: Normal human blood, both undiluted and diluted with plasma. INTERVENTIONS: Two experiments were conducted. In the first, blood unmodified or after adding HCl or sodium bicarbonate was rendered hypercarbic (P(CO2) >70 torr) by gas equilibration. Rapid Pco2 reduction in > or =10 steps to a final P(CO2) < or =20 torr was then performed. In the second experiment, blood unmodified or diluted to a hemoglobin concentration of approximately 4 G% was mixed anaerobically (9:1, vol:vol) with varying concentrations of lactic acid in saline (0-250 mmol/L). MEASUREMENTS AND MAIN RESULTS: In the first experiment, blood gas analysis at each step during the progressive P(CO2) reduction revealed that base excess remained nearly constant (SD all specimens < or =0.6 mmol/L) whereas P(CO2) changed by >80 torr. In the second experiment, simultaneous blood gas and plasma lactate analyses showed that changes in base excess correlated closely with changes in both plasma and whole blood lactate concentrations (r2 > or = 0.91) despite concurrent P(CO2) elevations as great as 200 torr. Quantification by base excess of change in whole blood lactate concentration was precise with slight negative bias (mean negative bias, 1.1+/-1.9 mmol/L) in both diluted and undiluted blood. There was significant underestimation of change in plasma lactate concentration in undiluted blood, presumably because base excess is a whole blood variable. CONCLUSIONS: Base excess calculated using the Van Slyke equation accurately quantifies metabolic (nonrespiratory) acid-base status in blood in vitro. This accuracy is little affected by large simultaneous alterations in P(CO2), or by very low hemoglobin concentrations similar to that used to calculate standard base excess.

Acid-Base Equilibrium↗

Artifactual elevation of measured plasma L-lactate concentration in the presence of glycolate.

OBJECTIVES: To determine whether glycolate, a toxic metabolite of ethylene glycol that is chemically similar to lactate, can cause artifactual elevation of measured L-lactate concentrations. DESIGN: Prospective in vitro study. SETTING: Intensive care unit and chemical pathology laboratory in a university-affiliated hospital. SUBJECTS: Heparinized normal human blood and four commercially available L-lactate analyzers. INTERVENTIONS: Four analyzers were tested, three of which used L-lactate oxidase and one of which used L-lactate dehydrogenase. Glycolic acid (10 g/L) in saline was added to blood in a series of aliquots. Corresponding plasma L-lactate concentrations and blood pH, PCO2, and hemoglobin concentrations were measured and base excess was calculated initially and after the addition of each aliquot. One of the two L-lactate oxidase-type analyzers, which was found to show interference, was then used to measure plasma L-lactate and glucose concentrations in blood with glycolic, oxalic, or formic acid added until the base excess was reduced by >15 mmol/L. MEASUREMENTS AND MAIN RESULTS: Artifactual plasma L-lactate elevations were observed in two analyzers, both of the L-lactate oxidase type. Small concentrations of glycolic acid (causing reductions of base excess of 2-5 mmol/L) were accompanied by artifactual plasma L-lactate elevations of 4-8 mmol/L. Artifactual plasma L-lactate elevations increased with further glycolic acid-induced reductions in base excess. Oxalate and formate did not interfere with plasma L-lactate measurements, and measured plasma glucose concentrations were unaffected by all three acids. CONCLUSIONS: Glycolate causes large artifactual elevations in plasma L-lactate measurements by two analyzers in common use, with potential for misdiagnosis of lactic acidosis in ethylene glycol poisoning. A possible cause of the interference is incomplete specificity of the analytical reagent L-lactate oxidase, allowing cross-reaction with glycolate.

Acidosis, Lactic↗

Accuracy of intramucosal pH calculated from arterial bicarbonate and the Henderson-Hasselbalch equation: assessment using simulated ischemia.

OBJECTIVES: To determine the accuracy of intramucosal pH (pHi) calculated using arterial bicarbonate instead of mucosal capillary bicarbonate in the Henderson-Hasselbalch equation. DESIGN: Simulation of progressive ischemia in mucosal capillary blood. SETTING: University research laboratory. SUBJECTS: Normal human blood diluted with plasma. INTERVENTIONS: Three venous blood specimens were heparinized and diluted to a mean hemoglobin concentration of 5.0 (+/-0.9) g/dL by addition of plasma (2:1, vol:vol). Mucosal capillary aerobic flow stagnation was simulated by multiple exposures of each cooled specimen to a gas mixture containing 90% nitrogen and 10% CO2. When PCO2 measured at 37 degrees C (98.6 degrees F) was approximately 120 torr (16 kPa), the assigned anaerobic threshold, subsequent anaerobic flow stagnation was simulated by mixing the hypercapnic specimens in sealed syringes with five to six successive small aliquots (<100 microL) of lactic acid (10 g/L). MEASUREMENTS AND MAIN RESULTS: The relationship between Pco2 and pH in the specimens was compared with the relationship between the same PCO2 values and pHi calculated by substituting bicarbonate concentrations of 22 and 26 mmol/L in the Henderson-Hasselbalch equation. As PCO2 rose from 50 torr (8 kPa), conventionally calculated pHi increasingly underestimated simulated mucosal capillary pH, with bias >0.1 pH unit at the simulated anaerobic threshold of 120 torr (16 kPa). As PCO2 rose further the values converged, becoming equivalent at PCO2 approximately 150 torr (20 kPa). From PCO2 > or =200 torr (26.7 kPa), conventional pHi progressively overestimated simulated mucosal pH. The difference was >0.3 pH units at PCO2 = 250 torr (33.3 kPa). CONCLUSIONS: In the mucosal PCO2 range usually encountered clinically, the arterial bicarbonate substitution causes underestimation of mucosal capillary pH. With moderate mucosal capillary lactic acidosis the error becomes small, and in severe regional ischemia there is significant overestimation of mucosal capillary pH.

Anaerobic Threshold↗

The oxyhaemoglobin dissociation curve in critical illness.

OBJECTIVE: To review the status of haemoglobin-oxygen affinity in critical illness and investigate the potential to improve gas exchange, tissue oxygenation and outcome by manipulations of the oxyhaemoglobin dissociation curve. DATA SOURCES: Articles and published peer-review abstracts. SUMMARY OF REVIEW: The P50 of a species is determined by natural selection according to animal size, tissue metabolic requirements and ambient oxygen tension. In right to left shunting mathematical modeling indicates that an increased P50 defends capillary oxygenation, the one exception being sustained hypercapnia. Increasing the P50 should also be protective in tissue ischaemia, and this is supported by modeling and experimental evidence. Most studies of critically ill patients have indicated reduced 2,3-DPG concentrations. This is probably due to acidaemia, and the in vivo P50 is likely to be normal despite low 2,3-DPG levels. It may soon be possible to achieve significant P50 elevations without potentially harmful manipulations of acid-base balance or hazardous drug therapy. CONCLUSIONS: Despite encouraging theoretical and experimental data, it is not known whether manipulations of the P50 in critical illness can improve gas exchange and tissue oxygenation or improve outcome. The status of the P50 may warrant more routine quantification and consideration along with the traditional determinants of tissue oxygen availability.

Journal Article↗