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Biomedical subjects

R K Webb

Publications and source records attributed to R K Webb.

16 recordsLinked to original sources
PubMed1992

Ventilation/perfusion indices do not correlate with the difference between oxygen consumption measured by the Fick principle and metabolic monitoring systems in critically ill patients.

OBJECTIVE: To determine whether the difference between oxygen consumption (VO2) measured by metabolic gas monitoring systems and by the Fick principle is related to venous admixture, deadspace/tidal volume ratio, or alveolar-arterial oxygen tension gradient in critically ill patients. DESIGN: A prospective study. SETTING: An 11-bed general ICU in a 900-bed teaching hospital. PATIENTS: Twenty critically ill patients admitted to the ICU who required mechanical ventilation, right heart catheterization, and arterial and mixed venous gas measurements for normal clinical management. RESULTS: Thirty-three recordings were analyzed. The mean VO2 measured by the metabolic gas monitoring system was 308 +/- 63.9 (SD) mL/min and was significantly greater than the mean VO2 measured by the Fick principle of 284 +/- 72.0 mL/min. The difference between the two measurements of 24.3 +/- 47.6 mL/min correlated poorly with venous admixture (r2 = .0009), dead-space/tidal volume ratio (r2 = .0064) and alveolar-arterial oxygen tension gradient (r2 = .017). CONCLUSIONS: If the difference in VO2 measured by metabolic gas monitoring systems and the Fick principle is due to intrapulmonary VO2 then in critically ill patients the ventilation/perfusion indices of venous admixture, deadspace/tidal volume ratio and alveolar-arterial oxygen tension gradient correlate poorly with intrapulmonary VO2.

Adult↗
PubMed1992

A longitudinal study of 100 consecutive admissions for carbon monoxide poisoning to the Royal Adelaide Hospital.

A longitudinal study of one hundred consecutive admissions to the Royal Adelaide Hospital for carbon monoxide poisoning was conducted from 1986 to 1989. Twenty-five patients left hospital with persistent symptoms and signs of this poisoning. Five subsequently recovered. Twenty-four other patients, who were well when they left hospital, did not attend for a review one month after discharge. Extensive neuropsychiatric testing at this time showed 32% (24 of 76) had obvious sequelae of their exposure. Overall, the frequency of neuropsychiatric sequelae in the patients who only received oxygen at atmospheric pressure was 63% (N = 8) on discharge and 67% (N = 6) on one month follow-up. The frequency of sequelae among those who were given one hyperbaric oxygen treatment only was 46% (N = 24) on discharge and 50% (N = 20) on one month follow-up. In contrast, the frequency of sequelae in patients who had two or more hyperbaric oxygen treatments was only 13% (N = 68) on discharge (P less than 0.005) and 18% (N = 50) on follow-up (P less than 0.005). the frequency of sequelae was also significantly greater if hyperbaric oxygen was delayed (P less than 0.05). No markers of severe poisoning could be identified.

Adolescent↗
PubMed1991

The P50 is reduced in critically ill patients.

A prospective study was designed to measure the P50 in 20 critically ill patients, and compare it with the P50 measured in 20 normal individuals. Arterial blood gases, lactate, haemoglobin (Hb) and phosphate (PO4) levels were also measured and compared with the P50 in the critically ill patients. The mean P50 of the critically ill patients was 24.5 mmHg (SD +/- 2.9) and was significantly lower than the mean P50 of 26.2 (SD +/- 2.2) in the normal individuals (p less than 0.05). In the critically ill patients, strong correlations were observed between the P50 and the arterial pH and base excess (BE) levels, with coefficients of 0.79 and 0.69 respectively whereas correlations between the P50 and arterial oxygen tension (PO2), carbon dioxide tension (PCO2), lactate, Hb and PO4 levels were poor, with correlations of 0.001, 0.008, 0.07, 0.13 respectively. It is concluded that the P50 is commonly reduced in critically ill patients, and has a strong correlation with arterial pH and BE.

Adult↗
PubMed1991

A comparison of the performance of 20 pulse oximeters under conditions of poor perfusion.

The performance of 20 pulse oximeters with finger probes was evaluated by comparison of their readings with directly measured arterial blood oxygen saturations. The samples were taken from patients who had undergone cardiac surgery under hypothermic cardiopulmonary bypass and had poor peripheral perfusion. The mean difference (bias, accuracy), standard deviation (precision) and drop-out rate for each pulse oximeter was determined. An overall ranking of performance of each pulse oximeter was calculated using five criteria (accuracy, precision, number of readings within 3% of standard, percentage of readings given within 3% of standard, expected overread limit in 95% of cases). Two pulse oximeters achieved a combination of accuracy and precision such that 95% of measurements would be expected to be within 4% of the co-oximeter value; these two also had the lowest drop-out rate.

Carboxyhemoglobin↗
PubMed1991

Potential errors in pulse oximetry. I. Pulse oximeter evaluation.

There is no absolute reference for oxygen saturation, although multiwavelength in vitro oximeters are accepted as the 'gold standard'. Regardless of whether fractional or functional saturation is used by manufacturers to calibrate their oximeters, evaluation against fractional saturation is recommended since this is the clinically relevant variable. The use of standard notation and comparisons based on bias and precision is recommended. The accuracy of pulse oximetry is intrinsically limited by the use of only two wavelengths, and is dependent on the initial calibration population. The empirical algorithms used to convert the signal to its 'readout value' and the quality control of hardware may both be important sources of variability between oximeters. Change in blood temperature may introduce errors in pulse oximeter and in vitro oximeter saturation readings, but these will be clinically insignificant. Changes in blood pH should not decrease pulse oximetry accuracy.

Humans↗
PubMed1991

Potential errors in pulse oximetry. II. Effects of changes in saturation and signal quality.

The published studies of pulse oximeter performance under conditions of normal, high and low saturation, exercise, poor signal quality and cardiac arrhythmia are reviewed. Most pulse oximeters have an absolute mean error of less than 2% at normal saturation and perfusion; two-thirds have a standard deviation (SD) of less than 2%, and the remainder an SD of less than 3%. Some pulse oximeters tend to read 100% with fractional saturations of 97-98%. Pulse oximeters may be suitable hyperoxic alarms for neonates if the alarm limit chosen is directly validated for each device. Pulse oximeters are poorly calibrated at low saturations and are generally less accurate and less precise than at normal saturations; nearly 30% of 244 values reviewed were in error by more than 5% at saturations of less than 80%. Ear, nose and forehead probes respond more rapidly to rapid desaturation than finger probes, but are generally less accurate and less precise. Ear oximetry may be inaccurate during exercise. Low signal quality can result in failure to present a saturation reading, but data given with low signal quality warning messages are generally no less accurate than those without. Cardiac arrhythmias do not decrease accuracy of pulse oximeters so long as saturation readings are steady.

Animals↗
PubMed1991

Pulse oximeter probes. A comparison between finger, nose, ear and forehead probes under conditions of poor perfusion.

The performances of 10 pulse oximeters using finger probes were compared with the same pulse oximeters using alternative probes (eight finger probes, two nose probes and a forehead probe) in poorly perfused patients. All readings were then compared with directly measured arterial blood oxygen saturations. The mean difference (bias, 'accuracy'), standard deviation (precision) and 'drop out' rate for each pulse oximeter combination was determined. An overall ranking of performance of each pulse oximeter was calculated using five criteria (accuracy, precision, number of readings within 3% of standard, percentage of readings given within 3% of standard, expected overread limit in 95% of cases). Nose and forehead probes performed poorly. Some ear probes performed well compared to some finger probes, but the overall performance of probes in other sites compared to finger probes was worse, (p = 0.05). Two of eight ear probes and no nose or forehead probes would be expected to be within 4% of the reference value in 95% of readings. The use of finger probes rather than probes in other sites is recommended in the patient with poor peripheral perfusion.

Adult↗
PubMed1991

Potential errors in pulse oximetry. III: Effects of interferences, dyes, dyshaemoglobins and other pigments.

Electrosurgery, patient motion and some types of lighting can cause errors in saturation readout; it is recommended that probes should be shielded from ambient lighting. Intravenous dyes can introduce gross but transient errors, which may also be present in in vitro measurements. Carboxyhaemoglobin causes overestimation of fractional saturation by an amount less than, but possibly close to, the percent of carboxyhaemoglobin present. Methaemoglobin causes the pulse oximeter readout to tend towards 85%. Fetal haemoglobin and bilirubin introduce no significant error, although they may interfere with in vitro measurements. Skin pigmentation can result in a slight decrease in accuracy. Nail polish may cause up to 6% underestimation of saturation; it is recommended that probes should be mounted sideways on fingers with nail polish or long nails. Adhesive tape or a vinyl glove across the probe has no demonstrable effect on accuracy. A blood sample should be analysed by a multiwavelength in vitro oximeter when an erroneous pulse oximeter reading is suspected, although errors may be introduced in the in vitro reading by fetal haemoglobin, bilirubin and intravenous dyes.

Coloring Agents↗
PubMed1990

An acute pain service in an Australian teaching hospital: the first year.

The Acute Pain Service began at the Royal Adelaide Hospital in April 1989. Funding, education programmes, policies, procedures, protocols, techniques (particularly patient-controlled analgesia, epidural opioid analgesia and subcutaneous morphine therapy) and daily organisation of the service are described in this article, and the experience with the 1053 patients referred to the Service during the first year of operation is reported. The occurrence of major complications was small. Mild-to-moderate respiratory depression occurred in four (0.5%) of the 747 patients who received patient-controlled analgesia and in none of the 177 who received epidural opioids. Five patients receiving patient-controlled analgesia had persistent nausea/vomiting; 320 (35%) of all patients receiving patient-controlled analgesia or epidural opioids suffered nausea/vomiting that required no treatment or was alleviated by treatment with an antiemetic. Around 13% of patients reported mild-to-moderate itching. In our experience, the combination of appropriately trained nursing and medical staff, standardised orders and procedures, and proper supervision can lead to safe, more effective management of acute pain.

Acute Disease↗
PubMed1977

Relationship between phosphaluria and acute hypercapnia in the rat.

Standard clearance studies were performed in mechanically ventilated intact and acutely thyroparathyroidectomized (TPTX) rats to document and characterize the effect of hypercapnia (HC) on urinary phosphorus excretion (U(P)V). HC as compared to normocapnia (NC) was associated with an increase in U(P)V in intact (62.5 vs. 7.93 mug/min) and TPTX (30.5 vs. 0.59 mug/min) rats, an increase in filtered load of phosphorus in intact (218 vs. 191 mug/min) and TPTX (243 vs. 146 mug/min) rats, an increase in blood bicarbonate concentration in intact (27.8 vs. 26.0 meq/liter) and TPTX (24.5 vs. 22.3 meq/liter) animals, and a decrease in blood pH in intact (7.15 vs. 7.42) and TPTX (7.07 vs. 7.39) rats. Additional TPTX rats with NC and HC were studied during phosphorus infusion at a comparable filtered load of phosphorus (NC = 307 mug/min and HC = 328 mug/min). U(P)V was 18.5 mug/min in NC and 85.2 mug/min in HC animals. Intact NC animals infused with NaHCO(3) achieved a blood bicarbonate of 45.9 meq/liter compared to 26.0 meq/liter in intact NC NaCl-infused rats. U(P)V was 10.0 mug/min in the NaHCO(3) and 7.93 mug/min in NaCl-infused animals. In intact HC animals infused with NaHCO(3), blood pH was 7.36 compared to 7.42 in NC intact NaCl-infused animals. U(P)V was 83.2 mug/min in the HC bicarbonate-infused and 7.93 mug/min in the NC NaCl-infused rats. These experiments demonstrate that elevated blood carbon dioxide tension per se increases U(P)V. Increases in filtered load of phosphorus and blood bicarbonate which are associated with HC contribute to the phosphaturia as does parathyroid hormone. The phosphaturia is not dependent upon reduction of extracellular pH.

Acidosis↗
PubMed1975

Acute effects of lithium on the renal concentrating mechanism in a primate.

Although chronic lithium therapy has been associated with a defect in the urinary concentrating mechanism, short-term renal effects of lithium have received little attention in the intact animal. Solute-free water reabsorption (T-cH2O) and free water clearance (CH2O) were measured in primates of the genus Galago under control conditions and while animals were receiving either 0.5 mmol/kg-h or 1.0 mmol/kg-h lithium chloride (135 mM) intravenously. CH2O was unchanged by lithium infusion (P greater than 0.10), whereas T-cH2O was significantly depressed at all levels of osmolal clearance (P smaller than 0.01). Spontaneous recovery of near-normal T-cH2O was documented in two animals within 1 wk following acute lithium infusion. In addition it was observed that lithium-induced depression of T-cH2O could be partially prevented by pretreatment with intravenous amiloride. These results suggest that alterations in the renal concentrating mechanism can occur rapidly following the onset of lithium administration. They also imply that impairment of the renal concentrating mechanism by lithium is due at least in part to antagonism of the action of vasopressin on the collecting duct.

Amiloride↗