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Biomedical subjects

W E Fordyce

Publications and source records attributed to W E Fordyce.

At least 37 records · Page 2Linked to original sources
PubMed1990

Evaluation of resuscitation proficiency in simulations: the impact of a simultaneous cognitive task.

In order to evaluate the impact of simulation complexity on resuscitation skill performance, 15 pediatric residents were observed in bag-valve-mask ventilation on an infant manikin. Performance was evaluated in a simple exercise in which ventilation was performed as a single isolated task. For each subject, this was compared to performance when a cognitive task involving clinical problem solving was simultaneously presented. Performance was expressed as frequency, tidal volume, and estimated hypothetical alveolar Pco2 in each resuscitation. A correlation was observed (P less than 0.05) between simple and complex resuscitation simulations for each measure of performance. The only subject with inadequate performance in the complex exercise was also identified as deficient in the simple exercise. These observations suggest that an adequate evaluation of performance of some resuscitation skills may be obtained in simple, efficient simulation exercises.

Carbon Dioxide↗
PubMed1989

Learning factors in pain.

The concept of pain is analyzed from the perspective of behavioral science. Distinctions between pain and suffering are drawn and the impact of learning or experience is discussed. Implications for management of pain, exercise and restoration of functional performance, and use of pain-related medications are described.

Behavior↗
PubMed1988

Arterial-end tidal PCO2 equilibration in the cat during acute hypercapnia.

We have studied the problem of pulmonary capillary-alveolar CO2 exchange in the cat during acute hypercapnia. Three cats, anesthetized with xylazine and pentobarbital sodium and prepared with acute tracheostomy and femoral arterial catheter, and three awake cats, prepared with a small tracheal catheter and femoral arterial catheter, were subjected to acute hypercapnia (FICO2 = 0.00, 0.06, and 0.08). During steady states, end tidal PCO2 was determined with an infrared analyzer, and arterial PCO2 was measured with a Radiometer ABL-2 analyzer in simultaneously drawn samples. In vitro studies indicated that our blood sampling techniques resulted in a 6% reduction in PCO2. Blood PCO2 readings were corrected for (1) non-ideal performance of the analyzer as determined by tonometry, (2) 6% reduction due to sampling, and (3) differences between electrode and rectal temperature. Mean arterial-end tidal PCO2 differences were not significantly different from zero in any condition in either group (except for 0.08 CO2 in the awake group when the difference was 2.0 Torr). These findings in the cat agree with the classical view that PCO2 in pulmonary capillary blood approaches PCO2 in alveolar gas. Further, our findings provide evidence that CO2 loss from blood samples is an important technical factor which can cause systematic underestimation of blood PCO2 and, hence, contribute to the observation of negative PCO2 gradients.

Acute Disease↗
PubMed1988

Gain of the ventilatory exercise stimulus: definition and meaning.

The ratio G = delta VE/delta VCO2 where delta VA is change in ventilation and delta VCO2 is change in CO2 production, is often used to quantitate the ventilatory response to exercise and is the overall system gain (G). However, the actual variable of interest often is the gain for the exercise stimulus (GEX). Exercise stimulus refers to a stimulus or group of stimuli other than the mean levels of arterial PO2 (PaCO2), PCO2 (PaCO2), and pH (pHa) that act to increase ventilation during exercise. GEX will be equal to G only if the response to exercise is precisely isocapnic, normoxic, and without metabolic acidosis. A mathematical model was used to examine the relationship between G and GEX when 1) the response to exercise is not strictly isocapnic and 2) when the resting PaCO2 is shifted away from its normal value. It was found that 1) when the exercise response was not strictly isocapnic, G was a poor estimate of GEX and 2) when resting PaCO2 was changed while GEX wa assumed to remain constant, G was a function of the resting PaCO2. However, this dependence of G on resting PaCO2 is a system property that was caused by the nonlinear properties of the gas exchange processes and was not a fundamental property of the controller. It is concluded that G may not always be a good estimate of GEX and may lead to incorrect conclusions concerning the nature of the exercise stimulus.

Carbon Dioxide↗
PubMed1988

Psychological factors in the failed back.

Pain is a complex phenomenon. Lack of understanding of its nature leads to two common mistakes in the failed back, firstly to look for a discrete physical cause and secondly to ascribe pain to psychological causes. This paper explores the nature of pain in the failed back and discusses the implications for treatment.

Back Pain↗
PubMed1987

Hypoxic ventilatory control in the awake cat five years after carotid body resection.

Steady state breathing patterns, alveolar gases, and arterial blood gases and pH were measured during air, acute hypoxia, and acute hyperoxia in four awake cats 5 years after combined carotid body resection (CBR) and aortic depressor nerve section. Steady state breathing patterns and alveolar gases were also measured in these animals following 3 days of hypoxia (PIO2 = 110 Torr). The results show that the awake cat without carotid bodies and aortic depressor nerves hypoventilates during normoxia in relation to intact cats. Acute hypoxia resulted in respiratory acidosis, decreased tidal volume (VT), and decreased breath duration (TTOT). Exposure to hypoxia for three days resulted in no hyperventilation (isocapnia) but increased VT and TTOT from their levels during acute hypoxia. Acute hyperoxia resulted in respiratory alkalosis and increased VT. Moderate degrees of acute inspiratory hypoxia (FIO2 less than 0.12) induced a behavioral 'arousal' in these cats; this is in direct contrast to the lack of response seen shortly after CBR. Presumably, the recrudescence of chemosensitivity via unsectioned aortic chemoreceptor afferents played a key role in the arousal responses. However, there is no evidence in the cat for recrudescent chemoreceptor input to the respiratory control system with measurable steady state effect. We conclude that the peripheral chemoreceptors are essential for normal resting ventilatory control and for acclimation to chronic hypoxia.

Adaptation, Physiological↗
PubMed1987

Characteristics of a simple measure of respiratory impedance.

The ratio of mouth pressure developed 0.1 sec after occlusion at end-expiration (P0.1) to average inspiratory flow rate (VT/TI) has been proposed as 'effective inspiratory impedance', Imeff. We have studied a simple mathematical model of lung mechanics, consisting of an effective resistance, an effective compliance and a single pressure generator, to learn how Imeff is altered by changes in resistance (R), compliance (C), inspiratory duration (TI), and the degree of curvature of the inspiratory pressure wave form. The degree of curvature was varied between concave with respect to the time axis to convex and included a linear inspiratory muscle pressure function. Assuming a linear pressure function, we obtained an explicit equation for Imeff as a function of R, C, and TI. Using the same model we also studied the classical impedance as a function of R, C and frequency (of a sinusoidal excitation pressure). We found that Imeff was increased by increases in R, increasing degrees of concavity, decreases in C, and by decreases in TI. For this model the classical impedance was about 5 times larger than Imeff. Classical impedance was increased by increases in R, decreases in C, and decreases in excitation frequency. In conclusion, measurements of effective inspiratory impedance need to be interpreted in terms of R, C, TI, and the shape of the inspiratory muscle pressure function.

Adolescent↗
PubMed1986

Acute back pain: a control-group comparison of behavioral vs traditional management methods.

Back-pain patients with onset in the preceding 1-10 days and comparable on a back examination were randomly assigned to traditional management (A regimen) and behavioral treatment methods (B regimen). Patients were compared at 6 weeks and 9-12 months on a set of "Sick/Well" scores derived from patient reported vocational status (V), health-care utilization (HCU), claimed impairment (CI), and pain drawings (D) and on two measures of activity level. No differences were found at 6 weeks, but at 9-12 months, A-group S's were more "sick." No A/B differences were found on activity-level measures. Group A S's showed significant increases in claimed impairment from preonset to follow-up, whereas Group B S's had returned at follow-up to preonset levels.

Acute Disease↗
PubMed1985

Characteristics of the ventilatory exercise stimulus.

Simple mathematical models were used to quantitatively examine a number of hypotheses concerning the nature of the exercise stimulus. The modelling demonstrated the following for an exercise intensity of 5 times the resting metabolic rate. (1) During the steady state, a deviation in the coupling between VE and metabolic rate by +/- 25% of the value necessary for isocapnia, results in a deviation of PaCO2 of +/- 2 torr from isocapnia. (2) In the transient phase, a mismatch between VE and Q (and thus CO2 flow) of 50% results in a change of PaCO2 of only 1 torr. (3) When resting PaCO2 is changed by 10 torr and it is assumed that the coupling between VE and VCO2 does not change, PaCO2 deviates from isocapnia by less than 2 torr. It is concluded that (1) to experimentally test hypotheses of the exercise stimulus requires resolution of small changes in PaCO2; (2) good regulation of PaCO2 does not necessarily imply precise coupling between VE and VCO2; (3) the ventilatory exercise stimulus need not be a precise function of metabolic rate; (4) in the steady state, the normal CO2 controller will be very effective in minimizing changes in PaCO2 due to a mismatch between ventilation and metabolic rate.

Arteries↗
PubMed1984

Ventilatory responses to low levels of CO2 inhalation in the cat.

The steady-state ventilatory and end-tidal PCO2 (PETCO2) responses to low-level CO2 inhalation have been studied in four awake cats. Four cats anesthetized with Dial-urethane were also studied before and after vagal section or blockade. Awake cats breathed gas mixtures with FICO2 equal to 0.0015 (control), 0.01 and 0.03 in oxygen or 0.0015, 0.01 and 0.02 in air, while anesthetized cats inhaled FICO2 of 0.0000 (control), 0.005 and 0.01 in oxygen. In order to obtain accurate, unbiased determinations of the respiratory system responses to small increases of FICO2 above control values, we used a protocol in which control conditions preceded and followed each CO2 test. The pairwise response for each variable was calculated from the mean of the two 'bracketing' control values. We found that low-level CO2 inhalation in the cat resulted in consistent and significant increases in PETCO2 (82 of 86 trials) and VT (76 of 86 trials) but inconsistent changes in TTOT. We conclude that low-level CO2 inhalation in the cat results in hypercapnia detectable by a replicated, unbiased experimental design.

Anesthesia↗
PubMed1984

Role of the carotid bodies in ventilatory acclimation to chronic hypoxia by the awake cat.

Steady-state breathing patterns during air and hypoxia (PIO2 = 84 Torr) were measured in awake cats in the following conditions: (1) during 7 months of exposure to air following carotid body resection (CBR; N = 6); (2) during 7 months of hypobaric hypoxia (PIO2 = 84 Torr; N = 5) following CBR; (3) during 5 months of exposure to hypobaric hypoxia (N = 4) while intact and then following CBR. Also, in groups (1) and (2) the aortic nerves were sectioned (ANX) at the end of the acclimation periods. The results show that the awake cat hypoventilates if the carotid bodies have been removed, and hypoxic sensitivity is reduced during long-term exposures to either hypoxia or normoxia. ANX caused a slight increase in respiratory frequency, indicating a minor role for the aortic bodies. CBR after acclimation to hypoxia resulted in decreased tidal volume but no change in respiratory frequency. The slight ventilatory acclimation to hypoxia in CBR cats was solely due to increased respiratory frequency. The phenomenon of 'hypoxic tachypnea' was modulated by acclimation, indicating that the effect of hypoxic acclimation upon respiratory frequency is due to central mechanisms.

Adaptation, Physiological↗
PubMed1984

Measuring functional impairment associated with pain: psychometric analysis of an exploratory scoring protocol for activity pattern indicators.

Behavioral science theorists who study pain have advocated the development of measures designed to assess aspects of behavior. Recently, Diller , Fordyce , Jacobs, and Brown developed a 64-item self-report activity measure. Assessment of functional impairment associated with pain is a potentially appropriate application for the Activity Pattern Indicators (API). The API provides a description of actual functioning; frequency of behavior is the unit of measurement. Currently, no agreed upon scoring protocol is available for this measure. We propose to design, in accordance with measurement theory, a psychometrically sound yet practical scoring protocol. The API data presented allow an acceptable degree of reliability and sensitivity to group differences. Results of the present study support continued psychometric exploration of: the current scoring protocol, alternative scoring protocols, and the Activity Pattern Indicators.

Activities of Daily Living↗
PubMed1982

Evidence in man for a fast neural mechanism during the early phase of exercise hyperpnea.

Recently, the rapid increase in ventilation at the onset of exercise has been attributed to reflexes stimulated by the concomitant increase in cardiac output. To evaluate these 'fast-humoral' hypotheses in supine man, the heart rate, ventilation, and end-tidal PCO2 and PO2 were observed during four procedures: the onset of mild dynamic exercise by the lower legs (1) with and (2) without inflation of occluding cuffs around the upper thighs, (3) rapid induction of circulatory occlusion at the level of the upper thighs, and (4) abrupt release of circulatory occlusion after 2.5 min of ischemia. Exercise resulted in abrupt hyperpnea, alveolar hyperventilation, and tachycardia whether or not there was circulatory occlusion. Circulatory occlusion engendered abrupt bradycardia and transient, hyperventilatory hyperpnea. Release of circulatory occlusion resulted in relatively large tachycardia and, after a delay, small hyperpnea and alveolar hypoventilation. The results demonstrate that the early response to exercise is not inherently isocapnic hyperpnea and that, contrary to the prediction of the fast-humoral hypotheses, the presumed increase in cardiac output following cuff release does not produce a ventilatory response similar to that of exercise. These findings support the existence of a neurally mediated factor during the early stages of exercise hyperpnea.

Adult↗