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Biomedical subjects

C S Roussos

Publications and source records attributed to C S Roussos.

10 recordsLinked to original sources

Facilitating changes in supervisees' clinical behaviors: an experimental investigation of supervisory effectiveness.

This research was conducted to determine whether supervisees altered their clinical behaviors as a consequence of a joint data-analysis method of clinical supervision. Four beginning graduate student clinicians assigned to articulation clients were supervised in accordance with tenets of Cogan's Clinical Supervision Model and Anderson's Continuum of Supervision. Supervision focused on the targeted dependent variables of clinician "explanations," "informative feedback," and "directive responses to off-task utterances." Visual inspection of multiple baseline data indicated that target behaviors improved after they became the focus of supervision. The supervisory procedures implemented in this study effected positive changes in the supervisees' clinical behaviors. Qualitative discoveries that relate to the practicalities of daily supervision are discussed.

Clinical Competence

Flow dependence of gas distribution and the pattern of inspiratory muscle contraction.

We measured regional distribution of xenon-133 boli at 0.25, 0.75, and 1.5 l/s in four normal seated subjects during inspirations performed predominantly with intercostal and accessory muscles (IC) or with the diaphragm, accompanied by outward abdominal motion (Ab). In six additional subjects we inferred the topographical distribution of helium boli during similar breaths and flow rates from the slope of the alveolar plateau recorded during a slow expiration (less than 0.5 l/s). Distribution of the helium boli was studied during natural as well as IC and Ab inspirations. At each of the flow rates IC breaths distributed relatively more of the inspired bolus to upper lung regions than did Ab inspirations. Natural breaths at 0.25 l/s resulted in distributions similar to those of Ab inspirations, whereas at 1.5 l/s the distribution approached that of IC inspirations. A three-compartment model, representing upper, middle, and lower lung regions, was used to simulate bolus distribution. The experimental data showed substantial departure from predictions based on regional time constants alone. However, additional small differences in applied pressure (less than 0.50 cmH2O) between the regions satisfactorily accounted for the gas distribution.

Abdominal Muscles

Respiratory muscle fatigue: a cause of respiratory failure?

1. The question whether respiratory muscle fatigue ever causes respiratory failure is over 40 years old, but we still have no definitive answer to this question. Skeletal muscle fatigue occurs when the rate of energy consumption of the muscle is greater than the energy supplied, so that energy stores are utilized and eventually become depleted. 2. Five factors which are important in the development of muscle fatigue (a, the tension developed by the muscle; b, the maximum tension the muscle can develop; c, the energy stored within the muscle; d, the energy supplied to the muscle; e, the efficiency of the muscle). These can be affected in many diseases, so disposing to fatigue, thus respiratory muscle fatigue is likely to be a common occurrence. 3. Respiratory muscle fatigue can in principle easily be diagnosed at the bedside by application of a simple electromyographic technique used to detect fatigue in other skeletal muscles.

Electromyography

Diaphragmatic contraction and the gradient of alveolar expansion in the lateral posture.

Using 133Xe we measured the vertical distribution of regional volume in four subjects in the lateral decubitus posture at 20, 40, 60, and 80% of vital capacity (VC). To study the influence of diaphragmatic tone, all measurements were performed either when transdiaphragmatic pressure (Pdi) was low, i.e., diaphragm was "relaxed" (RD) or during voluntary diaphragmatic contraction (VDC). The latter was achieved by tensing the abdominal muscles while keeping the glottis open. Under both conditions the gradient of alveolar expansion tended to be curvilinear, with a discontinuity at the level of the mediastinum. At all lung volumes the difference in regional volume between dependent and nondependent lung regions was less during VDC than during RD. At 70% total lung capacity (TLC) this difference, expressed as percent of regional TLC (%TLCr), decreased from 19.7 +/- 1.7 (mean +/- 1 SE) %TLCr during RD to 3.9 +/- 1.5% TLCr during VDC. It is likely that diaphragmatic tension influences the pleural pressure gradient and regional volume distribution 1) by modifying the transmission of the abdominal hydrostatic pressure gradient to the thorax, and 2) by an upward displacement of the mediastinum.

Diaphragm

Diaphragmatic fatigue in man.

The time required (tlim) to produce fatigue of the diaphragm was determined in three normal seated subjects, breathing through a variety of high alinear, inspiratory resistances. During each breath in all experimental runs the subject generated a transdiaphragmatic pressure (Pdi) which was a predetermined fraction of his maximum inspiratory Pdi (Pdimax) at functional residual capacity. The breathing test was performed until the subject was unable to generate this Pdi. The relationship between Pdi/Pdimax and tlim was curvilinear so that when Pdi/Pdimax was small tlim increased markedly for little changes in Pdi/Pdimax. The value of Pdi/Pdimax that could be generated indefinitely (Pdicrit) was around 0.4. Hypoxia appeared to have no influence on Pdicrit, but probably led to a reduction in tlim at Pdi greater than Pdicrit for equal rates of energy consumption. Insofar as the behavior of the diaphragm reflects that of other respiratory muscles it appears that quite high inspiratory loads can be tolerated indefinitely. However, when the energy consumption of the respiratory muscles exceeds a critical level, fatigue should develop. This may be a mechanism of respiratory failure in a variety in a variety of lung diseases.

Diaphragm

Convection, diffusion and cardiogenic mixing of inspired gas in the lung; an experimental approach.

In 8 open-chested dogs, we measured the FN2 within 26 airways, 2.5-8.6 mm in diameter, during constant flow inflations with 0.5 liter of O2. At low flows the FN2 did not fall to zero but reached a plateau, at a value that was inversely related to inspiratory flow. When inspiratory flow is constant, the measured FN2 represents one point on a stationary front separating inspired and alveolar gas. At all points on the front the convective and diffusive transport of N2 is equal and opposite in direction. We quantitated cardiogenic gas mixing by comparing in vivo and post mortem the flow which resulted in a given stable FN2 value within the same airway. In vivo, this flow and therefore the calculated effective diffusion coefficient (D') was more than 5 times greater than that post mortem. Our results confiem some of the predictions made from model analyses of gas transport in the lung. However, calculations based on molecular diffusion as the sole mixing mechanism necessarily overestimate diffusion times and the magnitude of stratification.

Animals

Influence of diaphragmatic contraction and expiratory flow on the pattern of lung emptying.

Transdiaphragmatic pressure (Pdi) and expiratory flow (V) were monitored during vital capacity single breath N2 washouts in 7 seated subjects. Transient increases in V were produced (1) actively, by subjects increasing mouth pressure while expiring through a constant resistance of (2) passively, by the operator transiently decreasing the resistance. Voluntary contraction of the diaphragm (increased Pdi) was achieved when abdominal muscles were tensed while maintaining V constant. In 5 subjects a transient increase in Pdi of 25-150 cm H2O consistently produced a transient increase in expired N2 concentration of 1.80 +/- 0.06% (Mean +/- 1 SE); in 1 subject N2 concentration decreased by 0.8% to 2.7% N2, and in one subject the alveolar plateau was uninfluenced by changes in Pdi. Passive increases in V up to 21/sec had no effect on FEN2 in any of the subjects. Active increase in V changed FEN2 only when associated with increases in Pdi. Qualitatively similar results were obtained during helium (He) bolus washouts. However, whereas diaphragmatic contraction, maintained throughout expiration, had no measurable influence on the N2 washout, it changed the slope of the He alveolar plateau in 6 out of 7 subjects. We conclude that in normal subjects the alveolar N2 plateau is relatively insensitive to flow variations up to 21/sec. The fluctuations in FEN2 observed when the expiratory flow is varied are due to concomittant changes in Pdi. We propose that diaphragmatic contraction changes the pattern of lung emptying by altering the vertical gradient of pleural pressure.

Diaphragm

Influence of diaphragmatic contraction on ventilation distribution in horizontal man.

The washout of a bolus of helium (inhaled from residual volume) during relaxed expiration (RE) through a resistance was compared with that during expiration with voluntary diaphragmatic contraction (VDCE) achieved by tensing the abdominal muscles while maintaining constant expiratory flow (less than 0.4 l/s). In six subjects in the lateral decubitus position, phase IV during RE started at 58 +/- 1.6% vital capacity (VC) (mean +/- 1 SE). During VDCE, when the transdiaphragmatic pressure (Pdi) exceeded 30 cmH2O, phase IV commenced at 8.2 +/- 0.8% VC. The expired He concentration (FEHe) at lung volumes greater than 70% VC was 1.3 +/- 0.05 times that during RE. In supine subjects VDCE flattened the slope of the alveolar plateau and decreased closing volume by 3.7 +/- 0.4% VC. Our results suggest that when the diaphragm is relaxed in the horizontal subject, the hydrostatic gradient of pressure within the abdomen enhances early emptying of dependent lung zones. Diaphragmatic contraction results in more homogeneous emptying. We conclude that diaphragmatic tone influences the vertical gradient of regional volume, and hence of pleural pressure. The latter is not constant, being less during inspiration than during expiration. Therefore, differences in the changes of applied pressure between dependent and nondependent lung regions influence ventilation distribution in subjects in the horizontal posture.

Diaphragm