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Biomedical subjects

C K Mahutte

Publications and source records attributed to C K Mahutte.

65 records · Page 4Linked to original sources

Magnitude scaling of externally added loads to breathing.

Externally added resistive and elastic loads to breathing elicit a sensation the psychological magnitude of which was described by a power function: psi = k theta n. The perceived magnitude (psi) was related to the physical magnitude (theta) by the exponential term (n). The exponent described the increase in sensation for an increase in load. In normal subjects, the mean exponent for added resistive loads was 0.80 +/- 0.35 SD, and for elastic loads was 0.99 +/- 0.45. Intrasubject variability (mean coefficient of variation = 7%) was much less than intersubject variability (coefficient of variation = 230%). The exponents for elastance and resistance were highly correlated (r = 0.92). In these studies, the subjects freely adopted their tidal volume and flow rate. During the addition of resistive loads, the subjects tended to reduce their flow rate, especially at the highest loads, and during the elastic loads, they tended to reduce their tidal volume. Fixing tidal volume during the addition of elastic loads and flow rates during the addition of resistive loads caused an increase in exponent. This finding implied that the tidal volume and flow rate, or factors related to them such as muscular effort, are important attributes of the sensation elicited by loaded breathing.

Adult↗

Joint mechanics as a determinant of motor unit organization in man.

To support a given weight a muscle which inserts close to the axis of a single joint must develop more force than a muscle which inserts further from the axis. Using available anatomical and histochemical data we have shown an association between the mechanical leverage of a muscle at a joint and the proportion of type II (fast twitch, large tension) muscle fibres. We suggest that the mechanical leverage at joints determines the proportion of fast and slow motor units within a muscle in a teleologically appropriate manner. This determination probably occurs before the differentiation of motorneurones into fast and slow types.

Biophysical Phenomena↗

Resistive load detection during passive ventilation.

By using standard psychophysical techniques resistive load detection was estimated in five normal subjects during spontaneous breathing and during passive ventilation in a Drinker respirator. 2. During assisted ventilation a gross deterioration in resistive load detection occurred. 3. The findings imply that active respiratory muscle contraction plays an essential role in the detection of added resistive loads.

Adult↗

Changes in the perception of inspiratory resistive loads during partial curarization.

1. The ability of normal subjects to estimate the magnitude of resistive loads and to detect resistive loads was determined using standard psychophysical techniques. The experiments were repeated during maintained partial neuromuscular blockade with D-tubocurarine. 2. During curarization the ability to detect the presence of a small inspiratory resistive load was not significantly impaired. This finding is consistent with the view that changes in the usual breath-by-breath relation between pressure and flow mediate detection. 3. The size of resistive loads was over-estimated during partial curarization. Subjects thus placed more reliance on sensing the increased motor command required during curarization than on alternative peripheral signals related to pressure, flow or resistance. 4. The exponent for the power function relating the perceived magnitude of a resistive load to its actual size (Stevens, 1957) was reduced during partial neuromuscular blockade. 5. These results suggest that detection of resistive loads depends upon sensing apparent information arising from an unexpected pressure-flow disturbance but that estimation of the size of an added load depends, in part, on sensing the outgoing motor command.

Adult↗

Effect of timing, flow, lung volume, and threshold pressures on resistive load detection.

The acuity of resistive load detection (RLD) has been tested by comparing threshold detection (delta R50) under control conditions with that obtained when loads were applied at different times in inspiration, with different inspiratory flows, at different lung volumes, and with different background loads. For loads applied suddenly during established inspiratory flow, the mean delta R50 was 0.94 +/- 0.04 (+/- SEE) cmH2O . 1(-1) . s compared with 0.42 +/- 0.13 cmH2O . 1(-1) . s (P < 0.01) for loads applied before inspiration, suggesting that information generated early in the breath is important and the RLD is not subserved by a simple peripheral proprioceptive mechanism. Rapid voluntary inspiration through nonlinear resistances did not improve RLD (mean delta R50 0.86 cmH2O . 1(-1) . s compared with a control of 0.56 cmH2O . 1(-1) . s; P < 0.05) despite the much greater pressures and resistances at high flow rates, further suggesting that detection of a resistive load occurs early in inspiration. Alteration of the background load by breathing at increased lung volume (1 liter above FRC) or by breathing against a standing pressure of 1 or 3 cmH2O (i.e., pressure independent of volume or flow) did not significantly reduce RLD. This suggests that the change in pressure due to the added load, expressed as a fraction of the total driving pressure, cannot subserve RLD. Our results suggest that external resistive load detection is subserved by the relation between pressure and flow over the early part of inspiration.

Adult↗

Influence of rate of induction of hypoxia on the ventilatory response.

1. We have studied the influence of rate of induction of hypoxia on the duration of the phases of the respiratory cycle in seven conscious healthy subjects.2. Nine hypoxic procedures were performed on each subject, comprising three different rates of induction of hypoxia each at three different levels of P(CO2). Ventilation vs. arterial O(2) saturation plots were constructed and patterns of response were analysed in terms of ventilation vs. tidal volume and tidal volume vs. inspiratory duration (T(I)) and vs. expiratory duration (T(E)).3. The highest ventilatory responses were observed during steady-state hypoxia when P(CO2) was held at a level similar to the control mixed venous level; progressive hypoxia at this P(CO2) failed to stimulate ventilation to comparable levels. The ventilatory response was not influenced by rate of induction of hypoxia when P(CO2) was maintained at an end-tidal P(CO2) close to the control level.4. As tidal volume increased in response to hypoxia, T(I) and T(E) shortened. The progressive decrease in cycle duration occurred at all levels of P(CO2) and at all rates of induction of hypoxia, but was most marked under eucapnic conditions during steady state.5. It is concluded that steady-state hypoxia may produce a higher ventilatory response than progressive, non-steady-state hypoxia. Inspiratory time shortens as tidal volume increases irrespective of the rate of induction of hypoxia.

Adult↗

A noninvasive method for measuring the PCO2 of mixed venous blood.

A breath-holding method for measuring the PCO2 of mixed venous blood has been developed. Two gas mixtures, 100 per cent O2 and 12 per cent CO2 in O2, were inspired, and the expired gas was analyzed after 5 and 15 sec of breathholding. The oxygenated mixed venous PCO2 was calculated using an exponential equation. The method was applied in healthy subjects, patients with lung disease, and unconscious mechanically ventilated patients. The mixed venous PCO2 correlated well with arterial PCO2 (r = 0.96), the PCO2 obtained by rebreathing (r = 0.97), and the PCO2 in blood drawn from the pulmonary artery (r = 0.97). The method is noninvasive, has a low coefficient of variance, and allows arterial PCO2 to be estimated by multiplying the breath-holding mixed venous PCO2 by 0.8.

Adult↗

A mathematical expression to describe the ventilatory response to hypoxia and hypercapnia.

A mathematical expression has been developed to describe the ventilatory responses to changes in arterial oxygen saturation (SaO2) and arterial carbon dioxide tension (PCO2). The derivation is based on the experimental observations: (1) that ventilation is a linear function of PCO2 under isoxic conditions, and (2) that ventilation is a linear function of SaO2 under isocapnic conditions. It is assumed that all functions are continuous and single valued, with the implication that for any given SaO2 and PCO2 there is a unique ventilatory response. The analysis following from these three assumptions has enabled us to derive the following expression for ventilation: VI(SaO2, PCO2) = alpha1 - SaO2 - PCO2 + alpha2 - SaO2 + alpha3 - PCO2 + alpha4 where the alpha's are constants for an individual. This equation, which follows uniquely from the assumption stated, is simpler and contains fewer parameters than previous expressions used to describe ventilation.

Humans↗