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H Manning

Publications and source records attributed to H Manning.

13 recordsLinked to original sources
PubMed1992

Oxygen cost of resistive-loaded breathing in quadriplegia.

We hypothesized that, in quadriplegia, chest wall distortion would increase the energy cost of ventilation. To assess this, we measured the oxygen cost of breathing (VO2 resp) and changes in chest wall configuration during inspiratory resistive-loaded breathing tasks in five quadriplegic and five normal subjects. Each subject performed three breathing tasks that spanned a range of work rates (Wtot). Configurational changes of the abdomen and upper, lower, and transverse rib cage were assessed with magnetometers. We found that 1) in both groups, VO2resp increased linearly with Wtot over the range of tasks performed, 2) the mean slope of the regression line of VO2resp vs. Wtot was greater for quadriplegic than for normal subjects (3.7 +/- 0.8 vs. 2.0 +/- 0.7 ml O2/J, P less than 0.01), 3) efficiency of breathing (Wtot/VO2resp) was less for quadriplegic than for normal subjects (1.9 +/- 0.6 vs. 3.5 +/- 1.4%, P less than 0.001), 4) during inhalation, upper and lower rib cages behaved similarly in the two groups, but the quadriplegic subjects had a decrease in transverse rib cage and a much greater increase in abdomen than normal subjects, and 5) functional residual capacity decreased in normal but not in quadriplegic subjects during the breathing tasks. We conclude that the lesser efficiency of breathing in quadriplegia may be related to the elastic work of chest wall distortion, shorter mean operational diaphragm length, and possibly differences between normal and quadriplegic subjects in mechanical advantage of available inspiratory muscles.

Adult↗
PubMed1992

Dissociation between dyspnea and respiratory effort.

Breathlessness induced by hypercapnia may be related to the sensation of respiratory effort or to the central or peripheral effects of CO2. To examine the relationship among breathlessness, respiratory effort, and hypercapnia, we studied eight normal naive subjects. By using a visual feedback system, subjects maintained a constant ventilation of 50-60 L/min. PETCO2 was held at 40 mm Hg during the first 2 min of each trial (control period), then for 4 min (test period) was either kept at 40 mm Hg or elevated to 50 mm Hg. At the end of each control and test period, subjects were asked to give separate ratings for dyspnea (an unpleasant urge to breathe) and for the sense of respiratory effort (analogous to lifting a weight) on a 50-cm visual analog scale. Hypercapnia was associated with a significant reduction in effort ratings (-7.3 +/- 6.4, mean +/- SD, p < 0.05) and a concomitant increase in dyspnea (+6.6 +/- 6.0, p < 0.05). We conclude that dyspnea associated with hypercapnia is dissociated from changes in respiratory effort, and that CO2 has a direct central effect that leads to breathlessness. Our data also suggest that the sense of effort at a given level of ventilation is less when the ventilation is the result of "reflex" stimuli to breathe rather than "voluntary" signals to the respiratory muscles.

Adult↗
PubMed1990

Hypoxemia alone does not explain blood pressure elevations after obstructive apneas.

In patients with obstructive sleep apnea (OSA), substantial elevations of systemic blood pressure (BP) and depressions of oxyhemoglobin saturation (SaO2) accompany apnea termination. The causes of the BP elevations, which contribute significantly to nocturnal hypertension in OSA, have not been defined precisely. To assess the relative contribution of arterial hypoxemia, we observed mean arterial pressure (MAP) changes following obstructive apneas in 11 OSA patients during non-rapid-eye-movement (NREM) sleep and then under three experimental conditions: 1) apnea with O2 supplementation; 2) hypoxemia (SaO2 80%) without apnea; and 3) arousal from sleep with neither hypoxemia nor apnea. We found that apneas recorded during O2 supplementation (SaO2 nadir 93.6% +/- 2.4; mean +/- SD) in six subjects were associated with equivalent postapneic MAP elevations compared with unsupplemented apneas (SaO2 nadir 79-82%): 18.8 +/- 7.1 vs. 21.3 +/- 9.2 mmHg (mean change MAP +/- SD); in the absence of respiratory and sleep disruption in eight subjects, hypoxemia was not associated with the BP elevations observed following apneas: -5.4 +/- 19 vs. 19.1 +/- 7.8 mmHg (P less than 0.01); and in five subjects, auditory arousal alone was associated with MAP elevation similar to that observed following apneas: 24.0 +/- 8.1 vs. 22.0 +/- 6.9 mmHg. We conclude that in NREM sleep postapneic BP elevations are not primarily attributable to arterial hypoxemia. Other factors associated with apnea termination, including arousal from sleep, reinflation of the lungs, and changes of intrathoracic pressure, may be responsible for these elevations.

Adult↗
PubMed1980

Mind that child!

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Child↗