Letter: Vital capacity and myocardial-infarction risk.
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Biomedical subjects
Publications and source records attributed to D E Leith.
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Lung volumes and quasi-static deflation volume-pressure relationships were measured in male golden hamsters anesthetized with pentobarbital. Volume was measured with a pressure plethysmograph, and pleural pressure was estimated by the use of a water-filled esophageal catheter. Mean body weight +/- SE was 122.3 +/-3.0 g, mean lung weight was 0.74 +/- 0.2 g or about 0.6% of body weight. Mean lung volume at 25 cmH2O transpulmonary pressure (TLC25) was 7.2 +/- 0.14 ml, 9.78 +/- 0.17 ml/g lung weight or 5.92 +/- 0.06 ml/100 g body weight. Mean functional residual capacity was 2.4 +/- 0.06 ml or 33.3% of TLC25. Mean vital capacity was 5.2 +/- 0.13 ml. Mean quasi-static compliance of lung was 0.63 +/- 0.03 ml/cmH2O. Chord compliance of chest wall between lung volumes of 1 and 4 ml above RV was 3.39 +/- 0.53 ml/cmH2O. At FRC, the chest wall recoiled inward, so that pleural pressure was positive (1.4 +/- 0.13 cmH2O) and the lung was resisting further collapse. The slope of the lung's deflation volume-pressure curve changed at FRC, ERV was small (0.36 +/- 0.03 ml), and RV was determined by complete airway closure. Thus the mechanisms determining FRC are unusual and include an influence of airway closure.
We studied respiratory mechanics in young volunteers before and after 5-wk training programs limited to the ventilatory muscles. Four strength trainers (S) performed repeated static maximum inspiratory and expiratory maneuvers against obstructed airways. Four endurance trainers (E) performed voluntary normocarbic hyperpnea to exhaustion. Subjects spent 30-45 min each day in these exercises, 5 days a week. Four control subjects (C) did no training. We attempted to minimize the effect of learning. S increased pressure maximums by about 55%, but vital capacity and total lung capacity by only about 4%. Initially all subjects could sustain hyperpnea at about 81% of their control 15-s maximum voluntary ventilation (MVV) for 15 min; E increased this to about 96% and increased their MVV by 14% as well. No other statistically significant changes were recognized in any group. We conclude that ventilatory muscle strength or endurance can be specifically increased by appropriate ventilatory muscle training programs.
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In 10 patients with severe, acute respiratory failure we studied the effects of positive end-expiratory pressure when intermittent positive pressure ventilation (IPPV) with inspired oxygen (F(IO2)) up to 0.5 failed to maintain arterial oxygen tension (P(aO2)) above 70 torr.Positive end-expiratory pressures (PEEP) of 0, 5, 10, and 15 cm H(2)O were applied for 30-min periods each and in random order. Blood gas exchange, lung volumes, compliance, and hemodynamics were studied at each level of PEEP. P(aO2) (F(IO2) = 1.0) rose linearly with elevation of PEEP, the mean increase being from 152 to 347 torr, or 13 torr/cm H(2)O PEEP. Mean functional residual capacity (FRC) was 1.48+/-0.78 liters at zero PEEP (i.e., IPPV) and the increase was essentially linear, reaching 2.37 liters at 15 cm H(2)O PEEP. P(aO2) and FRC showed a close correlation. Total and lung static compliance were greater during ventilation with high than with low levels of PEEP. The increase in P(aO2) correlated with the specific lung compliance. Dynamic lung compliance decreased progressively with rising levels of PEEP except for an increase with 5 and 10 cm H(2)O PEEP in patients with initial values of 0.06 liter/cm H(2)O or higher. Cardiac index fell in some patients and rose in others and there was no correlation of mean cardiac index, systemic blood pressure, or peripheral vascular resistance with level of PEEP. The most probable explanation for the effect of PEEP on P(aO2) and compliance is recruitment of gas exchange airspaces and prevention of terminal airway closure.
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The clinical usefulness of two pulse oximeters was evaluated at two probe sites in nine anesthetized horses. The hemoglobin saturation determined by the pulse oximeters (SaOx) was compared with the hemoglobin saturation calculated from the measured arterial oxygen tension (SaO2). The mean and standard deviation (SD) were calculated from the differences in saturation measurements, over the saturation range of 80% to 100%, for each oximeter used at the tongue probe site and for one oximeter used at the ear. The oximeter results tended to underestimate the SaO2 with mean differences of -3.7% on the tongue and -6.0% on the ear. The limits of agreement were defined as the mean difference +/- 2 SD. Each oximeter used at the tongue produced limits of agreement of +1% to -8%, which meant that 95% of the SaOx values were 1 percentage point above or 8 percentage points below the SaO2. The variability of the differences and limits of agreement were larger when the ear was used as the probe site and at saturations less than 80%. Although both oximeters tended to underestimate the SaO2, they appeared to be clinically useful in detecting changes in arterial hemoglobin saturation.