Yongyudh Ploysongsang

Reproducibility of the Vesicular Breath Sounds in Normal Subjects

Nonfiltered (NF) lung sounds from the apical area of the heart along with lung volumes and ECG signals were recorded from 5 normal subjects. The signals were digitized and subjected to three methods of heart sound cancellation: 75-Hz high-pass filtering (75 HF), ECG-triggered blanking (BL) and adaptive noise cancelling (AF) [IEEE Trans. Biomed. Engng 33: 1141-1148, 1986]. The sound signals were then subjected to the fast Fourier transform algorithm to obtain power spectra. Five breaths from each subject were analyzed, and their spectra were similar and slightly skewed to the right. The average values of mean, median and mode frequencies of the whole breath of 5 subjects, respectively, were for NF: 64.62 +/- 3.74, 44.57 +/- 2.06 and 36.75 +/- 1.79 Hz; for 75 HF: 150.42 +/- 17.49, 114.02 +/- 6.43 and 86.16 +/- 3.13 Hz; for BL: 81.76 +/- 6.02, 52.36 +/- 2.79, 41.10 +/- 3.15 Hz; for AF: 96.87 +/- 11.58, 68.23 +/- 10.44 and 52.25 +/- 8.97 Hz. These values showed no differences between subjects. The F values obtained by the two-way analysis of variance of all breaths of all subjects (mean, median, mode) were: NF: 0.161, 0.341, 0.089; 75 HF: 0.455, 0.042, 0.085; BL: 0.108, 0.082, 0.057; AF: 0.130, 0.204, 0.113 (all p greater than 0.1). The data revealed a remarkable lack of variation within and between subjects, suggesting similar sites and mechanisms of production and transmission.

Inspiratory and Expiratory Vesicular Breath Sounds

Unfiltered breath sounds (NF) from the apical area of the heart, lung volume and ECG signals were recorded in 5 normal subjects. The signals were digitized and subjected to three methods of heart sound cancellation: 75-Hz high-pass filtering (75 HF), ECG-triggered blanking (BL) and adaptive filtering (AF). The sound signals were then subjected to the fast Fourier transform algorithm to obtain power spectra. Inspiratory and expiratory phase sounds of five breaths of each subject were analyzed separately. The inspiratory and expiratory sound power spectra were very similar and skewed slightly to the right, and therefore characterized by median frequencies. The differences between inspiratory and expiratory median frequencies were insignificant for NF: 42.90 +/- 2.03 (mean +/- SD) vs. 46.64 +/- 2.53 Hz (p greater than 0.1); for 75 HF: 106.43 +/- 10.27 vs. 118.22 +/- 6.30 Hz (p greater than 0.5); for BL: 44.46 +/- 3.33 vs. 66.73 +/- 2.93 Hz (p greater than 0.1), for AF: 49.72 +/- 5.68 vs. 79.20 +/- 13.07 Hz (p greater than 0.1). We conclude that the lack of significant differences suggests similar mechanisms and sites of production of inspiratory and expiratory vesicular breath sounds.

Factors Influencing the Production of Wheezes during Expiratory Maneuvers in Normal Subjects

We recorded wheezes, pleural pressure, plethysmographic lung volumes and mouth flow rates in 6 healthy subjects during maximal expiratory maneuvers breathing air and a mixture of 80% He-20% O2 (He) before and after methacholine inhalation. During expiratory flow maneuvers a critical pleural pressure was needed before wheezes occurred. All but one wheeze occurred in the last two thirds of vital capacity during forced exhalation where flow limitation existed. At a flow rate of 2 liters/s, the critical pleural pressure breathing air was 21 +/- 5.8 cm H2O (mean +/- SD), whereas that of breathing He was higher: 32 +/- 7.8 cm H2O (p less than 0.02). In addition the wheezes occurred at lower lung volumes (associated with small airway diameters) when He was breathed instead of air. This was seen both before (p less than 0.02) and after (p less than 0.01) methacholine. These findings suggested that for a given flow rate a lighter gas such as He had to acquire a higher linear velocity so that the convective acceleration was sufficient to produce wheezes. This was achieved by either an increase in the driving critical pleural pressure or narrowing of bronchi by a larger compressing pleural pressure or smaller lung volumes.

Lung function tests in connective tissue diseases associated with Raynaud's phenomenon

13 patients with various connective tissue diseases associated with Raynauds phenomenon were studied with pulmonary physiologic techniques to see the alterations of lung functions and also whether spasm of pulmonary circulation occurs in these patients. We found that an increase in the dead space ventilation was common and associated with normal tidal volume. We interpreted this finding as evidence of redistribution of blood flow in the lung by spasm of blood vessels going to well-ventilated lung units generating a high dead space ventilation. We also found commonly that the distribution of inspired air in the lung was uneven, the diffusing capacity was reduced and the dynamic compliance decreased with increasing frequency of breathing suggestive of disease in small airways. The restrictive defect, the obstructive defect, the reduction of lung compliance and the arterial hypoxemia were relatively uncommon and probably occurred when the diseases were more advanced.

Serial Physiologic Studies of a Chronic Obstructive Pulmonary Disease Patient in Acute Respiratory Failure: Clues for Weaning?

A patient with severe chronic obstructive pulmonary disease was studied during acute respiratory failure. On the day of intubation his respiratory rate was 42, the tidal volume 295 ml, and the maximal inspiratory pressure 8 cm H2O. These parameters improved with rest by mechanical ventilation to 16, 620 ml, and 30 cm H2O, respectively, on the day of successful weaning. Daily tidal volumes correlated significantly with maximal inspiratory muscle pressures (r = 0.936; p less than 0.001). Respiratory system compliances and resistances were measured by the inflation, the end-inspiratory occlusion, and the interrupter methods. In general, inflation compliance and occlusion compliance were comparable and significantly smaller than the interrupter compliance (p less than 0.002 and p less than 0.003, respectively), whereas inflation resistance and occlusion maximal resistance were also comparable but significantly smaller than the interrupter resistance (p less than 0.0008 and p less than 0.0006, respectively). The former was due to increased hysteresis of the pressure volume curves and the latter due to expiratory compression of airways. The compliance was low, and the resistance was high on the day of intubation and became much higher and lower, respectively, on the day of successful extubation. These physiological changes were associated with weaning difficulty. We conclude that respiratory failure and weaning are complex physiologic events under the influence of muscle strength, lung mechanics, gas exchange, and control of breathing. Therefore, prediction of weaning success based upon one or two measured parameters as has been done is probably inadequate in difficult patients.

Effects of Breathing Pattern and Oxygen upon the Alveolar Arterial Oxygen Pressure Difference in Lung Disease

It was suggested by analysis of theoretical lung models that low V/Q units are unstable and can be converted into shunt by breathing O2. We tested this theory in 21 subjects with various lung diseases (mostly chronic obstructive pulmonary disease) by having them breathe O2. We also increased the tidal volumes in these patients to see whether this maneuver could prevent the development of shunt. We found that mean P(A-a)O2 increased from 30 +/- 2.8 (mean +/- SEM) Torr breathing room air to 135 +/- 20.7 Torr breathing O2 for 10 min (p less than 0.0001), to 124 +/- 20.4 Torr breathing O2 for 20 min (p less than 0.0001), and to 125 +/- 19.0 Torr breathing oxygen with inspiratory capacity breaths (p less than 0.0001). The corresponding shunt increased from about 2.8% of the cardiac output to 7.9 +/- 1.01, 7.3 +/- 1.03 and 7.3 +/- 0.98%, respectively. We conclude that: (1) breathing pure oxygen can convert low V/Q units to shunt, hence measurement of P(A-a)O2 and shunt by oxygen technique will overestimate the actual values; (2) 10 min of oxygen breathing will cause complete atelectasis of low V/Q units, and (3) increased tidal volume does not prevent absorptive atelectasis.