Does interstitial lung edema compress airways and arteries? A morphometric study.

We compared areas and diameters of small airways and arteries in three groups of anesthetized dogs: 1) control (n = 5), 2) hydrostatic edema induced by fluid overload (n = 13), and 3) increased permeability edema induced with alpha-naphthylthiourea (n = 5). We measured pulmonary arterial and wedge pressures in all groups and cardiac output in the hydrostatic edema group. Postmortem, lobes were frozen at functional residual capacity and samples taken for measurements of extravascular lung water (Qwl/dQl) and for light microscopy. We also examined lobes from hydrostatic edema experiments fixed at transpulmonary pressures of 5 and 27 cmH2O. From the histology slides, bronchovascular bundles with respiratory bronchioles (n = 706) and bronchioles (n = 467) were photographed and airway and vessel areas and diameters measured. Alveolar and airway luminal edema were graded. We found that only in hydrostatic edema, pulmonary arterial and wedge pressures increased and vascular resistance fell with fluid infusion. Mean Qwl/dQl values were 3.80 +/- 0.17, 6.81 +/- 0.96, and 9.34 +/- 0.62 (SE) in control, hydrostatic, and increased permeability edema groups, respectively. By quantitative histology, airway and arterial areas and diameters did not decrease in edema and rose with increasing transpulmonary pressure. Variable quantities of air-space edema were seen. We conclude that interstitial edema does not compress small airways or arteries and that other mechanisms, including alveolar and airway luminal edema, may explain reported increases in airway resistance.

Decay of inspiratory muscle pressure during expiration in conscious humans.

In eight conscious spontaneously breathing adults we studied the decay of pressure developed by the inspiratory muscles during expiration (PmusI). PmusI was obtained according to the following equation: PmusI(t) = Ers X V(t) - Rrs X V(t), where V is volume and V is flow at any instant t during spontaneous expiration, and Ers and Rrs are, respectively, the passive elastance and resistance of the total respiratory system. Ers was determined with the relaxation method, and resistance with the interrupter method. All subjects showed marked braking of expiratory flow by PmusI. The mean time for PmusI to reduce to 50 and 0% amounted, respectively, to 23 and 79% of expiratory time. During expiration, 24-55% of the elastic energy stored during inspiration was used as resistive work and the remainder (45-76%) as negative work.

Statistical "biases" in respiratory disability determinations.

The manner in which pulmonary function test results are employed in the assessment of respiratory disability may be affected by 4 statistical choices: (1) choice of prediction equation(s), (2) adjustment factors (such as sex and race), (3) criterion values, and (4) method of comparison of observed to predicted normal test values. The records of 900 respiratory disability applicants were employed to estimate the direction and magnitude of the effect of these choices on the overall number of persons who would be declared "disabled" and upon the manner in which personal characteristics (e.g., sex, race, height, age) affect the likelihood of being declared "disabled." Choice of prediction equation had minor effects, and adjustment for race and sex had more significant effects. Choice of criterion value affected the overall number and, in certain instances (e.g., Social Security Disability Insurance), the distribution of "disability" declarations. Method of comparison (percent of predicted, difference of predicted minus observed or minimal value criterion) had major effects upon the distribution of "disability" declarations between population subgroups. Preliminary analysis therefore suggests that these statistical choices should be carefully manipulated in the design of a disability system to facilitate achievement of the system's goals.

Unilateral pulmonary artery aplasia presenting with chest pain and pleural effusion.

A 58-year-old woman with a pleural effusion and left chest pain was found to have unilateral absence of the left pulmonary artery. She is unique in that she had recurring pleural effusions and chest pain for 26 years, which has not been previously described with this rare disorder.

Pulmonary function studies in acute pulmonary histoplasmosis.

We performed follow-up pulmonary function studies on three patients with acute pulmonary histoplasmosis over a period of several months, and found that the disease is benign and usually responds well to treatment or is self-limiting. There are four major changes in lung function, namely a restrictive defect, an impairment of diffusing capacity, stiff lung, and obstruction in small airways. These changes usually lead to disturbance of ventilation-perfusion ratios and impaired gas transport across alveolar capillary membranes, resulting in arterial hypoxemia. There is also hypocapnia from alveolar hyperventilation commonly found in restrictive and stiff lung syndrome.

Demonstration of regional phase differences in ventilation by breath sounds.

We measured phase and amplitude of compensated breath sounds (Ib/Tn), which are indexes of regional ventilation, with two microphones placed near the apex and base 10 cm apart on the chest wall, lateral to the right anterior axillary line in four seated normal subjects. We compared phase and amplitude of Ib/Tn with phase and amplitude of esophageal pressure changes (Pes) measured by two balloons positioned 10 cm apart and at approximately the same horizontal levels as the microphones. When breathing tidally below closing volume (CV), apical Ib/Tn was louder and earlier than basal Ib/Tn, whereas basal Pes was greater and earlier than apical Pes. Above CV basal Ib/Tn was louder than apical and the phase differences either disappeared or followed phase differences in PES. The results suggest that below CV, ventilation of lower zones lags behind upper ones probably due to airway closure. Pes measurements indicate that this may lead to an amplification of pleural pressure swings at the base. Above CV, all airways are open, the ventilation of lower zones is greater than that of upper zones, and the sequence of ventilation follows the sequence of pleural pressure changes.

Pancreatic pleuropericardial effusions presenting as tumor of the lung.

A 45-year-old man presented with what was thought to be a mass in the left upper lung and a pericardial friction rub. He was subsequently discovered to have a loculated pleural effusion and pericardial effusion associated with chronic pancreatitis. This is the first instance we were able to find of pancreatitis mimicking bronchogenic carcinoma with pericardial metastasis.