Patients with severe air-flow obstruction receiving mechanical ventilation are at risk of inadvertent pulmonary hyperinflation with morbidity and mortality caused by pneumothorax and circulatory depression. Nine patients with severe air-flow obstruction (5 asthma, 4 chronic air-flow obstruction) requiring mechanical ventilation were studied while sedated and therapeutically paralyzed. Pulmonary hyperinflation during steady-state ventilation was quantified by measuring total exhaled volume during 20- to 40-s apnea (end-inspiratory lung volume, VEI). Patients were studied at 3 levels of minute ventilation (VE) (10, 16, and 26 L/min) and at each VE, 3 levels of tidal volume (VT) (0.6, 1.0, and 1.6 L) and 3 levels of inspiratory flow (VI) (40, 70, and 100 L/min for VT = 1.0 L). There were progressive increases in VEI when VT was increased or when expiratory time (TE) was decreased either by an increase in rate (and hence VE) or by a decrease in VI (at a constant VE) reaching lung volumes as high as 3.6 +/- 0.4 L above FRC. Alveolar, central venous, and esophageal pressure rose in parallel with lung volumes, and hypotension was seen in most patients at highest lung volumes. Peak airway pressure (Ppk) was predominantly related to inspiratory flow and did not reflect changes in lung volume. Levels of ventilation required for normocapnia prior to paralysis (15.7 +/- 2.3 L/min) were associated with hypotension in 7 patients and probable hyperinflation in excess of 1.96 +/- 0.17 L above FRC. VEI is a simple, reproducible measurement of pulmonary hyperinflation and may be more important than Ppk in the causation of barotrauma.(ABSTRACT TRUNCATED AT 250 WORDS)

Case reports of neurogenic pulmonary edema (NPE) often indicate that the edema resolves quickly. Because plasma epinephrine concentration may be elevated in NPE, and epinephrine has been shown to increase the rate of alveolar liquid clearance (ALC), we determined if ALC was increased in a canine model of NPE produced by the intracisternal administration of veratrine. ALC was determined by instilling autologous plasma into a lower lung lobe and using the increase in instillate protein concentration after 4 h to calculate the volume of fluid cleared from the airspaces by mass balance. To prevent pulmonary hypertension and edema, which would confound the mass balance analysis, carotid arterial blood was allowed to drain into a reservoir as pulmonary arterial pressure started to rise after veratrine administration. ALC in animals administered veratrine (n = 6) was 30.4 +/- 1.6 (SE)% of the instilled volume compared with 14.1 +/- 2.1% observed in control animals. The increase in ALC could be inhibited by adrenalectomy, beta2-adrenergic blockade using ICI 118,551, or sodium channel blockade using amiloride and could be duplicated by infusing epinephrine to increase plasma epinephrine concentration to levels observed in NPE. These data indicate that the increased ALC was mediated by adrenal epinephrine and suggest that edema resolution in patients with NPE might be accelerated by endogenous epinephrine.

We evaluated the ability of canine isolated nonperfused lung lobes to absorb fluid from their air spaces by simultaneously measuring alveolar liquid clearance (ALC) in three lobes removed from the same dog. Autologous plasma was instilled in the air spaces of each lobe, and the increase in plasma protein concentration resulting from fluid reabsorption was used to calculate ALC. ALC after 4 h was 16.5 +/- 0.6% (SE) of the instilled fluid volume under baseline conditions and was 30.2 +/- 1.3% after terbutaline (10(-5) M) administration. These values were similar to those previously reported for intact dogs. Propranolol (10(-4) M) and ouabain (10(-3) M) reduced ALC in terbutaline-stimulated lobes to 20.4 +/- 0.8 and 3.9 +/- 1.4%, respectively. There was no significant difference in ALC among the three lobes under either baseline conditions or after terbutaline administration. These data indicate that the sodium and water transport mechanisms of the canine alveolar epithelium remain viable during 4 h of nonperfusion and that there are no intrinsic differences in the transport properties of individual lung lobes. The ability to study several lobes simultaneously without the need for perfusion will allow for the design of experiments in which multiple interventions can be studied by using lung lobes from the same animal.