No abstract

Central and pulmonary vascular engorgement is a characteristic feature of congestive heart failure. It has been suggested many times that this vascular engorgement might be responsible for certain phenomena associated with congestive failure, such as stiffening of the lungs, dyspnea, and orthopnea. However, the simultaneous occurrence of pulmonary edema and other changes has made it difficult to single out the effects of simple vascular engorgement.The present study was undertaken to investigate the pulmonary and circulatory effects of acute, reversible central and pulmonary vascular engorgement in normal man.Central and pulmonary vascular engorgement was produced by rapid application of pressure over the surface of the body. Two methods were used to accomplish this: inflation of an aviator's "G suit," and submersion in water while breathing against atmospheric pressure.The results indicate that vascular engorgement of the degree found in congestive heart failure can markedly stiffen the lungs. In addition, it was found that the production of acute central and pulmonary vascular engorgement in normal subjects by the present experimental means is quickly followed by changes which reduce the engorgement and which may represent an adaptive circulatory response. These changes could be modified by pre-treatment with drugs which alter vascular tone or by applying a painful stimulus. METHODS

Using a specially designed needle system, pressures were recorded directly from the pleural space in seated normal men. Respiratory pressure changes (ΔP) measured simultaneously from different pleural sites and the esophagus are not the same but become so after a large pneumothorax is produced. Since esophageal ΔP is little affected by a pneumothorax of 2–300 ml, it is suggested that, in the absence of pneumothorax, esophageal ΔP represents a better measure of the over-all elastic behavior of the lung than any local pleural ΔP. In the absence of pneumothorax, ΔP is less in the upper than in the lower chest. This may be an expression of a gradient either of distribution of ventilation or of elastic forces opposing expansion of the lung. In three of four subjects, end expiratory pressure was more positive in the low chest than in the high chest. Acute central vascular engorgement (pressure suit inflation) caused similar changes in esophageal and intrapleural ΔP. These observations confirm the previously observed decrease in lung compliance during acute central vascular engorgement and provide evidence of local differences in respiratory pleural pressure change in man. Submitted on August 20, 1962

In 1956 Otis and co-workers (1) compared the behavior of a single pulmonary pathway to an electrical circuit consisting of a capacitor and resistor in series with a sinusoidally varying voltage source. In a pulmonary pathway driven by a sinusoidally varying pressure, the resultant flow curve is also a sine wave and leads the pressure curve by an amount 9, which is determined by the relationship, O= tank ( 1/27rfRC), [1] where 9 is the phase angle in degrees between the pressure and flow curves, f is the frequency in cycles per second, R is resistance in centimeters of water per liter per second, and C is compliance in liters per centimeter of water. The product RC is the time constant and at any given frequency determines the phase angle of the system. A sinusoidally driven system of multiple parallel pathways can be considered as a single pathway only if the time constants of the individual pathways are the same. With different time constants, the effective resistance and compliance of the system will decrease with increasing frequency.Otis and co-workers observed a constant pulmonary compliance (CL) at frequencies of 10 to 120 respirations per minute in three normal subjects. Two of these subjects breathed a histamine aerosol and at 120 respirations per decreasing CL following epinephrine as compared with values before epinephrine. One patient with emphysema showed marked fall of CL over the range of 20 to 55 respirations per minute. Defares and Donleben (2) reported a small percentage of normal subjects with frequency dependent pulmonary compliance. Frank, Mead, and Ferris (3) studied nine healthy elderly adults at increasing frequencies and consistently found small decreases in CL. Others (1, 4, 5) have demonstrated constant CL in normal subjects with increasing frequency.Although the chest wall and lungs moving together determine the characteristics of the total respiratory system, the effect of respiratory frequency on total thoracic and chest wall mechanics has not been extensively studied. This study was undertaken to evaluate total thoracic, pulmonary, and chest wall compliance, resistance, and impedance as a function of frequency in normal subjects. MethodsThe subjects sat in a body plethysmograph with the head protruding through a rubber neckpiece. The plethysmograph was constructed of 1-inch plywood and measured 20 X 26 X 34 inches on the inside. Sinusoidally varying plethysmograph pressures were produced by a 16-inch diameter piston driven by an electric motor at a frequency of 10 to 130 cycles per minute. The piston stroke was adjusted to produce peak to peak plethysmograph pressures of 20 to 40 cm H20. The plethysmograph pressure was measured by a Statham PM5TC strain gauge. The esophageal pressure was measured by a 15-cm long thin wall balloon attached to a 50-cm long polyethylene tube with internal diameter of 0.070 inch.The tube was passed through the nares for a distance of 35 cm and inflated with 1 ml of air. The balloon was attached to one side of a Statham PM5TC differential strain gauge ...

In a re-examination of the effects on lung compliance of acute central vascular engorgement produced in normal subjects by inflation of a ‘G suit’ it was found that the reduction in complicance, previously reported, during suit inflation was in part due to artifactual changes in esophageal pressure. When the esophageal balloon used for pressure recording was positioned higher on the esophagus than in the previous study, and when decreases in mid-position, which usually accompany the abdominal compression associated with suit inflation, were prevented, the complicance reductions in a small group of subjects were approximately one-half as great as those obtained with the balloon low in the esophagus and with the mid-position uncontrolled. Extrinsic pressures from distended mediastinal structures, greater in the distal esophagus, and greater at low lung volumes are thought to be responsible. Additional observations are presented which support this possibility. It is concluded that respiratory esophageal pressure change may not be a valid index of lung surface pressure change in the presence of central vascular congestion. Those measurements of pulmonary compliance during clinical and experimental central vascular engorgement which have used esophageal pressure must be accepted with this reservation. Submitted on March 18, 1960

The surface tension of extracts from normal lungs is extremely low owing to the presence of a specific surfactant. 1 Experiments of Finley et al. 2 showing an abnormally high surface tension of lung extracts obtained 12 to 16 hours after ligation of the pulmonary artery (PA) were confirmed by Long and associates. 3 These studies suggested that the surfactant is decreased or absent after PA ligation.The present studies were designed to correlate the pressure-volume characteristics of the lung with changes in the surface tension of lung extracts and to investigate the long term effects of PA ligation. Surface tension measurements of the lung extracts, pressurevolume curves and histological studies of lungs were made in one group of dogs four hours after the pulmonary artery was ligated and in another group of dogs two weeks after the pulmonary artery was ligated. A comparative study was also made of the results obtained by two different methods of surfactant extraction and by two different methods of surface tension measurements. MethodsThe right PA was ligated in each of 12 healthy mongrel dogs weighing 14 to 17 kg. Surgery and experimental measurements were done under thiopental (Pentothal) anesthesia. Respiration was controlled with a positive pressure respirator, administering 100% oxygen through an endotracheal tube until the PA ligation was completed (20 to 30 minutes). The dog was ventilated with room air for the remainder of each experiment. A right lateral thoracotomy was performed through the fourth intercostal space and the thoracic cavity widely exposed. Four hours after ligation of the right pulmonary artery, separate pressure-volume measurements of each lung were performed in the following manner: The indwelling endotracheal tube was connected to a three-way Luer lock stopcock with one arm leading to a calibrated 100 ml syringe and the other to a water manometer. A noncrushing clamp was applied to one main stem bronchus and the lung to be tested was inflated with air until all the lung units appeared grossly distended. The lung was then allowed to deflate passivelv. This was repeated two or three times and further volume-Dressure studies were made using the retained lung volume at zero transpulmonarv pressure (atmospheric pressure) as the base line for the volume measurements.The lung was inflated with 100 ml increments of air and the pressure changes were recorded after stabilization of the transpulmonary pressure (15 to 20 seconds). Inflation was continued seriatim until all the lung units appeared distended. The right lung which had the PA ligated, was studied first and the maximum pressure was recorded when the right lung was distended and the pressure produced in the intact lungs was kept in a comparable range. Most lungs were completely inflated when transpulmonary pressure reached approximately 40 cm H 2 O. Inflation was more irregular and more undistended units were observed during inflation in lungs two weeks after PA ligation than in the intact lungs. Deflation was performed by stepwise remo...

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To evaluate the effects of oxygen breathing at atmospheric pressure on pulmonary surfactant, cats, rabbits, and rats were continuously kept in 98% oxygen until death occurred. Pulmonary surfactant was extracted by mincing of the lung and by foam fractionation of the lung. Surface tension of the extracts was measured on a Wilhelmy balance. Lung extracts prepared by both methods from the cats and rabbits kept in oxygen had greater surface tension than lung extracts from control animals. Surface tension of extracts prepared by foam fractionation of lungs of rats kept in oxygen did not differ from that of extracts of lungs of control rats, whereas surface tension of extracts prepared by mincing lungs of rats kept in oxygen had minimum surface tension greater than that of lung extracts of control rats. This species difference in the effects of oxygen breathing on pulmonary surfactant may reflect a difference in the pathogenesis of oxygen intoxication. oxygen intoxication; surface tension Submitted on October 19, 1964