The ventilatory apparatus is analogous to a mechanical system composed of an engine coupled to a pump. The engine comprises the chest wall and the diaphragm, while the pump embraces the airways and the lungs. Although the two units operate as a single assembly, their functions are distinct. The engine converts metabolic energy into mechanical work; the pump translates this work into a rhythmic exchange of air.According to this schema, the useful work of the chest wall and diaphragm is that performed on the surfaces of the lungs. Hence, the efficiency with which this work is accomplished is defined by the formula written below. Per cent efficiency mechanical work performed on the lungs X 100 total energy used for breathing Using this formula, we have calculated the efficiencies of seven normal subjects, of six patients with chronic pulmonary emphysema, and of five patients who were obese. A presentation of these data is the purpose of this report. METHODS a) Estimnation of the energy used for breathing. The energy used for breathing was estimated by using a modification (1) of the method of Liljestrand (2). In brief, the procedure entailed measuring the oxygen uptake first at rest, then at from 10 to 20 different levels of voluntary hyperpnea. At each level the subject breathed a gas mixture containing a small concentration of carbon dioxide; this prevented the development of hypocapnia and enabled the subject to maintain an augmented volume of ventilation for 20 minutes, a sufficiently long period for the establishment of a steady state. During the * This investigation was supported by a research grant (Public Health Service) (Grant H-2001 C) from the National Heart Institute, National Institutes of Health.final two minutes of each period the ventilation was measured and collections of expired gas were made. Two samples of this gas were analyzed for oxygen and carbon dioxide; duplicate analyses were required to check within 0.03 volume per cent.In each of the experimental periods, the subject breathed at a frequency of 30 breaths per minute by following the rhythm set by a metronome. This frequency was chosen because the subject could achieve a large minute volume of ventilation with a small tidal volume of air. Although the size of the tidal volume did not affect the measurement of energy, it appeared to be an important factor in the measurement of work. The reasons for this importance are outlined in Part b of this section; they indicated that measurements of work were most reliable when the tidal volumes were small.The data from those experiments in which the respiratory quotients lay outside the range of 0.70 to 0.95 were discarded. The data from the remaining runs were plotted on coordinate axes, and the curve that provided the best visual fit was drawn through the points (Figure 1, A). Since such a curve did not directly indicate the total oxygen used for breathing, this quantity was estimated by following these steps: 1) The oxygen used for quiet breathing at a frequency of 30 was calculated by multiplyi...

MAJOR obstacles complicate the study of the pulmonary circulation in man: the inaccessibility of the pulmonary vessels for direct cannulation, and the multiplicity of extravascular factors that influence pressure-flow-volume relationships within the lungs. New technics have largely circumvented the first difficulty; the second difficulty is minimal in the normal resting subject, but is exaggerated by either physiologic stress, e.g., exercise, or by abnormalities of the heart or lungs.Observations on a variety of experimental preparations have afforded considerable insight into the regulation of the pulmonary circulation. Particularly rewarding have been the demonstrations by Beyne in the dog' and by von Euler and Liljestrand in the cat,2-4 that acute hypoxia, hypereapnia, or both elicit pulmonary hypertension. These observations constitute a landmark in studies of the regulation of the pulmonary circulation since they afforded an experimental tool for the production of a pulmonary pressor response, and provided a hypothesis,2-4 which could be tested, concerning the adaptation of pulmonary capillary perfusion to alveolar ventilation. Others have subsequently reproduced the pressor response to acute hypoxia in animals5 and in man ;6 attempts to reproduce the pulmonary pressor response to acute hypercapnia have yielded far less consistent results.7The present studies were designed to eluci- report compares the effects of acute hypoxia and of exercise on pressure-flow relationships in normal subjects, in patients with restricted vascular beds, and in a patient with sympathetic denervation of the lungs. The second paper, because of the special technics involved, is confined to the effects of acute hypoxia on the pulmonary blood volume. The third considers the effects of acute hypereapnia on pressure-flow relationships in the pulmonary circulation.Methods All patients underwent a preliminary period of adjustment to the laboratory, its personnel, and facsimiles of the experimental protocol; this consisted of trial runs on a variety of hypoxic breathing mixtures coupled with collections of arterial blood and expired gas. Those who tolerated these procedures well subsequently served as experimental subjects.All tests were performed in the postabsorptive state, without medication. Venous catheterization of the right heart was performed in the usual manner8 and the tip of the catheter was placed in the pulmonary artery. The combination of the right heart catheterization, arterial cannulation, and the open-circuit method for collection of expired gas supplied the samples necessary for the calculation of the oxygen uptake (Vo,), the respiratory exchange ratio (RE), and the cardiac output (Q) by application of the Fick principle.For the recording of pulmonary and systemic arterial pressures, Statham gages were used as pressure transducers, in conjunction with highsensitivity carrier amplifiers and photographic registration of the cathode-ray images.The protocols were designed to satisfy criteria for the "steady state."9 In br...

It is generally accepted that the tone of the peripheral arterioles plays an important part in regulating the systemic blood pressure in man. Whether the small vessels of the lungs exercise similar control over the pressure in the pulmonary artery is not so certain. This uncertainty has stemmed largely from the fact that the human pulmonary vessels have exhibited an erratic response to many vasoactive drugs (1-15). As a consequence, most physiologists have concluded either that the pulmonary vessels are incapable of intrinsic changes in tone, or that the effect of such changes, if they occur, is less important in determining the pulmonary arterial pressure than is the effect of mechanical factors alone.There is, however, considerable evidence to suggest that acute hypoxia increases the pulmonary vascular tone (16)(17)(18)(19)(20). This stimulus raises the pulmonary arterial pressure by a greater amount than might be expected to result from the increase in blood flow which occurs. Moreover, the pulmonary wedge and systemic pressures are not altered (19), and there is no consistent variation in the central blood volume (19,21). From these observations it may be inferred that hypoxia constricts the vessels of the lungs.Active dilatation of these vessels has not been so adequately demonstrated. Most drugs which lower the pulmonary arterial pressure have a concomitant action on the systemic pressure, and it 1 This investigation was supported by a research grant [H-2001 (C) ] from the National Heart Institute of the is difficult to determine whether the changes in the pulmonary circulation represent a primary or a secondary effect. However, one of us (P.H.) observed that a single dose of acetylcholine can lower the pulmonary arterial pressure without affecting the pressure in the systemic vessels (22,23). The response was transient, and was found only in patients with a moderate degree of pulmonary hypertension.Since it seemed possible that this fall in pressure occurred as a result of active vasodilatation, the present project was undertaken with two objectives in view: 1) to investigate the effect of a continuous infusion of acetylcholine into the pulmonary artery of normal subjects, and 2) to inquire whether the action of the drug was enhanced when the pulmonary arterial pressure in these same subjects had been raised by making them hypoxic. METHODSEach subject was studied in the unanesthetized basal state. Respiratory studies were carried out on a previous day to acquaint the subject with the laboratory personnel and to accustom him into the effects of breathing a low oxygen mixture.Catheterization of the pulmonary artery was accomplished in the usual way (24,25). The position of the catheter was adjusted so that the tip lay just beyond the pulmonic valve. In those subjects in whom the wedged pressure was also measured, a special doublelumen catheter was used which allowed the tip to be wedged while the proximal lumen opened into the main pulmonary artery. With the catheter in place, a cannula was introduced into...

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When a small volume of dissolved Kr85 was rapidly injected into the venous circulation, only about 5% of the injected gas appeared in the systemic arteries. Further, when a similar solution was infused over a 10-minute period, the fraction reaching the systemic arteries was less than 15% of that contained in the pulmonary arterial blood. Because the problem of recirculation was minimized, an infusion of Kr85 was used to measure continually the output of the right ventricle. The values obtained, both at rest and during steady-state exercise, agreed satisfactorily with direct Fick measurements. Although similar comparisons could not be made in the interval when flow was changing, the values measured with the Kr85 method appeared to be of reasonable magnitude. Submitted on September 2, 1958

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The effects of inhaling 5 per cent carbon dioxide in air on the pulmonary arterial blood pressure and flow were studied in 5 subjects with normal pulmonary circulations and in 10 patients with chronic pulmonary emphysema. In the 5 control subjects, with an average increase in arterial P CO CO2 of 6 mm. Hg (37 to 43) and a 3-fold increase in minute ventilation, both pulmonary arterial blood pressure and flow remained unchanged. In the 10 patients with chronic pulmonary emphysema with a similar increase in arterial P CO CO2 (45 to 52) and a 2-fold increase in minute ventilation, there was a 14 per cent increase in cardiac output and a rise in pulmonary arterial mean pressure of 4 mm. Hg. In these patients an increment in pulmonary arterial pressure was invariably associated with an appreciable increment in blood flow. The present study affords no support for the view that the breathing of air enriched with carbon dioxide elicits pulmonary vasoconstriction in either normal subjects or in patients with chronic pulmonary disease.