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The changes in the circulation of patients with heart disease and with emphysema have been studied many times when the patient was at bed rest. There is little information as to the changes produced when the circulatory requirements exceed the resting level. This information is probably of more importance than resting measurements as the greater part of existence is one of activity. Chronic emphysema produces changes in the heart in many patients. Congestive failure leads to water logging of the lungs. It was felt that simultaneous measurements of the cardiac output and pulmonary arterial pressure in normal persons and in those with emphysema and heart failure would aid in the understanding of the alterations of cardiac and pulmonary functions occurring in these diseases. The purpose of this paper is to present these data and to discuss their significance. METHODSIntracardiac catheterization was performed in the usual manner (1). The catheter was passed for a distance of 1 to 2 inches into the right or left main branch of the pulmonary artery. Pulmonary arterial pressures were recorded by a Hamilton manometer and mean pressures determined by planimetric integration, covering a period of at least 2 respiratory cycles. Atrial pressures were determined either in the same fashion, using a sufficiently sensitive Hamilton manometer, or by the use of a saline manometer. Systemic arterial pressures were measured in most cases from the brachial artery, using a Hamilton manometer. The point of zero reference was 5 cm. beneath the fourth left costochondral junction. Mixed venous blood samples were taken from the pulmonary artery in nearly all cases; otherwise, they were from the ventricle or atrium. Arterial samples were taken through an in-lying needle, usually in the brachial artery but occasionally in the radial or femoral arteries.

In man, hypocapnia induced by hyperventilation causes a drop in arterial pressure. The calculated peripheral resistance is decreased, indicating a net vasodilatation. The forearm blood flow is markedly increased, and the vascular resistance of the forearm is much reduced. Persons with impaired function of the sympathetic nervous system continue to show these effects. The increase in forearm flow is not prevented by brachial block. These results suggest that hypocapnia acts directly on blood vessels to produce a net over-all vasodilatation and fall in blood pressure, and that this effect is not mediated through the nervous system, as usually supposed.

By photographic techniques measurements have been made in the human retina of vessel size, arteriovenous oxygen difference across the retina, and mean retinal circulation time. By combination of these methods estimates can be made of relative changes in retinal blood flow rate and in the rate of oxygen delivery from the retinal vascular system. Observations are presented on the response of the normal and diseased retinal circulation to a variety of stimuli, particularly changes in blood oxygen and carbon dioxide tensions.

In many normal people a sizable part of the lung is ventilated at a much slower rate than the remainder. Means have been devised for measuring the volume and ventilation rate of these "slow spaces" (1-4). It is also established that a change in body position from sitting to recumbent will alter the size of the various subdivisions of the lung volume (5, 6). In the course of some observations on intrapulmonary gas mixing, it was found that changes in body position caused significant changes in size and ventilation rate of the "slow spaces." It is the purpose of this paper to present the results of a study of the effects of various body positions on lung volumes and on the size and ventilation rate of the poorly ventilated regions of the lung. METHODSThe functional residual capacity. (FRC) and the vollume (Vs) and minute ventilation rate (Vs) of the most poorly ventilated lung space were measured by an opencircuit helium method (4). The subject breathes a mixture of 50 per cent helium and 50 per cent oxygen for fifteen minutes to achieve a nearly uniform concentration of helium throughout the lungs. At the end of a normal expiration he is switched to tank oxygen, and the expired gas is thereafter collected for subsequent measurement of volume and helium concentration. In addition, the helium concentration of the expired gas is continuously followed by a sensitive katharometer between he- homogeneously ventilated lung space. The straight line toward which the curve tends during the last few minutes of the washout is drawn in "by eye." From the slope of this line, the point at which it intersects the ordinate at zero time, and from the minute ventilation rate of the subject, it is possible to estimate the ventilation rate and volume of the slow space.In the present study the expressions k. and f are used to characterize the slow space. k. is the "turnover rate"of the slow space, or ratio of its minute ventilation to its volume (V./V.). For the lung as a whole, k is usually between 2 and 3 if the subject is in a basal or nearbasal state. For the whole lung, k represents the ratio between total minute ventilation and the functional residual capacity. The present subjects were not basal and the ratio between minute ventilation and FRC was about 4, for seated subjects. The relative size of the slow space is expressed as the ratio, f, between the volume of the slow space and the functional residual capacity. The present method is not well suited to the measurement of rapidly ventilated lung spaces because of the lag in response of the katharometer to change in helium concentration. A 95 per cent response occurs in 20 seconds. In addition, it requires 5 to 8 seconds for expired gas to pass from the subject to the sampling point. Although an allowance can be made for these delays, inexactness in the allowance may introduce serious errors into the estimates of ventilation rate and volume of lung spaces which have a very rapid turnover rate. The analytical system can measure accurately k values of at least 3.0, as demonstra...

SYSTEMIC DISORDERS often cause pathological changes in the optic fundus. These changes have diagnostic value because of their empirical association with specific illnesses. The value of funduscopic examination would be even further increased by a better understanding of how certain of these fundic lesions are produced. With the ultimate object of investigating this problem, several photographic techniques for study of the retinal circulation and metabolism in man have been adapted or developed and used by the authors and their associates. These techniques are: (1) measurement by fundus photography of changes in the diameter of retinal vessels in response to various stimuli, a procedure previously used by others;1,2 (2) estimation by fundus photography of the arteriovenous blood oxygen difference, (3) a method of photographing fluorescence in circulating blood in the retina, and ( 4) a method for measuring the mean retinal circulation time using fluorescein. It is the purpose of this presentation to summarize some results obtained by these special techniques and to interpret them in relation to the work of others in this rapidly expanding field. MethodsThe methods have been described elsewhere3-8 and will be outlined only briefly here. In most of this work the Zeiss fundus camera has been used. For the measurement of change in vessel diameter, fundus photographs were made with the subject usually in a seated position, first in the control state and then after various test pro¬ cedures. From these photographs, measurements were made of the arteries and veins near the disk using a dissecting microscope with a scale in the ocular. Changes in diameter were ex¬ pressed as a percentage of the control value, and the mean changes for arteries and veins were calculated separately. For examination of patients with retinopathy, the procedure most often used was the inhalation of 100% oxygen, which constricts retinal vessels. The terms, "ret¬ inal arterial reactivity" and "retinal venous re¬ activity," denote the mean percentage decrease in diameter of these vessels after inhalation of oxygen for 5 minutes.The method for measuring oxygen saturation of retinal venous, or arterial, blood was similar in principle to other photometric methods for measuring blood oxygen saturation. However, rel¬ ative light intensities were estimated by the density of the images which they produced on photographic film rather than by a photo¬ electric cell. For fundus photographs a beamsplitting device was used that allows making two simultaneous film exposures, one through a red interference filter with peak transmission at 640 µ, and the other through a green filter with peak transmission at 510 µ. The optical den¬ sity of reduced hemoglobin is much greater than that of oxyhemoglobin at 640 µ, but is the same at 510 µ. The per cent oxygen satura¬ tion of hemoglobin and whole blood bears a linear relationship to the ratio of optical den¬ sities at these red and green wavelengths. In retinal photography the light which strikes the optic disk is la...

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

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