No abstract

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.