John B. Hickam

Reflex Venomotor Activity in Normal Persons and in Patients with Postural Hypotension

Reflex venomotor activity has been observed and measured in normal subjects by means of the pressures developed within isolated segments of superficial veins. Strong contractions are caused by the Valsalva maneuver, tilting, cold, exercise, and hyperventilation. After the Valsalva and after tilting there is a brief elevation of central venous pressure. Pulmonary vascular pressures are also increased after the Valsalva. This is taken to indicate a widespread venoconstriction with central shifting of blood. Persons with postural hypotension show little or no segment or central venous pressure response to these stimuli, indicating impaired reflex venomotor activity.

The Effect of Hypocapnia on Arterial Blood Pressure

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.

Normal and Impaired Retinal Vascular Reactivity

Normal retinal arteries and veins will constrict when the arterial blood oxygen tension is increased and dilate when it is lowered. A technic, employing fundus photography, is described for measuring this reaction. The amount of constriction on breathing oxygen, and its trend with age, have been measured in normal subjects. The arteries of persons with well-established hypertension and diabetes usually show marked impairment of this constrictor reaction, presumably because of sclerotic changes. It is suggested that measurements of this reaction may prove to be a useful, quantitative extension of present retinal vascular grading technics.

Circulatory changes produced by the Valsalva maneuver in normal subjects, patients with mitral stenosis, and autonomic nervous system alterations.

The cardiac output has been measured during the immediate post-Valsalva maneuver recovery period in normal subjects, patients with clinically significant mitral stenosis, and patients with alterations of the autonomic nervous system. When compared with the resting value, it was found that normal subjects had a decrease in cardiac output during the immediate post-Valsalva recovery period, while patients with mitral stenosis had an increased output following the same stress. Three patients with alterations of the autonomic nervous system had a variable response. Changes in total peripheral vascular resistance usually were directionally opposite to changes in the cardiac output. The difficulties of attaching clinical significance to a patients response to the Valsalva maneuver are considered.

Rupture of mitral chordae tendineae

Abstract The histories and pathologie observations in seven cases of rupture of the mitral chordae tendineae are reviewed. Patients with bacterial endocarditis were excluded from the series. All showed fibrosis and chronic injury of the mitral valve. In two, the lesions were those of rheumatic heart disease; in the remainder, the changes suggested quiescent rheumatic disease, but were not pathognomonic. The chordae of the two valve cusps were ruptured with equal frequency in this series, and usually more than one was broken. The point of rupture lay close to the papillary muscle. The stumps consisted of hyalinized and partially degenerated connective tissue, with a covering of endothelium. Scarring extended into the subjacent myocardium. The corresponding papillary muscles underwent atrophy if all their chordae were broken, but showed hypertrophy if a number were left attached. It was clear from inspection that rupture of the chordae must have allowed a high degree of mitral regurgitation. All hearts were dilated and hypertrophied, with an average weight of 580 grams. The histories of the patients did not indicate that external violence or vigorous exertion were etiologic factors of primary importance in rupture of the mitral chordae tendineae. The symptoms after rupture of the mitral chordae tendineae are those of congestive heart failure, which may be insidious or abrupt in its onset and progressive or remittent in its course. Months or even years may elapse between rupture and the onset of frank congestive failure. Rupture of the chordae is suggested by the sudden appearance of a loud precordial systolic murmur, maximal at the apex and left sternal border, where it is usually accompanied by a thrill. An apical diastolic murmur may also be present. Auricular fibrillation sometimes occurs. Roentgenograms show cardiac enlargement, and fluoroscopic examination may demonstrate systolic pulsation of the left atrium. The differential diagnosis includes bacterial endocarditis, rupture of a valve cusp, rupture of a papillary muscle, and perforation of an infarcted interventricular septum.

Atrial septal defect. A study of intracardiac shunts, ventricular outputs, and pulmonary pressure gradient

Abstract Patients with atrial septal defect provide an unusual opportunity for the study of certain problems connected with the regulation of cardiac output and the hemodynamics of the pulmonary circulation. It is frequently possible to pass a catheter through the septal defect into the venous side of the pulmonary circulation. Blood samples and pressure determinations from this site extend the significance of the usual observations which can be made in the course of an intracardiac catheterization. It is possible to determine the pressure gradient through the pulmonary vascular tree, to estimate the right and left ventricular outputs, to estimate the magnitude and direction of intracardiac shunts, and to observe changes in some of these quantities as a result of exercise or other stimuli. This paper reports observations on four patients with atrial septal defect in whom it was possible to catheterize pulmonary veins.

Hyperventilation in Postural Hypotension

In normal subjects hyperventilation causes a drop in arterial blood pressure, apparently because of the direct effect of hypocapnia on the peripheral vessels. In persons with disease of the autonomic nervous system, the drop in blood pressure is much greater because it is not effectively opposed by reflex vasoconstriction. Consequently, hyperventilation caused by anxiety may greatly intensify postural hypotension in such patients and contribute significantly to their disability. A pertinent case is reported.

The Relation between Retinal and Cerebral Vascular Reactivity in Normal and Arteriosclerotic Subjects

It has been found that retinal arterial reactivity to oxygen is diminished in persons with retinal arteriosclerosis, and that cerebral blood flow and the increment in cerebral flow upon inhalation of carbon dioxide are diminished in persons with cerebral arteriosclerosis. The present study demonstrates that there is a significant positive correlation between retinal arterial reactivity on the one hand, and cerebral blood flow and reactivity, on the other. This finding is taken to mean that arteriosclerosis severe enough to affect measurements of this sort is apt to involve retinal and cerebral vessels together.

Effect of circulatory changes on the pulmonary compliance of normal subjects and patients with mitral stenosis.

Fulfillment by the lungs of their bellows function depends largely on their resiliency and elasticity. Unless the lungs can readily comply with the changes in the thoracic cage during inspiration and expiration, ventilation will be seriously impaired. Pulmonary compliance is expressed as the ratio of lung volume in liters to intraesophageal pressure in centimeters of water. The present study is concerned with the role of pulmonary vascular engorgement in reducing compliance in normal subjects and in patients with mitral stenosis.

The Relationship Between Impaired Retinal Vascular Reactivity and Renal Function in Patients with Degenerative Vascular Disease

In hypertension and diabetes retinal vascular changes which are evident on fundiscopic examination are usually accompanied by renal vascular changes which are evident on microscopic examination. It has been found that the retinal vessels of most patients with hypertension or diabetes fail to constrict normally when the blood oxygen tension is elevated. This investigation evaluates the clinical significance of decreased retinal vascular reactivity in patients with degenerative vascular disease by relating it to kidney function as measured by common clinical tests. The results of the study show that impairment of retinal arterial reactivity usually occurs in the course of degenerative vascular disease, particularly in hypertension, in advance of clinical evidence of altered kidney function. When clinical tests of renal function demonstrate renal damage, loss of retinal arterial and venous reactivity is marked.