Pulmonary Hypertension in Mitral Stenosis

Bayliss, Richard; Etheridge, M. J.; Hyman, Albert L.

doi:10.1016/s0140-6736(50)91855-1

Cited by 56 publications

(7 citation statements)

References 10 publications

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“…In mitral stenosis, especially in the low output group, the venous component might be expected to increase because of the rise in central venous pressure that usually occurs in this type of patient on exercise Bayliss et al, 1950). It has been observed that patients with mitral stenosis in congestive failure with high central venous pressure show no significant increase in the intrathoracic blood volume (Kopelman and Lee, 1951), and it is unlikely that any slight increase in central venous pressure could cause much increase in this volume.…”

Section: Discussionmentioning

confidence: 99%

Circulatory Changes in Mitral Stenosis at Rest and on Exercise

Ball¹,

Kopelman²,

Witham³

1952

Heart

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There is some increase in the pulmonary artery pressure in many patients with mitral stenosis and this pressure may rise considerably on exercise as was first shown by Hickam and Cargill (1948). have described a method of calculating the area of the mitral orifice in life and Gorlin et al. (1951 a and b) have attempted to evaluate the factors causing this pulmonary hypertension at rest and on exercise. Although in these cases, the stenosed mitral valve must be the primary cause, other changes that may occur in the pulmonary vasculature or in the pulmonary blood volume may also be of importance. Lagerlof et al. (1949) and Borden et al. (1949) using the Hamilton method, injecting dye directly into the pulmonary artery, showed no increase in the pulmonary blood volume in patients with mitral stenosis at rest. Kopelman and Lee (1951) verified these findings with dye injected into an antecubital vein and also showed no significant increase in the intrathoracic blood volume in mitral stenosis even when in congestive cardiac failure. This was in contrast with patients in left ventricular failure who showed a well marked increase in intrathoracic blood volume.The Hamilton dye method has been used in a further study of patients with mitral stenosis to determine the changes in cardiac output and intrathoracic blood volume that occur during mild exercise.MATERIAL AND METHODS Sixteen patients with mitral stenosis were investigated. Some of these had auscultatory signs of aortic valve involvement but mitral stenosis was considered to be the predominant lesion. None had clinical signs of congestive cardiac failure at the time of the investigation. Previous experience has shown that the presence of a giant left atrium or of tricuspid regurgitation prevents a reliable result with the method used, and no patient investigated had either of these conditions. Nine subjects without evidence of cardiovascular disease were similarly investigated.The Hamilton dye method consists of the injection of a known amount of dye (Evans Blue T 1824) into an antecubital vein and the collection of rapidly timed arterial samples. From these a time-concentration curve can be constructed and the cardiac output and mean circulation time calculated as described by Hamilton et al. (1932). By the application of Stewart's formula (1921) the volume of blood between injection and sampling points can be determined and this has been referred to as the " intrathoracic blood volume."In a series of five duplicate tests at rest, the coefficient of variation for the intrathoracic blood volume was found to be 6-5 per cent: although the number is small, changes in the intrathoracic blood volume of more than 13 per cent are probably significant. Similarly changes in the cardiac output of the same order are probably significant, the summation of errors in the technique being 6 per cent (Hamilton et al., 1948;Kopelman and Lee, 1951). It has been found that the cardiac output obtained by this method corresponds *

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Section: Discussionmentioning

confidence: 99%

Circulatory Changes in Mitral Stenosis at Rest and on Exercise

Ball¹,

Kopelman²,

Witham³

1952

Heart

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“…There is considerable evidence to support the contention that the narrowing is initially a functional one (Bayliss et al, 1950;Davies et al, 1954), but the possibility is not excluded that this may persist after valvotomy. Harrison (1954) has found hypertrophy of the muscular coats of the pulmonary arterioles at necropsy in patients with mitral stenosis-changes which would be consistent with persistent pulmonary hypertension.…”

Section: Special Problems Of Mitral Valve Disease (A) Active Rheumatimentioning

confidence: 99%

Mitral Valve Disease and Mitral Valvotomy

Goodwin¹,

Hunter²,

Cleland³

et al. 1955

BMJ

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“…More recently it has been shown that this pressure, which is due to an increase in the pulmonary vascular resistance, may rise still further on effort (Bayliss et al, 1950;. There is considerable debate as to the mechanism and significance of this increase in pulmonary vascular resistance for, as the author of a recent annotation in the Lancet remarked, " it is not fully understood.…”

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The Nature of the Increased Pulmonary Vascular Resistance in Mitral Stenosis

Wade¹,

Mackinnon²,

Vickers³

1956

Heart

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It has been known for many years that in certain cases of mitral stenosis the pulmonary arterial pressure may be disproportionately high. More recently it has been shown that this pressure, which is due to an increase in the pulmonary vascular resistance, may rise still further on effort (Bayliss et al., 1950;. There is considerable debate as to the mechanism and significance of this increase in pulmonary vascular resistance for, as the author of a recent annotation in the Lancet remarked, " it is not fully understood."In view of its theoretical and practical importance we decided to reinvestigate this problem with especial reference to the role of the autonomic nervous system. In a previous paper we reported the results of injecting adrenergic-blocking agents into the pulmonary artery in cases of mitral stenosis (Mackinnon et al., 1956), concluding that they had no effect. In this paper we report the effects of hexamethonium bromide and of atropine. We find that hexamethonium will frequently lower the high resistance, but will bring forward evidence that this is an indirect action secondary to lowering the pulmonary capillary or venous pressure and independent of the autonomic system. We find that atropine has no consistent effect on pulmonary dynamics.MATERIAL AND METHODThe material consisted of 18 patients suffering from mitral stenosis, all of whom had attended the Department of Cardiology at the Manchester Royal Infirmary. They were all examined in the usual manner. All were subjected to cardiac catheterization; three grains of seconal and 0 5 ml. of procaine amide were given one hour beforehand and all pressures were recorded electrically by means of a capacitance manometer. Systemic pressures were obtained through a Cournand needle placed in the brachial artery. Mean pressures were obtained by electrical damping and all pressures were referred to a point 5 cm. below the sternal notch. Blood gases were analysed on the Van Slyke-Neill manometric apparatus and expired air was collected in a Tissot spirometer and analysed on the Haldane apparatus.Ten patients were selected because there was clinical evidence of pulmonary hypertension. At catheterization, after the basal measurements had been made, they were exercised on a bicycle-ergometer. The work varied in degree from patient to patient according to their capacity, the oxygen consumption usually varying from 250 to 400 ml./m.2/min. The effort was invariably continued at a constant rate for six minutes, the output being estimated again between the fourth and sixth minutes; this was considered sufficient time for a steady state to be obtained Donald et al., 1954) and this was confirmed by minute to minute measurements of pressures and pulse rate. After a period of fifteen to thirty minutes for recovery, checked by frequent pressure and pulse readings, hexamethonium bromide was injected through the cardiac catheter and the circulatory measurements repeated at rest and under identical conditions of exertion. The dose of hexamethonium was that which had been pr...

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Pulmonary Hypertension in Mitral Stenosis

Cited by 56 publications

References 10 publications

Circulatory Changes in Mitral Stenosis at Rest and on Exercise

Circulatory Changes in Mitral Stenosis at Rest and on Exercise

Mitral Valve Disease and Mitral Valvotomy

The Nature of the Increased Pulmonary Vascular Resistance in Mitral Stenosis

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