M. Irené Ferrer

The Influence of Hydrogen Ion Concentration and Hypoxia on the Pulmonary Circulation

Pulmonary hypertension has been found to be reversible in certain patients with, cor pulmonale due to chronic bronchitis, bronchiolitis, and/or emphysema. In these individuals, as disturbances in gas exchange are corrected, pulmonary artery pressures fall (1). The high degree of correlation between the level of pulmonary artery pressures and the degree of hypoxemia (2, 3) as well as the pressor response to acutely induced hypoxia (4, 5) has implicated a reduced oxygen tension within the lungs as a major factor in the appearance of pulmonary hypertension (6). Since these patients almost invariably demonstrate hypercapnia, carbon dioxide tension has also been invoked as a cause of pulmonary hypertension (3). Anatomic reduction of the pulmonary vascular bed cannot be assigned a dominant role in the genesis of this hypertension because of its reversibility. Nonetheless, we may assume that the effects of reactivity of the vascular compartment to various stimuli will be more readily discernible in the presence of a restricted bed. Liljestrand has recently come to the conclusion that an increased hydrogen ion concentration in the blood is the chemical stimulus for pulmonary

Some Effects of Digoxin upon the Heart and Circulation in Man Digoxin in Chronic Cor Pulmonale

The effects of acute digitalization upon the dynamics of the circulation were observed in patients with chronic cor pulmonale, using the technic of cardiac catheterization. The state of the circulation was further investigated in the same patients following recovery from failure. The mode of action of intravenous digoxin is discussed, and a tentative concept of the pathogenesis of chronic cor pulmonale is presented.

Influence of chronic pulmonary disease on the heart and circulation

Abstract 1.1. Studies of both cardiac and pulmonary function were made in forty-eight cases of chronic pulmonary disease. The pathogenesis of pulmonary hypertension and the evolution of chronic cor pulmonale have been considered. 2.2. Pulmonary arterial hypertension was present at rest in thirty-nine of the forty-eight patients studied. 3.3. In chronic pulmonary emphysema anoxia was shown to be the important abnormality since it was directly or indirectly responsible for the circulatory complications found in these patients. The reversible nature of these circulatory complications in emphysema was demonstrated and its importance with regard to therapy was stressed. It would appear that in patients with chronic cor pulmonale and emphysema cardiac failure is generally characterized by a high cardiac output. 4.4. In patients with silicosis and emphysema the pulmonary hypertension is less likely to be reversible since it stems from anatomic alterations in the pulmonary vascular bed rather than from anoxia. When chronic cor pulmonale and cardiac failure develop in this type of patient, the cardiac output is not elevated. This emphasizes the point that chronic cor pulmonale in failure is not always of the high output type. 5.5. The circulatory changes found in the group of patients with diffusion fibrosis do not appear to be related to anoxia but probably spring from the anatomic lesions produced by the disease processes themselves.

Mechanical and Myocardial Factors in Rheumatic Heart Disease with Mitral Stenosis

Sixteen patients with rheumatic heart disease and pure mitral stenosis, studied by cardiac catheterization, are presented to illustrate the relative importance of mitral block and myocardial insufficiency in this disease. Analysis of hemodynamic data permitted a separation of those patients with predominantly mechanical mitral block from those in whom myocardial insufficiency appeared to be the predominant lesion. The importance of recognizing the existence of the latter group is emphasized, since commissurotomy will not be of benefit in such cases.

Some Effects of Nitroglycerin upon the Splanchnic, Pulmonary, and Systemic Circulations

Splanchnic, pulmonary, and systemic hemodynamics were studied in 18 patients afterthe sublingual administration of nitroglycerin. The drug, contrary to expectations, produced an over-all vasoconstrictive effect on the splanchnic circulation rather than vasodilatation. There was no evidence of venous pooling in this bed, and indeed the data may indicate a splanchnic supportive role in augmenting venous return to the heart with disengorgement of its own volume. In contrast, there was vasodilatation and pooling of blood in the pulmonary vascular bed. The systemic circulation probably sustains several effects by nitroglycerin, including arterial vasodilatation. A direct change in large artery distensibility probably explains the modest fall in systolic blood pressure seen. Further decline in arterial pressure may depend on venous pooling of a small or large degree. Probably the fall in systemic and specific organ flows is also linked to decreased venous return and the vascular readjustments provoked thereby. Pulsus alternans was produced by nitroglycerin, a previously unreported effect of the drug, but the mechanism by which it arose could not be defined.

The Relation between Electrocardiographic Evidence of Right Ventricular Hypertrophy and Pulmonary Arterial Pressure in Patients with Chronic Pulmonary Disease

Detection of right ventricular hypertrophy during life has often been exceedingly difficult. In a group of 40 patients with pulmonary artery hypertension either at rest or during exercise, in whom right ventricular hypertrophy of varying degree could therefore be anticipated, an attempt is made to correlate the pulmonary hypertension and the electrocardiographic evidence of right ventricular hypertrophy.

Hemodynamic Studies in Rheumatic Heart Disease

Hemodynamic studies were made in 42 patients with rheumatic heart disease with various valvular lesions and in different stages of cardiac function. These studies include observations not only at rest, but also during exercise, following the acute administration of Digoxin, and after recovery from failure. The relationship between symptomatology and hemodynamic findings were considered and the importance of differentiating between mechanical block and left ventricular myocardial failure as causes for pulmonary artery hypertension is stressed.

The Effect of Digoxin in the Splanchnic Circulation in Ventricular Failure

Splanchnic hemodynamics were examined in 22 patients with heart disease, 16 of whom had evidence of ventricular insufficiency at the time of study. The response of the splanchnic vasculature to the exhibition of intravenous digoxin was also studied in nine of these subjects.Ventricular insufficiency was associated with splanchnic vasoconstriction proportional to a generalized increase in peripheral vascularresistance. Splanchnic blood volume was disproportionately increased with respect to total blood volume in patients having visceral congestion with right ventricular failure and combined ventricular failure. A significant relationship between central venous pressure and splanchnic blood volume was demonstrated in these cases. The greater elevation of the former than of the latter suggested the presence of splanchnic venoconstriction.The vascular readjustment to digoxin resulted in a relative intensification of the already existing vasoconstriction of the splanchnic bed as compared to the diffuse systemic vasodilatation which occurred at the same time as the consequence of the inotropic action of the drug: estimated splanchnic blood flow and splanchnic blood volume diminished at a time when systemic flow rose and peripheral vascular resistance decreased. The ultimate distribution of the volume of blood translocated out of the splanchnic bed during this process remains to be determined.

A clinical consideration of cor pulmonale.

Definition T HE term cor pulmonale is genierally used to define the cardiac complications of certain forms of lung disease. From knowledge gathered in the recent past, it is apparent that a number of disease processes that attack pulmonary funetioni in a variety of ways can produce circulatory embarrassment. The mechanisms by which they do so may be fundamentally different and indeed the lungs themselves need not be directly inivolved. The terms cor pulmonale or pulmonary heart disease are far froin ideal, since they imply cardiac disorders secondary only to pulmonary parenehymal disease, whereas the name should be more inclusive and encompass cardiac abniormalities stemming fromii any form of pulmonary dysfunetion. It is therefore suggested that the name cor pulmonale always be coupled with the respolisible etiologic agent; for exanlple, cor pulmonlale due to chronic obstructive pulmonary emphysema, due to multiple pulmonary emboli (acute or chronic), due to exogenous obesity, due to berylliosis, due to poliomyelitis, etc. Inasmuch as mnany of the circulatory abnormalities and the cardiac enlargement itself may be reversible in some of these instances, it seems wise to eliminate the termns acute, subacute, or chronic as applied to these circulatory complicatioiis and use them solely in relationship) to the respiratory illness. Cor pulmonale would then be diagnosed only when evidences of right ventricular enlargement or failure are, or have been, shown to be present. Physiologic complications, such as anoxia, hyper-

Cor pulmonale (pulmonary heart disease): present-day status

In reviewing the present-day status of cor pulmonale, it is clear that considerable progress has been made in almost all instances of the disease. It is clearly a preventable form of heart disease in most cases and it is treatable and curable in its most common form, i. e., in COPD. One must agree with Petty, that today we have effective means of caring for the majority of respiratory cripples. Therapy for lung disease now appears even to have reduced the expected rate of pulmonary function deterioration in some patients. Surely with improved gas exchange and early detection of respiratory insufficiency the outlook for patients with respiratory diseases leading to cor pulmonale is better today than it was 30 years ago.