Florence W. Haynes

Studies of Congenital Heart Disease IV. Uncomplicated Pulmonic Stenosis

Congenital pulmonic stenosis is indicated by cardiac catheterization by the finding of a higher systolic pressure in the right ventricle than in the pulmonary artery. Eight cases of uncomplicated pulmonic stenosis are studied. The findings on history, physical examination, x-ray and fluoroscopy, and electrocardiogram have been analyzed and the variations in circulatory dynamics encountered in these individuals are described in detail.

Studies of the circulatory dynamics in mitral stenosis. II: Altered dynamics at rest

Abstract 1. 1. Twenty-one patients with mitral stenosis have been studied by the technique of cardiac catheterization. These patients were classified clinically and also according to the size of the orifice of the mitral valve. Six patients were in pulmonary edema during the study. 2. 2. As a consequence of mitral valvular stenosis, a balance develops between pulmonary vascular pressures and peripheral blood flow (tending toward an increase in pulmonary pressure and a decrease in blood flow). 3. 3. Cardiac and stroke indices were decreased at rest, although a wide range of values was seen. Patients with auricular fibrillation had slightly lower cardiac indices than patients with normal sinus rhythm. Tissue oxygen extraction per cubic centimeter of blood was increased so that oxygen consumption was maintained within the normal range in all. 4. 4. Pulmonary “capillary” pressures were increased above normal as a result of the increase in left atrial pressure proximal to the mitral stenosis. 5. 5. Pulmonary arterial pressures were increased above normal as a result of (a) the increase in pulmonary “capillary” pressure and (b) increased pulmonary arteriolar resistance. 6. 6. The presence of an elevated pulmonary arteriolar resistance was roughly related to the level of pulmonary “capillary” pressure and the degree of valvular stenosis. 7. 7. An inverse logarithmic relationship was observed between total pulmonary resistance and stroke output per square meter. 8. 8. As a result of the increased pulmonary vascular pressures, the pressure work of the right ventricle was greatly increased. 9. 9. Right ventricular incompetency, as judged by an elevated filling pressure, was seen in over one-half of the patients studied. Incompetence was believed due to (a) the increased pulmonary pressure load and (b) underlying myocardial damage from rheumatic fever.

THE PULMONARY BLOOD VOLUME IN MAN

The measurement of blood volume in the pulmonary vascular bed during life became theoretically feasible with the introduction of indicator dilution methods by Stewart (1) and Hamilton, Moore, Kinsman and Spurling (2). The principles and formulas set forth by these investigators have since undergone extensive scrutiny by theoretical analysis, in circulation models, and in vivo. As a result of these studies, there exists now general agreement that the introduction of an indicator substance into the central circulation, either directly or by peripheral venous injection, and downstream recording of its concentration change with time during the first transit permits the determination of three important circulatory parameters: 1) the cardiac output, 2) the mean transit time from injection to sampling site, and 3) by multiplication of cardiac output and mean transit time, the circulating volume of blood between injection and sampling sites, including all temporally equidistant points in the vascular bed. Practically speaking, then, the measurement of pulmonary blood volume in vivo requires determination of the mean transit time of an indicator from the pulmonary artery to the left atrium together with cardiac output. The development of right and left heart catheterization has made the pulmonary artery and left atrium accessible as injection and sampling sites in man. Injection of an indicator through a

STUDIES OF CONGENITAL HEART DISEASE. II. THE PRESSURE AND OXYGEN CONTENT OF BLOOD IN THE RIGHT AURICLE, RIGHT VENTRICLE, AND PULMONARY ARTERY IN CONTROL PATIENTS, WITH OBSERVATIONS ON THE OXYGEN SATURATION AND SOURCE OF PULMONARY “CAPILLARY” BLOOD

The venous catheter of Cournand and Ranges (1) permits the measurement of pressure and oxygen content of blood in the pulmonary artery, right ventricle, and right auricle of patients with congenital heart disease. To interpret the data so obtained, it is necessary to be cognizant of the variations in these measurements that occur in patients without congenital cardiac defects. The present report deals with the findings in a group of control patients.

Effects of exercise on circulatory dynamics in mitral stenosis. III.

Abstract 1. 1. Eight patients with mitral stenosis have been studied at rest and during exercise by the technique of cardiac catheterization. Three of the patients developed pulmonary edema on exercise. 2. 2. The resting balance between pulmonary pressure and peripheral blood flow was upset by exercise. The imbalance was related not only to the degree of stenosis but to the ability of the circulation to increase the cardiac output. 3. 3. Except for two patients with mild mitral stenosis, cardiac index failed to rise in normal fashion on exercise. Stroke index on the average did not change with exercise, although both increased and decreased stroke outputs were seen, depending on the pulse rate and diastolic filling period. Tissue oxygen extraction per cubic centimeter increased markedly on exercise. 4. 4. Pulmonary “capillary” pressure rose on exercise in association with increases in rate of mitral valvular blood flow. 5. 5. Pulmonary arterial pressure rose on exercise in association with the increase in pulmonary “capillary” pressure and in some cases with the increase in blood velocity flow. 6. 6. Pulmonary arteriolar resistance showed no consistent change on exercise, the average values at rest and during exercise being almost identical. 7. 7. Right ventricular work against pressure, already elevated at rest in most of the patients, became even greater on exercise. 8. 8. Almost all patients had elevated right atrial mean pressures at rest. Further rises occurred in two of the four in whom right atrial pressure was measured on exercise.

Cardiovascular Responses to Experimental Pulmonary Embolism

Abstract The basic circulatory response to pulmonary embolism is obstruction to blood flow through the lung. No circulatory changes occur until the cross-sectional area of the pulmonary vasculature is reduced by over 50 per cent. The roles of mechanical obstruction, vasoconstriction and humoral agents in this disorder are reviewed. In response to increased precapillary resistance to blood flow occasioned by embolism, pulmonary arterial and right ventricular systolic pressures rise; if this is severe enough, the right ventricle dilates, its enddiastolic pressure rises, and its coronary flow increases. In contrast to man, in whom embolism is commonly associated with manifestations of left ventricular failure, in the experimental animal the left ventricle is spared. Its output and systolic pressure fall, its work load is reduced, its end-diastolic pressure remains normal until terminally, and its coronary flow is unaltered or increases until terminally, when, with overall disruption of the cardiovascular system, it falls. It has been postulated by some that the fall of systemic arterial pressure cannot be entirely explained by the fall of cardiac output and that it represents in part a reflex hypotension. Heart rate and rhythm remain stable, except with massive embolism or in association with hypotension or apnea, when bradycardia and arrhythmias may occur.

Factors regulating pulmonary “capillary” pressure in mitral stenosis. IV☆

Abstract 1. 1. Pulmonary edema occurred at rest in six patients and during exercise in three other patients with severe mitral stenosis during cardiac catheterization. 2. 2. Pulmonary “capillary” pressure was 32 mm. Hg or higher in all nine patients. 3. 3. Pulmonary “capillary” pressure, actually an index of left atrial pressure, was elevated to such high levels in order to maintain blood flow through the mitral valve. 4. 4. Factors which resulted in an increased mitral valve flow rate, thus requiring an elevation in pulmonary “capillary” pressure, were (a) increased cardiac output and (b) decreased diastolic filling period. The latter was decreased by increases in (1) heart rate and (2) duration of ventricular systole. 5. 5. The degree of anatomic mitral stenosis affected the degree of pulmonary “capillary” pressure rise in exponential fashion. 6. 6. The mechanism of elevation of pulmonary “capillary” pressure was believed to be a momentary imbalance in ventricular outputs such that pulmonary blood volume and pressure were increased. 7. 7. It has been demonstrated that in patients with mitral stenosis, a normal cardiac output can be delivered only at the expense of high pulmonary “capillary” pressure. 8. 8. The role of tachycardia, even of a mild degree, in producing or aggravating symptoms of pulmonary edema is emphasized.

The angiographic diagnosis of acute pulmonary embolism: evaluation of criteria.

Abstract Abnormalities in the pulmonary angiograms of 52 patients were correlated with the clinical diagnoses in order to determine which angiographic signs are diagnostic of acute pulmonary embolism and which are abnormal but possibly related to other diseases affecting the pulmonary vasculature. Angiographic abnormalities were divided into two groups: those of major or morphologic significance, and those of lesser or physiologic significance. The signs of morphologic significance are intraluminal filling defects, cutoffs, and pruning. These major signs directly indicate arterial occlusion. The signs of physiologic significance are oligemia, asymmetrical filling, prolongation of the arterial phase, and bilateral lowerzone filling delay. These lesser signs indicate disturbance of flow. In an otherwise normal lung, they are highly suggestive of pulmonary embolism. In the presence of coexistent diseases that affect the pulmonary vasculature, correlations in this study show that only the signs of morphologic significance are reliable for the diagnosis of acute pulmonary embolism. In otherwise healthy patients, 95 per cent (20 of 21) who clinically had pulmonary embolism had one or more of the major or lesser angiographic abnormalities. In the entire group who clinically had pulmonary embolism (including patients with coexisting diseases that affect the pulmonary vasculature), 83 per cent (24 of 29) of the patients had one or more of the major or lesser angiographic abnormalities. However, 7 patients with nonembolic pulmonary vascular disease had lesser angiographic abnormalities (disturbance of flow). Utilization of the major signs alone reduced the number of positive angiographic interpretations to 79 per cent (23 of 29) in patients who clinically had pulmonary embolism, but eliminated all false-positive interpretations. Accuracy in making the diagnosis of acute pulmonary embolism by pulmonary angiography is enhanced by proper evaluation of the angiographic abnormalities of morphologic and physiologic significance as described in this study.

Chronic constrictive pericarditis: Further consideration of the pathologic physiology of the disease

Abstract 1. 1. The methods of catheterization of the heart and the pulmonary vessels make it practical, for the first time, to investigate the pressure and flow phenomena in the right side of the heart and in the pulmonary vascular system of patients with constrictive pericarditis. Six such patients have been studied by these methods. 2. 2. Every patient showed an elevation of pulmonary “capillary” pressure (which reflects pulmonary venous pressure). This demonstration of pulmonary congestion is interpreted as indicating that involvement of the left ventricle plays a more important and sinister role in the functional changes associated with pericardial constriction than has been demonstrated previously. 3. 3. Every patient also showed an elevation of pressure in peripheral veins and in right atrium, and pressure measurements in the right ventricle and pulmonary artery which indicate a reduced ability of the right ventricle to contribute to the forward movement of blood. These observations confirm and emphasize the previously recognized involvement of the right ventricle. 4. 4. In every patient before operation the mean pulmonary capillary pressure was approximately equal to the peripheral venous pressure. 5. 5. No patient exhibited pressure changes pointing to physiologically significant obstruction in great veins or auricles. 6. 6. The limitation of stroke volume and cardiac output per minute in constrictive pericarditis previously demonstrated by other methods is confirmed by these studies. 7. 7. Consideration of the course of events after operation suggests that myocardial atrophy, myocardial fibrosis, and incomplete release of the ventricles may all play a role in the slow, and in most cases, incomplete return to normal dynamics after operation. 8. 8. The specific therapeutic implications of this study are: (A) the objective of surgery is the adequate release of both ventricles; (B) no indications have been found for the decortication of great veins or auricles, and (C) the early use of antibiotics in acute tuberculous pericarditis may minimize myocardial fibrosis and may permit operative treatment before myocardial atrophy is severe. 9. 9. Finally, the fact that improvement after operation is often slow and often incomplete in terms of objective measurement should not lead physicians to ignore the more important fact that a well-planned operation for constrictive pericarditis has in the past usually made the difference between invalidism and activity. The studies reported in this paper may be expected to make future operations for this disorder even more effective.

THE RELATIONSHIP OF PULMONARY COMPLIANCE TO PULMONARY VASCULAR PRESSURES IN PATIENTS WITH HEART DISEASE

that the distensibility of the lungs, designated pulmonary compliance, is consistently reduced in the presence of cardiac dyspnea. Furthermore, this reduction of pulmonary compliance has been shown to be associated with increased work of breathing in the presence of mitral stenosis (10). This fac