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Five patients with severe chronic obstructive pulmonary disease (COPD) underwent detailed evaluation of pulmonary function (PF), respiratory mechanics and hemodynamics before and after 18 weeks of physical training (PT). PT consisted of daily progressive upright bicycle exercise. All patients demonstrated marked subjective and objective improvement in exercise tolerance. After PT exercise heart rates were significantly decreased (p

Twenty-one patients with partial anomalous pulmonary venous drainage with intact atrial septum have been studied. These include 13 patients not previously reported from our laboratories and eight patients with complete hemodynamics reported by others. Methods for identification of this abnormality and for identification of an intact atrial septum are described, including differential indicator dilution curves, catheter probing of the atrial septum and pulmonary angiography. Blood flow through anomalously draining lobes of the lung is usually higher than through normally drainage lobes attributable to the higher pressure differences across the anomalous lung, right atrial pressure being uniformly lower than left atrial pressure. The pulmonary vascular resistance when "standardized" to the flow of blood normally present in different portions of the lung indicated that no significant differences existed between normally and anomalously draining lobes. Six patients had coexisting rheumatic mitral stenosis and one had congenital mitral stenosis. Its influence on the hemodynamic changes produced by PAPVD is discussed.

Autologous blood clot was used to produce pulmonary macroembolism, and lycopodium spores to produce microembolism in normal mongrel dogs. Pressures were recorded from the pulmonary artery, left atrium and femoral artery; cardiac output and pulmonary blood volume (PBV) were determined using sequential indicator dilution curves from injections into the pulmonary artery and left atrium. Macro- and microembolism caused comparable elevations of pulmonary artery pressure and total pulmonary resistance. Macroembolism with blood clots resulted in marked decreases in PBV and pulmonary vascular compliance. However, microembolism with lycopodium spores caused only small decreases in PBV despite a large reduction in pulmonary vascular compliance. Prostaglandin E 1 infusion after microembolism had no effect on pulmonary hemodynamics, but caused significant systemic hypotension. After macroembolism PGE 1 infusion decreased PBV and decreased systemic arterial pressure.

Eight patients with mixed mitral stenosis and regurgitation underwent hemodynamic and angiographic study prior to mitral valve replacement. The stenotic orifice of the mitral valve was calculated employing the total left ventricular stroke volume by cineangiography as the numerator of the Gorlin Formula. Excellent agreement with the measured orifice of the mitral valve was obtained using a value of 37.9 (0.85 X 44.5) for the constant in the Gorlin formula as recommended by Cohen and Gorlin. Recalculation of this constant independently by our data yielded a value that was almost identical. Regurgitant flows and orifice sizes were calculated for each patient using the same constant as for calculation of the stenotic orifices.

Right auricular pressure, pulmonary "capillary" pressure (a measure of left auricular pressure) and cardiac output were measured at rest and during exercise in 14 patients with cardiovascular disease affecting primarily the left ventricle. In five patients these measurements were normal at rest, in nine abnormal. In all physiologic abnormalities developed on exercise in the sequence: increased pulmonary "capillary" pressure, increased right auricular pressure, decreased cardiac output. Definite abnormalities of left ventricular function were demonstrable when right ventricular function was entirely normal. These results are discussed in relation to the clinical status of the patients.

Diazepam, 5–10 rag, was given intravenously to treat anxiety occurring during cardiac catheterization in 15 patients. Anxiety was effectively relieved in 11 patients. Hemodynamic and ventilatory parameters were assessed before, and ten and 30 minutes after diazepam. The cardiac index decreased significantly in only three patients, each of whom had a control cardiac index in the high-normal range. No significant changes occurred in patients whose control cardiac indexes were below normal. Systolic blood pressure decreased by more than 10 mm Hg in eight patients. Pulmonary arterial pressure, heart rate, stroke volume and pulmonary and systemic resistance did not change significantly. Hypoventilation occurred in all patients. Ten minutes after diazepam minute ventilation had decreased by 28 per cent and tidal volume by 23 per cent. Paco2 increased by 5 mm Hg and Pao2 decreased by 10 mm Hg. The observed changes in blood pressure and ventilation were without clinical correlates and did not require therapy.

The effect of acute pulmonary embolism upon left circumflex coronary blood flow was studied in 11 open-chest, anesthetized dogs. Pulmonary embolization, in the absence of shock, was associated with increased left circumflex coronary blood flow, hypoxemia and electrocardiographic changes compatible with myocardial ischemia. Mean flow in the left circumflex coronary artery increased an average of 45 per cent after pulmonary embolization. No support was found for the concept of pulmonocoronary reflex spasm. The increase of left coronary blood flow was reduced or eliminated when hypoxemia was corrected by the administration of oxygen.

The clinical data (signs and symptoms, x-ray and electrocardiographic analysis) and hemodynamic findings in 10 patients with severe mitral and aortic stenosis have been presented. All patients had signs, symptoms, and radiologic stigmata of mitral stenosis. Normal sinus rhythm was present in 7 of the 10 patients, and right ventricular hypertrophy in only 3. Many of the features usually considered to be a sine qua non of severe aortic stenosis were absent in these cases. However, all patients had at least one manifestation other than the typical murmur of aortic stenosis (e.g., angina, syncope, abnormal carotid pulse, left ventricular enlargement by x-ray or ECG examination, calcification of the aortic valve, or dilatation of the aortic root). All patients with ECG evidence of left ventricular hypertrophy also had angina pectoris and significantly elevated timetension indices. This was due largely to a prolongation of the systolic ejection period. It is suggested that ECG evidence of left ventricular hypertrophy in this clinical setting, without significant mitral or aortic regurgitation, signifies severe left ventricular stress and severe aortic stenosis. A decrease in cardiac output secondary to mitral stenosis reduces the differences in pressure across the aortic valve and, there-fore, reduces the total left ventricular stress, as reflected by the time-tension index. It is believed that this reduction in output is the basic cause of inconstancy of symptoms and signs of aortic stenosis in patients with tight mitral and aortic stenosis. When aortic stenosis is suspected in patients with severe mitral stenosis, the only certain method of quantitative evaluation is catheterization of the left side of the heart, with simultaneous measurement of transvalvular pressure differences and blood flow.

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 pressor effect of series of subcutaneous injections of hog renin was studied in the dog, as well as the modification of the pressor effects of renin by reserpine, hydralazine ( l-hydrazinophthalazine) and hexamethonium. In 22 of 27 experiments, short series of subcutaneous renin injections (1–37 days) in doses of 550–1800 cat units/day were repeatedly followed by moderate elevations of systolic and diastolic blood pressure, whereas control injections of saline, ACTH or extracts of liver were without effect on the blood pressure. In a number of instances, but not in all, a definite increase in plasma renin could be demonstrated during the pressor effect of renin. The pressor effect of subcutaneous renin was still observed during oral administration of reserpine (0.25 mg/day) and hexamethonium (250–500 mg/day) but was often absent during the administration of hydralazine (25 mg/day). The pressor response to intravenous renin was increased in animals receiving reserpine and hexamethonium and decreased after hydralazine. In vitro experiments with these three drugs failed to indicate any significant effect on the formation or destruction of hypertensin.

Business response to political challenge or possibility has been the subject of much speculation and some recent exhortation. "Populist" and starkly "realist" elements in American political thought have tended to assume that powerful firms directly and unequivocally influence politicians.

Congenital heart lesions are notorious for their lack of characteristic signs and symptoms. The addition of venous catheterization, as developed by Cournand and Ranges (1), to the work-up of these cases presents an opportunity for the recognition of certain defects, for an estimation of the physiological magnitude of the shunts of blood, and for the study of the circulatory dynamics of these patients. Details of the procedure and methods of calculation of blood flows have been reported elsewhere (2, 3, 4, 5). Findings in representative types of congenital heart disease are herein described.2 Auricular Septal Defect In the presence of an auricular septal defect, blood usually flows from the left auricle to the right auricle. The venous catheter is helpful in the recognition of this defect by two methods, as described by Brannon, Weens, and Warren (6). The catheter may be introduced through the defect (4, 5) or arterial blood may be found in the right auricle (4). The following case report illustrates both ...

1. 1. Nineteen patients with severe aortic stenosis have been studied by left heart catheterization before and after transaortic valvuloplasty. 2. 2. The cardiac index was normal in patients with pure aortic stenosis but tended to be reduced in the presence of associated aortic regurgitation, mitral or coronary disease. 3. 3. Severe aortic stenosis, as it progresses, may become associated with a reduced cardiac output and, therefore, a small systolic mean pressure difference across the aortic valve. 4. 4. There was a small but significant postoperative increase in calculated aortic valve area in 11 patients, associated with a marked fall of left ventricular systolic pressure, transvalvular pressure difference, and left ventricular work, while cardiac output remained unchanged. A residual pressure difference across the aortic valve persisted in all but one patient, who developed severe regurgitation. 5. 5. Eight patients showed no change in valve area. The left ventricular systolic pressure and transvalvular pressure difference in these was also decreased postoperatively, but this was found to be the result of reduced cardiac output. 6. 6. Associated mitral stenosis, mitral regurgitation, or coronary disease did not preclude successful surgery for aortic stenosis. 7. 7. Six of the 8 operative failures occurred among 7 patients with clinically “insignificant” preoperative aortic regurgitation as the only complicating lesion. Operation in this group either did not relieve the stenosis or increased the regurgitation in proportion to the relief of stenosis so that measurable benefit was not observed. 8. 8. The meaning of the term “insignificant” as it pertains to pure aortic regurgitation and to regurgitation associated with severe aortic stenosis is discussed. 9. 9. Indications and contraindications for surgery for aortic stenosis are discussed.

Based on a myocardial mechanics approach to the analysis of left ventricular contraction, several indexes have been advanced as specific measures of myocardial contractility. Although two of these indexes, Vmax and [(d P /d t )/ P ]max, have been shown to be appropriately responsive to interventions known to alter the inotropic state, controversy has arisen as to whether they are unaffected by alterations in preload or initial cardiac muscle fiber length. This study was undertaken to determine which, if any, of the indexes obtained from myocardial mechanics analysis of left ventricular systole is independent of preload in the intact heart. Increases in left ventricular enddiastolic pressure were produced in seven dogs by infusion of dextran or whole blood and in eight patients by sudden elevation of the legs during cardiac catheterization. In dogs, elevation of left ventricular end-diastolic pressure was accompanied by a progressive decline in both Vmax and [(d P /d t )/ P ]max measured using total pressure ( P < 0.01). In contrast, Vmax measured using developed pressure was unaffected over a wide range of left ventricular end-diastolic pressures. Similarly, in the eight patients, increases in left ventricular end-diastolic pressure induced by sudden elevation of the legs were consistently associated with reductions in [(d P /d t )/ P ]max measured using total pressure ( P < 0.01), but these changes in pressure had no effect on developed pressure Vmax. In the intact heart, measurements of myocardial mechanics using developed pressure appear to be independent of preload, but similar measurements using total pressure are inversely dependent on preload. This finding raises doubt as to the validity of total pressure measurements as indexes of myocardial contractility.

Primary pulmonary hypertension is a distinct clinicopathologic entity characterized by pulmonary arterial and right ventricular hypertension. Right ventricular hypertrophy is uniformly present and may or may not be accompanied by right ventricular failure. The hypertension is the result, hemodynamically, of excessive increase in pulmonary vascular resistance and may reflect itself in the pulmonary vessels by a variety of vascular lesions. The pathogenesis of the ultimate vascular lesions remains obscure. The clinical, hemodynamic, and pathologic features of four patients with this condition have been presented. The clinical findings of cases reported in the literature as well as in our cases show a remarkable uniformity which, in our interpretation, is a reflection of the pulmonary hypertension. Thus, it is difficult if not impossible on clinical grounds alone to differentiate this lesion from any of the multitude of conditions in which pulmonary hypertension is a secondary concomitant. Cardiac catheterization has provided valuable information on the pathophysiology of primary pulmonary hypertension and may be of great value in differential diagnosis, particularly in excluding congenital heart disease. The abnormal hemodynamic data that may be demonstrated by this technic, however, are not sufficiently specific to permit one to make a conclusive diagnosis. In our opinion, such a definitive diagnosis is possible only by necropsy, and even here the exact mechanism may be difficult to define, although it is apparent now that many of the lesions in the pulmonary arteries represent the effect of pulmonary hypertension. In the face of such diagnostic difficulties and because there is no satisfactory treatment for primary pulmonary hypertension, it is in the patient's best interest that a search for a lesion that can be treated should not be abandoned.

Knowledge of the pulmonary blood volume is important in several areas of circulatory physiology. However, adequate methods for measuring this volume have not been established. The slope of an indicator-dilution curve across the central circulation has been used in several studies as an indication of this volume. In the present study the blood volume between pulmonary artery and left atrium was measured in 31 human subjects by an application of the well-established mean transit time principle. Slope volumes were also measured. There was poor agreement between the results of the two techniques. Unilateral pulmonary artery occlusion consistently reduced pulmonary blood volume by the mean transit time method, with only minor and less consistent changes in slope volumes. A close correlation between the slopes of curves from simultaneous pulmonary artery and left atrial injections suggested a predominant effect on both curves of factors at or distal to the left side of the heart. It was concluded that the slope method did not measure the pulmonary blood volume in man. Submitted on June 8, 1961

Sixty consecutive patients who survived an episode of acute pulmonary embolism documented by pulmonary angiography were assessed one to seven years later (average follow-up period, 29 months) to determine long-term prognosis. Thirty-nine were alive, 19 (32 per cent) had died, and two were lost to follow-up study. Survival largely depended on cardiac status before embolism. Of 42 patients without left ventricular failure, 36 survived. However, of 16 with failure before embolism, only three survived. Follow-up lung scans and arterial-blood gases in the survivors and autopsy in those who died demonstrated resolution of embolism in most patients. Of 43 with adequate follow-up data, resolution was complete in 28 (65 per cent) and partial in 10 (23 per cent); unresolved embolism persisted in only five patients (12 per cent), with resultant chronic cor pulmonale in only one. Recurrent embolism was documented in only one. The long-term prognosis of patients who survive acute embolism thus appears to be d...

The anatomy of the mitral leaflets, a classification of the variations in pathologic morphology of rheumatic stenosis, and the evolution of a practical technic for relief of that stenosis while restoring valve action are considered. The life cycle of patients suffering from mitral stenosis is reviewed and a clinical classification of these patients is presented. Some indications and contraindications for surgery are discussed in the light of strength and weakness of present surgical methods. Results of surgical treatment are reviewed.

Sotalol (MJ 1999), a beta-adrenergic blocking agent found to have no significant intrinsic myocardial depressant effects, was administered intravenously to 20 patients with heart disease. Eight of the patients had clinical and hemodynamic evidence of chronic heart failure. Doses ranged from 0.2 to 0.6 mg/kg. In all studies, heart rate decreased significantly, accompanied by comparable decreases in cardiac index and tension-time index. There were, however, no significant changes in stroke index, mean blood pressure, or left ventricular end-diastolic pressure—even in those patients with advanced heart failure, indicating that the changes noted were primarily rate-related and could not be ascribed to myocardial depression. To confirm this, further studies were performed in which heart rate was held constant by atrial pacing in normal and catecholamine-depleted dogs. Sotalol, at doses much higher than the minimal beta-blocking dose, did not change stroke index, blood pressure, left ventricular end-diastolic pressure, or estimated maximal velocity of isotonic shortening (V max ), confirming that myocardial contractility was unaffected. It is concluded that sotalol-induced beta blockade had no observable myocardial depressant action in dogs or adverse hemodynamic effects in cardiac patients, even when advanced chronic heart failure was present.

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.

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.