Citations

Sixteen patients were studied immediately and for 3 days following surgical closure of ventricular septal defect. In eight patients with absent or mild pulmonary vascular disease, convalescence was uneventful and only small deviations from normal in cardiac output, blood gas levels, and acid-base profile were observed. The remaining eight patients had pre-existing moderate or severe pulmonary vascular disease. Values for cardiac output were abnormally low at some time in the postoperative period in all but two of these eight patients. Failure to survive was clearly related to a low cardiac output in four of the five nonsurvivors. Reduction in cardiac output observed in this group of patients is believed to be based in major part on the pre-existing increased resistance to blood flow through the pulmonary vascular bed and also to impaired right ventricular function following operation. No evidence was obtained to suggest that major changes in pulmonary vascular resistance occurred in the immediate postoperative period in patients with moderate or severe pulmonary vascular disease following closure of ventricular septal defect. Right ventricular function following atriotomy or transverse ventriculotomy was less impaired than after vertical ventriculotomy.

A method is described for detecting and quantitating small left-to-right shunts by recording continuously and simultaneously the changes in blood oxygen saturation at a systemic artery and at selected sites in the right heart chambers or great vessels produced by a few breaths of an inert gas such as helium or nitrogen. The advantages of this technic for detecting and quantitating left-to-right shunts are (1) the same instrument, namely, the cuvette oximeter, used to determine blood oxygen saturation and indicator-dilution curves in conjunction with routine diagnostic catheterization procedures, also is used to record the inert gas curves, (2) only one right heart catheter is needed, (3) the method is relatively simple, (4) the shunt can be quantitated, and (5) shunts of less than 10 per cent of pulmonary flow can be detected. It is concluded that the technic is of considerable practical value as a means of excluding the presence of or demonstrating and determining the magnitude of small left-to-right shunts.

Sodium ortho-iodohippurate (Hippuran) I 131 renography has been performed by a standardized technic in patients with renal artery stenosis, pyelonephritis, primary aldosteronism, pheochromocytoma, and renal tubular acidosis with nephrocalcinosis, as well as in patients in whom the hypertension was apparently not secondary. Fifty of 94 patients studied were found to have abnormal renograms. In patients with renal artery stenosis, all of 37 patients studied had values on the renogram that were outside the range for normal subjects. Although the renographic findings were not considered diagnostic of renal artery stenosis, certain abnormalities of the renogram were commonly observed in the presence of such lesions. When a unilateral delay in the appearance of maximal radioactivity was associated with delayed disappearance ot the medium, renal artery stenosis was frequently observed. Less pronounced differences in the function of the two kidneys were observed in patients with bilateral renal artery stenosis. A state of antidiuresis was often found helpful in the detection of less severe differences in renal function. In patients with predominantly unilateral pyelonephritis, the renographic abnormalities were qualitatively consistent with the degree of impairment of renal function. Bilateral abnormalities were observed in two patients who had bilateral parenchymal disease. The abnormalities on the renogram did not permit distinction between renovascular and renal parenchynal disease. Pyelonephritis associated with obstructive uropathy revealed findings highly suggestive of renal artery stenosis. Distinction from renovascular lesions could be determined with the aid of urographic studies. Only three of 44 patients with essential hypertension had abnormal renograms. The renograms, normal and abnormal, revealed essentially equal function of the two kidneys. The patients with abnormal renograms were not found by other technics to have evidence of secondary hypertension. The patients who were found to have pheochromocytoma and primary aldosteronism had normal isotope renograms. The patient with renal tubular acidosis and nephrocalcinosis had a bilaterally abnormal renogram and severe impairment of total renal function. The presence of a normal isotope renogram, as performed in our laboratory, is considered strong evidence against the existence of a renal or renovascular cause for secondary hypertension.

Eighteen patients with the combination of ventricular septal defect and aortic insufficiency were studied. Nine also had infundibular pulmonary stenosis. Seventeen were treated by open-heart operations. The physical findings were those of a typical ventricular defect murmur and thrill together with an aortic insufficiency blow and a wide pulse pressure. A systolic murmur at the upper left sternal border with thrill is strongly suggestive of the additional lesion of infundibular pulmonary stenosis, but the presence or absence of infundibular pulmonary stenosis was indicated most accurately at cardiac catheterization and on inspection at operation. It was not of sufficient severity for signs of additional right ventricular hypertrophy to appear on the electrocardiogram. Retrograde aortography serves to demonstrate the severity of the aortic regurgitation. The problem of the surgical correction of these lesions will be the subject of a separate communication.

The problem of spontaneous calcific embolization was investigated at necropsy in 165 patients with calcific aortic stenosis. Minor coronary arteries contained calcific emboli in 18 patients (11 per cent), and major coronary arteries contained calcific emboli in 10 (6 per cent). Examination of the brain, kidney, and eye also disclosed spontaneous calcific emboli. In three instances of major coronary artery embolization, there was evidence of old silent infarction but no associated clinical disorder. Calcific embolization is apparently not rare in cases of calcific aortic stenosis, but this phenomenon does not appear to lead very often to extensive infarction or to clinically obvious disorders.

Physiologic observations were made on eight patients following repair of atrial septal defect or total anomalous pulmonary venous connection. A pattern of changes in cardiac output and atrial pressures during the first 3 postoperative days was noted. Cardiac output was abnormally low in some patients with obstructive pulmonary vascular disease or low atrial pressures. Transfusion of whole blood was effective in elevating cardiac output in the operating room and after operation. Left atrial pressure was higher than right atrial pressure in the operating room. Postoperatively left and right atrial pressures tended to become equal in some patients, and the levels were slightly elevated. Heart rate did not seem to be directly related to cardiac output. Ventilation was adequate with regard to elimination of carbon dioxide. Arterial oxygen saturation was maintained at 93 per cent or more by the use of oxygen-enriched mixtures. The difference in arteriovenous oxygen content was inversely related to cardiac output. Acidemia was present 2 to 4 hours after operation, but in general the pH of arterial blood had returned to normal by day 2. Some mechanisms possibly related to the observations are discussed.

Among 13,314 necropsies following death from neoplastic and nonneoplastic diseases performed at the Mayo Clinic from 1942 through 1958, 189 cases of secondary malignant lesions of the pericardium were demonstrated, an incidence of 1.42 per cent. Carcinoma of the lung and breast, the lymphomas, and leukemia constituted the large majority of the primary malignant lesions that caused the pericardial metastasis. Fifty-five of the 189 patients were adjudged to have had some impairment of cardiac function as a consequence of the pericardial metastasis and the following conclusions concern this group. 1. In 47 patients (86 per cent), the lesions were either the immediate or a contributory cause of death. 2. The most common mechanism whereby metastatic lesions in the pericardium interfered with cardiac function was by the development of pericardial effusion. Next in frequency was effusion combined with myocardial invasion and then cardiac constriction by tumor. Combinations of these processes with malignant encroachment on the great vessels and with invasion of coronary veins were the other mechanisms noted. Involvement of coronary arteries and the cardiac nerve supply was not noted. 3. Pericardial fluid was significant in causing tamponade in 31 cases. The fluid was frankly hemorrhagic in a small minority of these cases although fibrinous pericarditis was present in 45 (82 per cent) of the group. Pleural effusion was present in 48 (92 per cent) of 52 cases and was usually bilateral. Ascites was present in 22 (50 per cent) of 44 cases; the quantity was usually rather small. 4. Only one patient had metastasis to the pericardium without metastasis to other thoracic structures; exclusive of patients with leukemia, 43 (92 per cent) of 47 patients had extrathoracic metastatic lesions. 5. Dyspnea, cough, pleural effusion, hepatomegaly, and thoracic pain were the most commonly recorded signs and symptoms that might be related to the pericardial lesions. However, more specific signs and symptoms directing attention to pericardial or cardiac involvement were not commonly recorded. 6. The diagnosis of pericardial metastatic disease was suspected or established in only 16 (29 per cent) of the 55 patients, although 34 (62 per cent) either received treatment for congestive heart failure or were given roentgen therapy to mediastinal structures. 7. Of the 27 patients whose electrocardiograms were available, 25 had T-wave abnormalities, 22 had low QRS voltage, and 15 showed sinus tachycardia. 8. Thoracic roentgenograms, made on 53 patients, supplied clues to the diagnosis of pericardial malignancy in 28.