Citations

Arteriovenous fistula involving the portal vein or its tributaries is a rare condition that in some cases can be treated successfully by surgery if it is recognized. The clinical manifestations and diagnostic criteria are presented.

The diagnosis of Raynaud's disease was suspected in 756 female patients at the Mayo Clinic from 1920 through 1945. The diagnosis was substantiated from the records of the initial examination or from the follow-up data or examination in 474. The clinical characteristics, including diagnostic criteria, clinical course, complications, and sequelae are discussed.

Each of 21 patients was noted to have a low concentration of water in the serum immediately after whole-body perfusion. This indicated a loss of water either by the patient or the pump-oxygenator. Investigation suggested that the patient, and not the pump-oxygenator, was the source of water loss. Two of the 21 patients had a profuse, short-lived solute diuresis in the immediate postperfusion period. These phenomena are apparently benign and they require no specific treatment.

Anomalous connection of the right pulmonary veins to the superior vena cava associated with an interatrial communication in an unusually cephalad location has been diagnosed at cardiac catheterization in 8 patients. These patients had the clinical features seen in patients who have atrial septal defects in the region of the fossa ovalis. Differentiation was accomplished by (1) the roentgenographic position of the catheter in the right superior pulmonary vein, (2) demonstration of an abnormally high oxygen saturation of the blood in the superior vena cava, (3) the presence of a small right-to-left shunt from the superior vena cava and the absence of such a shunt from the inferior vena cava, and (4) demonstration of similar drainage of blood from the right superior pulmonary vein and superior vena cava. The syndrome is considered to be an anomaly of pulmonary venous development while the atrial septum forms normally.

Manifestations of left ventricular failure have been reported in the literature in some patients after surgical closure of atrial septal defects. The authors present their experience in their series of 85 cases and detailed hemodynamic measures in 16 patients.

While there are many anatomic varieties of congenital malformations of the heart and great vessels, most may be divided, from a functional point of view, into 3 types: (1) communication between the ventricles or between the aorta and pulmonary arteries, (2) anomalous drainage of pulmonary venous blood into the right atrium, and (3) obstruction to pulmonary venous flow. In each of these categories the responses of the pulmonary vascular tree have to be considered in understanding the altered dynamics. Depending on the type and degree of response in the pulmonary vascular bed, there may be a varying functional picture among patients having the same anatomic or functionally comparable malformation.

Various indirect methods of measuring blood flow in the peripheral blood vessels of man are available. Irrespective of the method used for measuring blood flow, certain fundamental factors concerned with the status of the subject or patient influence the measurement of blood flow. These factors are environmental temperature, position of the extremities and food. The present investigation indicates that a consideration of the basal metabolic rate or basal heat production is another important factor.

The case history of a patient with apparent spontaneous rupture of the posterior tibial artery is presented, with a brief review of the previously reported cases.

In a limited number of subjects having hypoxemia related to congenital malformations of the heart, no evidence was obtained of a correlation between the degree of hypoxemia or the extent of the polycythemia and the systemic blood flow. The circulatory response to exercise was characterized by a greater increase in the arteriovenous oxygen difference than in the systemic blood flow. A syncopal reaction in one patient was preceded by a greatly increased systemic blood flow and a small arteriovenous oxygen difference.

Calculated therapeutic doses of digitalis and its derivatives did not produce demonstrable microscopic changes in the myocardium of experimental animals. Toxic doses of digitalis (twice a therapeutic dose) induced myocardial lesions in animals. In those animals with experimentally induced mild to moderate hyperthyroidism, calculated therapeutic doses of digitalis did produce myocardial lesions. Toxic doses of digitalis administered to animals with mild to moderate hyperthyroidism caused extensive degenerative changes in the myocardium or promptly killed the animals without associated microscopic lesions.