Richard S. Cosby

Ventricular Fibrillation and Competitive Pacing

SUDDEN death in persons with artificial pacemakers is a continuing and disturbing problem. Causes include pacemaker-catheter displacement, electric-component failure, broken wires and rising pacing...

Pulmonary function in left ventricular failure, including cardiac asthma.

Unusually comprehensive studies of pulmonary function in hypertensive patients during left ventricular failure and cardiac asthma are presented. These findings are compared to those in mitral stenosis with congestive failure and in pulmonary emphysema with right heart failure. All patients were severely dyspneic and bedridden.

Interatrial septal defect.

Abstract Recent developments in the study of congenital heart disease have necessitated a more careful evaluation of clinical material. It is surprising that so few clinical studies of atrial septal defect comparable to that of Bedford, Papp, and Parkinson 1 are available in the literature. Our purpose is to describe the clinical and laboratory features in thirty-five cases of atrial septal defect and to evaluate the various diagnostic procedures at present available in the study of this, the most common lesion in congenital heart disease. The relative value and diagnostic significance of fluoroscopy, circulation times, angiocardiography, and venous catheterization will be discussed. The material consists of sixteen unselected clinical cases collected during a period of eighteen months in a large cardiovascular clinic. On all patients adequate histories, physical examinations, fluoroscopy, and laboratory tests were available. Four of these cases came to necropsy. Another series of nineteen unselected autopsy cases was used to obtain further information on the pathology of this congenital lesion. In this particular series the clinical information was less detailed and is not included in our study.

Variant angina: case reports and critique.

Abstract Variant angina, as herein described in three patients, is a rare clinical entity characterized by episodes of spontaneous pain and is rarely related to exertion. Marked elevation of the J point is common, although not invariable, and dysrhythmias, although characteristic and dramatic, are rare. It is distinguishable from preinfarction angina, with which it is often confused, by its chronicity. Coronary arteriography should be utilized early in an effort to identify obstruction in a single large coronary vessel because of the important possibility of serious dysrhythmias and sudden death.

Electrocardiographic changes in carbon monoxide poisoning

Abstract In 10 patients with severe carbon monoxide toxicity, electrocardiograms were abnormal in 9. In the 3 patients reported in detail, electrocardiographic changes consisted of arrhythmias (auricular fibrillation), ischemic changes and probable subendocardial infarction. In 2 severely ill patients the electrocardiographic pattern did not return to normal for four weeks, and the clinical course was compatible with moderately severe coronary artery insufficiency and myocardial damage. Anoxia, toxic changes and true coronary ischemia secondary to shock may all play a part in carbon monoxide poisoning, depending on concentration, duration of exposure and presence or absence of shock.

A correlation of the spatial vectorcardiogram with right ventricular hypertrophy

Abstract 1. 1. A vectorcardiographic study of thirty-four patients with congenital heart disease and mitral stenosis is reported. All patients had cardiac catheterization and none except one had left ventricular hypertrophy. 2. 2. With increasing right ventricular work, there is an increased rightward and anterior deviation of the horizontal plane loop and of the spatial vectorcardiogram to the right anterior inferior octant in both lesions. 3. 3. There is a better correlation between the vectorcardiogram and right ventricular work than between the electrocardiogram and right ventricular work. 4. 4. The vectorcardiogram shows the pattern of right ventricular hypertrophy clearly. The electrocardiogram is usually reliable only in the classical pattern of right ventricular hypertrophy but not when incomplete right bundle branch block is present. In nine patients with incomplete right bundle branch block, the vectorcardiogram clearly shows that this lesion also represents right ventricular hypertrophy, thus confirming previous studies in congenital heart disease and extending them to patients with mitral stenosis as well. 5. 5. The vectorcardiogram may serve as a gross quantitative estimate of the degree of right ventricular hypertrophy, especially in congenital heart disease.

The electrocardiogram in congenital heart disease and mitral stenosis; a correlation of electrocardiographic patterns with right ventricular pressure, flow, and work.

Abstract 1.1. Mean levels of right ventricular pressure, flow, and work, but particularly mean levels of right ventricular work, are considerably higher in congenital heart disease than in mitral stenosis. 2.2. In congenital heart disease only abnormal electrocardiograms appeared above a mean right ventricular systolic ejection pressure of 30 mm. Hg. In mitral stenosis normal or borderline electrocardiograms appeared frequently up to a mean pressure level of 60 mm. Hg. 3.3. In congenital heart disease almost all electrocardiograms were abnormal above a right ventricular work load of 1 kg. M./min./sq.M. In mitral stenosis, normal electrocardiograms often occurred at work levels above 1 kg. M./min./sq. M. 4.4. In both mitral stenosis and congenital heart disease, the pattern of partial right bundle branch block appeared at almost all levels of right ventricular pressure and work, and thus this pattern appeared to be almost as significant as the classic pattern of right ventricular hypertrophy in the detection of right ventricular hypertension and presumptive right ventricular hypertrophy. 5.5. Gross electrocardiographic differences between congenital heart disease and mitral stenosis were present in all precordial leads; this was most marked in V 3R and V 1 , where the R wave in congenital heart disease was three to four times as tall as the comparable R wave in mitral stenosis. 6.6. In congenital heart disease, the electrocardiogram is remarkably accurate (91 per cent of cases) in the detection of right ventricular hypertrophy. In this disease no definite correlation was present between abnormalities of individual waves such as the height of R or RS ratio over the right precordium and levels of pressure or work. 7.7. The electrocardiogram in mitral stenosis is less diagnostic (51 per cent of cases) in the detection of right ventricular hypertrophy. But when the electrocardiogram is abnormal, a definite correlation is present between the height of R and RS ratios over the right precordium and levels of right ventricular pressure and work. 8.8. These differences in the total electrocardiographic picture suggest fundamental differences in the genesis of right ventricular hypertrophy in the two diseases.

Transposed pulmonary veins; a correlation of clinical and cardiac catheterization data.

Abstract Ten patients with transposed pulmonary veins are described. These include four patients with partial and two with complete pulmonary vein transposition, in whom cardiac catheterization and clinical findings are correlated. The other patients presented (1) pulmonary valvular stenosis accompanied by partial pulmonary vein transposition, (2) a left superior vena cava entering a sinus venosus in common with the hepatic veins, accompanied by anomalous drainage of the right pulmonary veins into the right atrium, and (3) probable tricuspid atresia with partial pulmonary vein transposition (two cases). The diagnosis of anomalous pulmonary vein drainage in these cases was made at cardiac catheterization by roentgen visualization of the catheter in the anomalous vein, by a characteristic pulmonary vein pressure curve and finally by 90 to 95 per cent oxygen saturation in the blood sample from the anomalous vein. Surgical exploration and attempts to correct this anomaly should be reserved for those patients with complete transposition in whom limitation of physical activity is progressive.

Pulmonary stenosis with left to right shunt

Abstract 1.1. A series of cases exhibiting the combination of pulmonary stenosis and a defect permitting a left to right shunt is described. The series includes examples of the combination of pulmonary stenosis with atrial septal defect, transposed pulmonary veins and ventricular septal defect, respectively. 2.2. The clinical features of the cases were in general those of mild or moderate pulmonary stenosis. It is thought that electrocardiographic and radiologic findings may suggest the presence of an accompanying septal defect. 3.3. Atrial septal defect with left to right shunt occurred in the presence of mild or moderate pulmonary stenosis and a normal left to right atrial pressure gradient. These findings are contrasted with those in pulmonary stenosis with right to left shunts. 4.4. A shunt through transposed pulmonary veins may occur in the presence of severe pulmonary stenosis. 5.5. Cases of ventricular septal defect and pulmonary stenosis appeared to fall into two groups; those with slight to moderate elevation of right ventricular pressure and those in which the right ventricular and systemic pressures were similar. 6.6. The surgical implications of these combined lesions are discussed.

Cardiac catheterization in interatrial septal defect

Abstract 1.1. Ten proven and seven presumptive cases with atrial septal defects have been presented. 2.2. The importance of catheterization of the left auricle is emphasized, together with the differential diagnosis of atrial septal defect from transposed pulmonary veins. 3.3. A rise of oxygen content in the right atrium in comparison to the oxygen content of the superior vena cava is not necessarily present in proven atrial septal defects. 4.4. The cause for cyanosis in atrial septal defect lies primarily in the presence of a right to left shunt. 5.5. The direction of shunt is determined by the pressure gradient between the atria during the cardiac cycle. 6.6. Pulmonary vascular disease may contribute to the pulmonary resistance but is not a significant factor in the production of cyanosis.