Richard Bing Remembered

Richard Bing (Fig. 1), who died on 8 November 2010 at the age of 101 in his home at La Cañada, California, was the doyen of clinical and experimental cardiology. He was the first to perform catheterization in infants and children, to study metabolism of the human heart, and to use positron-emitting tracers to assess coronary flow. Active until he died, he was also an acclaimed composer and the author of several books of short stories. Bing came to New York in 1936 as a refugee scientist from Germany. He worked with Carrel and Lindbergh on organ preservation and published his first paper—at age 29, as a single author—in Science.¹ The last paper reporting original research with Dr. Bing as first author appeared when he was 92.² In between lie 63 years of productive and creative life in biomedical research. Dr. Bing's greatest contributions to cardiovascular medicine were perhaps in the field of congenital heart disease and occurred while he worked with Alfred Blalock and Helen Taussig at Johns Hopkins from 1945 to 1951. There he established the 3rd cardiac catheterization laboratory in the United States (the other 2 were those of Drs. André Cournand and Dickinson Richards in New York, and of Dr. Lewis Dexter in Boston), and the first one dedicated to the diagnosis of heart defects in “blue babies.”

Figure. Richard John Bing (1909–2010). Courtesy of Huntington Medical Research Institutes, Pasadena, California.

As I have mentioned above, Dr. Bing's career as scholar and investigator spanned well over 60 years. It was interrupted by war, setbacks, and new beginnings. In the following, I have selected passages from 3 papers written by Dr. Bing's contemporaries, none of them now with us, for presentation in a festschrift on the occasion of his 80th birthday in 1989. Although Richard Bing's Journal of Applied Cardiology is no longer published, the readers of the Texas Heart Institute Journal might enjoy the spirit in which the articles were written, because they recount a time of great excitement.

Dr. Leroy D. Vandam (1914–2004) was a fellow with Dr. Bing and later became the chairman of anesthesiology at the Peter Bent Brigham (Brigham & Women's) Hospital and Harvard Medical School in Boston. In his article “Ferment in Baltimore in the Forties,” he remembers Richard Bing as follows³:

More or less stranded at Hopkins, I, who was without any prior research experience, was both surprised and intrigued when Richard John Bing early in 1945 invited me to participate in the organization of a laboratory designated for the study of the pathophysiology of congenital heart disease. Thus began an association and friendship that would count so heavily in my future as an anesthesiologist first at Pennsylvania, then Harvard. Not only was Alfred Blalock farsighted in realizing the need for investigations that would lend credence to his surgery for correction of circulatory anomalies, but his choice of Richard Bing to carry out the mission could not have been more sensible. Bing, who possessed the genius, originality, and appropriate aggressiveness for this kind of pioneering endeavor, had already made a name for himself in investigations on the etiology of hypertension in man, and had done work in the laboratories of Alexis Carrel, Homer Smith, and others abroad—at the Rockefeller Institute, New York University, and the College of Physicians and Surgeons….

In a brief span of time, Bing had prepared himself to utilize cardiac catheterization as a diagnostic method, by visiting André Cournand's laboratory at Bellevue Hospital in New York City, the only other place besides Lewis Dexter's in Boston where work of that kind was being done. It was also important for Bing to learn as much as possible about other analytical methods for study of the circulation, respiration, and metabolism, some of which had been in vogue since the turn of the century. Logically, Blalock was primarily interested in the effects of pulmonic stenosis on the production of arterial oxygen unsaturation and the resulting cyanosis. However, Julius Comroe at Pennsylvania readily pointed out that cyanosis was largely the result of right-to-left shunting of blood, although in the light of later pulmonary function studies he might also have indicted ventilation–perfusion imbalance. Nonetheless, Bing had figured out a means to measure the pulmonary capillary circulation employing carbon dioxide as a factor in the Fick equation. This presumably permitted estimation of the collateral of effective circulation to the lung, and the degree of shunting to the systemic circulation. Here again, Cournand cautioned on the vagaries of employing carbon dioxide, a highly diffusible gas, in physiological measurements….

Once the laboratory began to function, there were many visitors from all parts of the world and others who would spend various periods of time learning procedures. But most memorable of all were the dozens of patients, plus parents and other relatives, who had been offered some hope in the amelioration of long-standing cyanosis and their incarceration at home. One cannot forget the vivid signs of congenital heart disease, the huckleberry blue lips, mucous membranes and fingernails, plus the pulmonary osteoarthropathy which extended beyond mere clubbing of the fingers to gross distortion of wrists and ankles. To be sure, every conceivable kind of congenital abnormality was encountered from patent ductus arteriosus and coarctation of the aorta, to all of the residuals of embryologic development of the heart.

Right-sided heart catheterization permitted the diagnosis of intracardiac defects by means of blood oxygen content and blood pressure gradients in the auricle, ventricle, and occasionally pulmonary artery. These data were supplemented by clinical history, physical examination and x-rays of the chest. Helen Brooke Taussig was a phenomenal diagnostician in this area. Further, the position of the catheter during fluoroscopy and its passage into the left side or pulmonary fields would further confirm the existence of an atrial or ventricular septal defect, a common chamber, and pulmonic valve patency (Eisenmenger's complex). According to this technique, it was not possible to distinguish mere stenosis from atresia. In coarctation of the aorta, not only was the pulse dampened in the femoral artery because of aortic constriction, but the diastolic pressure was elevated, suggesting a renoprival component to the hypertension.

The findings from the laboratory, embracing measurements in dozens of patients, began to appear as early as 1947, in the Bulletin of The Johns Hopkins Hospital, thus indicating the efficiency of the laboratory. Further, there was little delay in publication, because peer review in that journal was carried out by a small select committee of the Hopkins faculty. When revisions or corrections were made, the manuscripts could be delivered by hand in a short time to the office of the Executive Secretary, who resided just off North Charles Street. In that same year, an exhibit depicting results of the studies done in the laboratory was awarded a bronze medal at the Fifth International Congress of Pediatrics in New York City.

A native Texan, Dr. Dan McNamara (1922–1998), was a student of Helen Taussig's in Baltimore. Subsequently, he became the Chief of Cardiology at Texas Children's Hospital in Houston and professor of pediatrics at Baylor College of Medicine. He remembers Richard Bing's contributions to the knowledge of congenital heart disease as follows⁴:

While at The Johns Hopkins Medical School and Hospital in the 1940s, Bing was stimulated by the clinical diagnostic methods of Helen Taus­sig, who had learned to identify certain congenital malformations by the history, physical examination, and the radiographic, especially the fluoroscopic, image of the heart. But as a physiologist as well as a clinician, it became clear to Bing that the strictly clinical approach left serious limitations in consistently arriving at a reliable definition of anatomic and physiologic alterations sufficient for medical or surgical management of the patient. He proposed that cardiac catheterization, structured exercise tests, or ear oximetric study of arterial blood oxygen saturation, and other physiologic measurements would improve diagnosis of congenital cardiac defects and would further knowledge of the mechanisms of circulatory dysfunction and the body's adjustment to them. He began to carry out physiologic measurements in the large number of patients with congenital malformations who were referred to the clinics of Taussig and Blalock at Hopkins in the mid 1940s.

As a result, he was able to publish, for the first time, the hemodynamic features of some 20 different types of circulatory birth defects, which took congenital heart disease well out of the dark ages of that discipline. These included tetralogy of Fallot, single ventricle with pulmonary stenosis, transposition of the great arteries, Ebstein's malformation, Eisenmenger's complex, Taussig-Bing anomaly, atrial septal defect, ventricular septal defect, aortic valve atresia, truncus arteriosus, patent ductus with pulmonary hypertension, total anomaly of pulmonary venous return, pulmonary arteriovenous fistula, and systemic arteriovenous fistula.

While Bing fostered the importance of physiologic measurements in certain types of complex defects, he also emphasized the need for specific questions to be answered by cardiac catheterization through a careful clinical evaluation before the study was to be performed. His methods were intended as a support, not a replacement, for clinical evaluation.

It is difficult for cardiologists today to realize that cardiac catheterization as recently as forty years ago was largely a technique for research in basic pulmonary and cardiovascular physiology….

Bing offered a physiological classification which is used today by many workers in the field, often without knowing its source:

Pulmonary blood flow less than systemic blood flow and pulmonary artery pressure usually low (e.g., tetralogy of Fallot).

Pulmonary blood flow greater than systemic blood flow and pulmonary artery pressure either normal or increased (e.g., atrial septal defect, ventricular septal defect, or ductus arteriosus).

Pulmonary blood flow equal to systemic blood flow (e.g., aortic stenosis, coarctation, and isolated pulmonary stenosis)….

Today's students of congenital heart disease would do well to study Bing's published work of the 1940s and 1950s. If one is not distracted by outdated terms in use 40 to 50 years ago, such as “anoxia” (for hypoxemia) and “auricle” (for atrium), the substance of his writings remains pertinent and factual today and gives the interested reader a deeper understanding of the subject than might otherwise be gained.

Bing's role in demonstrating detailed physiologic aberrations in congenital cardiac defects and in developing what are now fundamental principles, such as effective pulmonary blood flow, have advanced the discipline of pediatric and congenital heart disease, and have doubtless stimulated other scientific investigators to continue in his path. In addition to the clinical pediatric cardiologist and heart surgeons, Bing introduced the physiologist as a vital member of the team for the management of patients with congenital heart malformations.

Dr. Lewis Dexter (1910–1995), one of the pioneer cardiologists in America, was professor of medicine at Harvard Medical School and director of the cardiac catheterization laboratory at Peter Bent Brigham Hospital in Boston. Dr. Dexter is credited, among other things, with the discovery of the pulmonary capillary wedge pressure. He recalls Richard Bing and the early days of cardiac catheterization as follows⁵:

Although cardiac catheterization had a history going back to the early 19th century, it was Richards and Cournand in 1941 who first showed its value for the study of human circulatory physiology. Others promptly took up the method and one of them was you, Richard, in 1945 at Johns Hopkins. At that time, you were particularly concerned with the study and diagnosis of “blue babies” (tetralogy of Fallot) for Dr. Blalock to correct surgically by the production of the Taussig-Blalock “ductus”….

In order to carry out such studies, let me describe the methods that were available in the mid-1940s. Fluoroscopy was required. This was before the invention of image intensification. In order to see the radio-opaque catheters, one had to dark-adapt for 15 minutes with red goggles and then carry out the procedure in a pitch-black room, peering at the dim picture on the fluoroscopic screen. My first x-ray and fluoroscopic machine cost $12,500….

At this time (1945), I visited you, Richard Bing, in Baltimore and I was very impressed with several things. First, your skill with the catheter. Next, your organization and surgical approach with gowns, masks, drapes, etc. Next, your lack of sedation in the little children. Your remarkable nurse, whose name I can't recollect, sitting by the patient's head, crooning to him in a soft voice, stroking his brow—she was the sedative. For many years, I gave no sedatives—only Novocain at the venotomy site; neither you nor I wanted to get false readings of arterial oxygen saturation in these congenitals. Finally, I was impressed with your precise recordings with the Hamilton manometer. You, Richard, were good enough to give me two, with the silver membranes, pedestals, and tiny mirrors. You were one of the real cornerstones in my career. It took me a bit of time to get them working but they did at last provide me with systolic, diastolic, and mean pressures, and thus allowed me to get on with my work. My eternal gratitude to you….

These early years were a real challenge. Each case produced data for which there was little prior experience for interpretation. But what fun we had. I studied two patients a week and three experimental dogs. How times have changed. Now, it's likely to be two dozen patients a week and no dogs! I think, Richard, you and I had remarkably fortunate times to live in.

The passing of Richard Bing marks the end of the beginning for modern cardiovascular medicine. He has inspired us to follow in his footsteps—not least because he overcame many adversities in his own life, even those of old age. Dr. Bing is survived by his son Dr. John Bing of Ewing, New Jersey; his daughter Judy Tasker of Thousand Oaks, California; and his son William Bing of Altadena, California. He is predeceased by his wife of 52 years, Mary Bing, née Whipple, and by his daughter Barbara.

Acknowledgments

The author thanks Pergamon Press (now Elsevier) for permission to quote from the Journal of Applied Cardiology, and Mrs. Roxy A. Tate for expert editorial help.