Forward and Backward Heart Failure

If you happened upon me at Parkland Hospital in July 1978, you might have found me attaching a water-filled manometer to a needle placed in an antecubital vein to measure a peripheral venous pressure and then injecting sodium dehydrocholate (Decholin) to measure circulation time. The peripheral venous pressure was supposed to reflect the central venous pressure and the Decholin time, the cardiac output. The Decholin time depends on the patient’s reporting a bitter taste after the injection of that bile salt into an antecubital vein, the normal transit time from arm to tongue being 13 to 17 seconds. More than bitter, the taste was vile and clearly apparent on the patient’s face before he or she verbally reacted. Better yet was when the patient would retch onto an unsuspecting nearby medical student, which was regarded as a hard end point. (Proper positioning of the medical student for this and for the insertion of nasogastric tubes was learned very quickly as an intern.)

When a patient was admitted to a medicine service with suspected heart failure, it was understood that a Decholin time and peripheral venous pressure would be measured. Heaven forbid if you could not recite those values to Dr. Donald Seldin, our legendary chief of medicine, in morning report the next day. For from these values, an entire construct of the physiology of heart failure was derived. A prolonged circulation time indicated “forward heart failure.” An elevated peripheral venous pressure confirmed “backward heart failure.” To report a relatively rapid circulation time in the face of heart failure would bring excitement to morning report, because discussion would then focus on beriberi heart disease, the favored differential for high-output congestive heart failure and the reason why an order for thiamine was included almost automatically on the admission order set. The framework of forward and backward heart failure was codified in the Forrester classification of heart failure.

Once the use of Swan-Ganz catheters became widespread, the Decholin time and the peripheral venous pressure became obsolete. They were flawed measurements to begin with; the circulation time subjective and dependent on the patient’s quickly reporting a taste, and the peripheral venous pressure on the opposite side of the heart and typically divorced from what needed to be measured, the left atrial pressure. It has probably been 10 years since I have heard anyone use the term forward or backward heart failure, but the concepts are still usefully applied in tailoring unloading therapy for patients with chronic heart failure.

Our Brain Natriuretic Peptide Was the Cardiothoracic Ratio

Another thing we measured carefully was the cardiothoracic ratio on chest x-ray, with an abnormal ratio being >50%. The precise heart size on the x-ray was relied on as a quantitative marker of heart failure, similar to brain natriuretic peptide today. Rulers hung by every view box, and results were written in wax crayon at the bottom of the film for easy reference. A patient’s progress from clinic visit to clinic visit was gauged by whether the ratio increased or decreased.

An enlarged heart was the sine qua non of heart disease from ancient times, so it was assumed that a patient could not have heart failure if the heart size was normal on chest x-ray. So, for example, if the chest film showed a pattern of pulmonary edema but the heart size was normal, the pulmonary edema was noncardiogenic by definition. M-mode echocardiography was in its infancy, and the concept of diastolic heart failure was mooted in research publications but had not yet influenced clinicians’ thinking.

I remember how astonished Dr. Seldin was in 1980 about a report in which Ross described a series of patients with acute myocardial infarctions, most of whom had pulmonary congestion with normal heart size. As he presented the study to us in morning report, he was incredulous. How could you have pulmonary edema with a normal heart size? The findings were inexplicable; yet he appreciated that there was something new and very important being described.

In short order, the imprecision of the cardiothoracic ratio became apparent. Subsequent publications refuted the ability of the cardiothoracic ratio to reflect the presence of heart failure or to predict the ejection fraction compared to the new, more golden standard of echocardiography or Swan-Ganz catheterization. On the basis of the seemingly logical scientific belief that one could not have congestive heart failure without an enlarged heart, the cardiothoracic ratio measurement had intuitive validity. The measurement and its interpretation flowed directly from scientific tenets of the time. It took the development of new measuring tools revealing contradictory findings to unravel what had previously been dogma.

Our Brain Natriuretic Peptide Was the Cardiothoracic Ratio

Another thing we measured carefully was the cardiothoracic ratio on chest x-ray, with an abnormal ratio being >50%. The precise heart size on the x-ray was relied on as a quantitative marker of heart failure, similar to brain natriuretic peptide today. Rulers hung by every view box, and results were written in wax crayon at the bottom of the film for easy reference. A patient’s progress from clinic visit to clinic visit was gauged by whether the ratio increased or decreased.

An enlarged heart was the sine qua non of heart disease from ancient times, so it was assumed that a patient could not have heart failure if the heart size was normal on chest x-ray. So, for example, if the chest film showed a pattern of pulmonary edema but the heart size was normal, the pulmonary edema was noncardiogenic by definition. M-mode echocardiography was in its infancy, and the concept of diastolic heart failure was mooted in research publications but had not yet influenced clinicians’ thinking.

I remember how astonished Dr. Seldin was in 1980 about a report in which Ross described a series of patients with acute myocardial infarctions, most of whom had pulmonary congestion with normal heart size. As he presented the study to us in morning report, he was incredulous. How could you have pulmonary edema with a normal heart size? The findings were inexplicable; yet he appreciated that there was something new and very important being described.

In short order, the imprecision of the cardiothoracic ratio became apparent. Subsequent publications refuted the ability of the cardiothoracic ratio to reflect the presence of heart failure or to predict the ejection fraction compared to the new, more golden standard of echocardiography or Swan-Ganz catheterization. On the basis of the seemingly logical scientific belief that one could not have congestive heart failure without an enlarged heart, the cardiothoracic ratio measurement had intuitive validity. The measurement and its interpretation flowed directly from scientific tenets of the time. It took the development of new measuring tools revealing contradictory findings to unravel what had previously been dogma.