Vol. 83, Issue 6, 1797-1798, December 1997

INVITED EDITORIAL
Invited Editorial on "Coupled vs. uncoupled pericardial constraint: effects on cardiac chamber interactions"

John V. Tyberg

Departments of Medicine and of Physiology and Biophysics, University of Calgary, Calgary, Alberta T2N 4N1, Canada

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IN THIS ISSUE, Masao Takata and his colleagues (10) provide an elegant model of atrioventricular, ventricular, and heart-lung interaction that comes as close to being a "unified field theory" of pericardial physiology as this observer expects to see. Starting from simple equations that plausibly define the essential behavior of cardiac and pericardial components, the authors provide a qualitative and quantitative analysis that encompasses salient findings of classic physical diagnosis as well as theoretical cardiac mechanics. In so doing, the paper caps a series of outstanding investigations from Robotham's laboratory.

Pericardial constraint is divided into two categories, "coupled" and "uncoupled." Coupled constraint (e.g., pericardial tamponade) is exerted by a uniform "liquid pressure" over the entire surface of the heart, thereby coupling changes in the volume of one chamber to changes in the volume of all the others. Uncoupled constraint (e.g., constrictive pericarditis) is exerted by regional "surface pressure," which independently restricts changes in the volume of each chamber. A minor quibble: although Agostoni (1) amply deserves the appreciation of pulmonary and cardiac physiologists for the enlightenment that his concepts of liquid pressure and surface pressure originally gave us, those distinctions may not now be as dichotomous or as useful as they once were. As physicists and engineers have steadfastly maintained, there is only one pressure, and that is liquid pressure. Given the technical achievement required to couple the thin layer of liquid between two biological surfaces directly to a conventional pressure transducer, liquid pressures can be recorded from pleural and pericardial spaces that are equal to surface pressures (5, 6). These findings suggest that the greatest value of using the paired terms is to provide a historical context, Takata et al. (10) have done.

The venous inflow and right-heart pressure waveforms that characterize pericardial disease were produced by numerical solution of the model of atrioventricular interaction. Coupled constraint yielded the patterns of pericardial tamponade (i.e., venous flow became predominantly systolic and the x descent in right atrial pressure became more prominent) and uncoupled constraint yielded the patterns of constrictive pericarditis (i.e., venous flow became mainly diastolic and the y descent became accentuated). The dependencies of "cross-talk" pressure and volume gains and effective right ventricular elastances on septal and pericardial elastances were demonstrated by an analytic solution of the model. It showed that greater gains in ventricular interdependence (that would increase the likelihood of pulsus paradoxus) were produced by coupled constraint, whereas greater effective right ventricular elastance (that would increase the likelihood of Kussmaul's sign) was produced by uncoupled constraint.

Milnor (8) commented, "Models, usually in the form of mathematical expressions, play an important role in hemodynamics. In essence, they embody the assumptions we make about conditions in the circulation and state them explicitly and quantitatively so that they can be tested by experiment." As such, they are "only" deductive and, in a strict sense, do not provide new information. As Milnor wrote earlier (7) "...Once a mathematical or analogue model has been completed, it can be used to compute the effects of changing any parameter, often with results that were not obvious before. At that point, there is a strong temptation to believe that the results reveal something about the circulation in vivo, which they do not. What they tell us are the implications of the hypotheses built into the model, hypotheses that may or may not be valid in living animals. Models are thus a kind of temporary assembly of working assumptions, and their purpose should be to provoke, not take the place of new experimental observations." Having been thus reminded of both the value and limitations of models, we experimentalists and physicians are challenged to test the implications and probe the predictions of Takata's work.

Perhaps further work with the model could shed light on the following, still-perplexing questions: Why do extreme degrees of acute volume loading tend to decrease left ventricular (LV) end-diastolic volume, even as pressure continues to rise (3)? Why does increased airway pressure increase LV end-diastolic volume (9) and cardiac output (4) in patients with heart failure? Why does lower body negative pressure increase LV end-diastolic volume in patients with the most severe heart failure (2)? The answers to these questions are important, not only to our understanding of fundamental cardiac mechanics but also with respect to the way we treat our patients with congestive heart failure.

Finally, advances in pericardial physiology might be described as Milnor (8) wrote of hemodynamics, "Progress in this field has been erratic, a succession of fallow periods alternating with sudden spurts of insight." Despite being only a "temporary assembly of working assumptions," the model of Takata and his colleagues seems very much like one of those all-too-rare, "sudden spurts of insight."

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