Abstract
The following is the abstract of the article discussed in the subsequent letter:
Norton JM. Toward consistent definitions for preload and afterload. Advan Physiol Educ 25: 53–61, 2001. Significant differences exist among textbook definitions for the terms preload and afterload, leading to confusion and frustration among students and faculty alike. Many faculty also chose to use in their teaching simple terms such as “enddiastolic volume” or “aortic pressure” as commonusage approximations of preload and afterload, respectively, but these are only partial representations of these important concepts. Straightforward definitions both of preload and afterload that are concise yet still comprehensive can be developed using the Law of LaPlace to describe the relationships among chamber pressure, chamber radius, and wall thickness. Within this context, the term “preload” can be defined as all of the factors that contribute to passive ventricular wall stress (or tension) at the end of diastole, and the term “afterload” can be defined as all of the factors that contribute to total myocardial wall stress (or tension) during systolic ejection. The inclusion of “wall stress” in both definitions helps the student appreciate both the complexities of cardiac pathophysiology and the rationale for therapeutic intervention.
To the Editor:
Cardiac preload and afterload are confusing terms because there are no clearly accepted definitions. Norton (2) reviewed 29 physiology textbooks, monographs, and reviews to provide a summary list of published definitions. The results clearly reveal the variability and inconsistency that confuse not only medical students but also clinicians and professors. He has proposed the Law of LaPlace as the basis for the definitions of both preload and afterload. Norton’s definitions are: “Preload represents all the factors that contribute to passive ventricular wall stress (or tension) at the end of diastole,” and “Afterload represents all the factors that contribute to total myocardial wall stress (or tension) during systolic ejection.”
Short, concise terms are indeed needed to help characterize the vigor of cardiac contractions, but Norton’s definitions have serious weaknesses. 1) They are virtually impossible to measure in a human; 2) they are vague in describing “all the factors that contribute to;” and 3) the definition of afterload does not specify a time for measurement during systole. Those who consider afterload to be the pattern of arterial pressure, arterial impedance, or myocardial wall stress during systolic ejection rarely, if ever, provide the user with an algorithm to estimate the magnitude of the influence of such afterload on cardiac function over this interval. What constitutes a useful definition of a term that represents a physiological concept? It should be 1) measurable, 2) based on the mechanisms of the related functions, and 3) help one understand the concept. The words themselves offer some help. “Pre” and “post” imply before and after contraction, respectively, and “load” implies a force or an amount of blood.
During the last two decades, I have developed a fivecompartment model of the circulatory system (3) based on five basic relationships: 1) mass balance implemented as the integral of inflow minus outflow of blood for each compartment; 2) capacitance characteristics of each compartment; 3) resistance to flow between compartments; 4) cardiac output as heart rate times (EDV − ESV); and 5) ventricular vigor of contraction, related to the ventricular endsystolic pressure volume relationship (ESPVR) and E_{max}. I suggest that definitions of preload and afterload should represent the two primary factors influencing the vigor of cardiac contraction. Thus:
1) Preload is the enddiastolic volume (EDV) at the beginning of systole. The EDV is directly related to the degree of stretch of the myocardial sarcomeres. This is the basis of the FrankStarling Law of the Heart. The EDV can be estimated using ultrasound imaging, and it occurs at a specific time in the cardiac cycle. If the EDV is increased and if the subsequent ejection stops at about the same endsystolic volume (ESV) as previous beats, then the stroke volume will be increased and cardiac output and work will be increased.
2) Afterload is the ventricular pressure at the end of systole (ESP). Ejection stops because the ventricular pressure developed by the myocardial contraction is less than the arterial pressure. This determines the endsystolic volume (ESV). The ratio of ESP to ESV is closely similar to the maximum systolic elastance (E_{max}), because it occurs within a few milliseconds of E_{max}. The ESP can be estimated from the arterial pressure at the time of outlet valve closure and can be approximated by the mean arterial pressure. Furthermore, the ESV at the cessation of ejection can be estimated using ultrasound imaging. The slope of the ESPVR and E_{max} can be estimated, under a constant level of contractility, by measuring the ESV at several magnitudes of ESP. The slope of the ESPVR provides a useful estimate of inherent cardiac contractility (See Ref. 5 and earlier studies by these authors).
Because the EDV equals the presystolic volume for a given beat of a ventricle, then the pre and postsystolic volumes define the stroke volume (if the valves are fully functioning and there are no ventricularseptal leaks). The product of stroke volume and heart rate determines the cardiac output—the primary function of the heart.
The definitions and consequences of afterload, as defined above, are not perfect. Problems of measurement, nonlinearity of the ESPVR, a nonzero intercept of the ESPVR at zero ESP, and the geometry of the chamber limit the application of E_{max} as an index of the contractile state of the myocardium (1, 3, 5). It is a better index than the ejection fraction or the rate of development of ventricular pressure at the beginning of systole. For more information about the relationship between ESPVR and E_{max} and their uses see Sagawa (4) and Kass and Maughan (1).
The Rothe and Gersting article (3), which describes the Cardiovascular Interactions (CVI) project, is available from the Web (http://advan.physiology.org/cgi/content/full/26/2/98).
A copy of the CVI project itself can be downloaded as zipped files from http://advan.physiology.org/cgi/content/full/26/2/98/DC1
Alternatively, the project may be obtained as a CD on request to C. Rothe (crothe@iupui.edu). The mathematical model and information file that accompanies the CVI project help clarify potentially daunting conceptual problems that limit clear understanding of the physiology of the cardiovascular system as a whole.
Footnotes

AN INVITATION TO READERS
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 © 2003 American Physiological Society