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LETTERS TO THE EDITOR
Department of Physiology, University of New England, College of Osteopathic Medicine, Biddeford, ME 04005. E-mail: jnorton{at}une.edu
The following is the abstract of the article discussed in the subsequent reply to the letter to the editor that was published in the previous issue: Rothe C. Toward consistent definitions for preload and afterload—revisited. Adv Physiol Educ 27: 44-45, 2003:
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 "end-diastolic volume" or "aortic pressure" as common-usage 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:
I greatly appreciate the thoughtful feedback from Dr. Carl Rothe (1) regarding my article on the definitions of preload and afterload (2), since his extensive experience in the teaching and quantification of cardiovascular phenomena was clearly evident in his remarks. I also believe that open discussion of differences of opinion regarding definitions, concepts, or models in a forum such as Advances in Physiology Education is entirely appropriate and should occur more often.
In response to Dr. Rothe’s comments about the basic definitions of preload and afterload, I agree that short, concise terms are indeed valuable. Perhaps my definitions could be restated in a less tentative fashion that expresses in words exactly what the LaPlace equations in my original article indicated: preload is the myocardial wall stress at the end of diastole; afterload is the myocardial wall stress during systolic ejection.
Although wall stress is virtually impossible to measure in humans, as Dr. Rothe indicates, this itself is not a reason for further compromising or simplifying the definitions of preload and afterload. If there are indexes of either preload or afterload that are measurable and that can be directly related to the terms in the LaPlace equation, these indexes can and should be used to reflect changes in preload and afterload, but they should not, in my opinion, be used as a substitute for the definitions above. For example, as Dr. Rothe suggests, end-diastolic volume (EDV) is directly related to filling, is the basis for Starling’s Law of the Heart, and can be quantified using imaging technology. EDV is also directly related to the "radius" term in LaPlace’s Law. This would make EDV an excellent index of preload, but is not sufficient reason to equate EDV with preload, as Dr. Rothe does. Similarly, the end-systolic pressure (ESP) and the relationship between ventricular ESP and end-systolic volume (ESV) can be used as quantifiable indexes of afterload and/or myocardial contractility, but should not be equated with afterload.
My definitions of preload and afterload have, as their common basis, ventricular wall stress as a means of defining "load." Dr. Rothe’s definitions as proposed in his letter are inconsistent, using volume on the one hand to define preload and pressure on the other hand to define afterload. I disagree with Dr. Rothe’s statement that "load" implies a force or an amount of blood. If the term "load" is consistently associated with tension or stress, then the prefixes "pre-" and "after-" adequately define when the particular stress is occurring. As Dr. Rothe points out, the words themselves help: "preload" becomes the wall stress before the onset of contraction, "afterload" the wall stress after the onset of contraction.
I recognize that there is some ambiguity in defining afterload as the myocardial wall stress during systolic ejection. Because ventricular pressures and ventricular geometry change constantly during ventricular ejection, so does ventricular wall stress. My definition of afterload, as the ventricular wall tension during systolic ejection, simply acknowledges this fact. A specific, standardized point at which an indicator of wall stress might be obtained, such as the end of systole, would be very helpful in assessing afterload clinically. Limiting the definition of afterload to pressure at this particular point during the ejection period, however, may obscure the impact that the entire period of systolic ejection has on active myocardial wall tension requirements and the associated myocardial oxygen consumption.
I suggest that, for the purposes of basic physiology instruction in medical and graduate school curricula, preload and afterload be introduced and defined in terms of wall stress and the Law of LaPlace, but that every attempt be made to link these concepts to concepts such as Starling’s Law and contractility and to the indexes of preload and afterload provided by clinical assessments of EDV, ESP, or ESV. In my opinion, these measurements are very useful in indicating changes in myocardial wall stress during diastole or systole, but the quantities that they measure should not be substituted for the more comprehensive definitions of preload or afterload that the Law of LaPlace provides.
References
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