Conceito de pré carga e pós carga em cardiologia
9 pág.

Conceito de pré carga e pós carga em cardiologia

DisciplinaFisioterapia8.990 materiais25.854 seguidores
Pré-visualização5 páginas
(afterload, in particular) relates to the
metabolic costs associated with the development of
myocardial wall tension and, therefore, chamber pres-
sure. The greater the tension requirement during sys-
tole, the greater the demand for oxygen and meta-
bolic substrate by the myocardium. In the presence of
cardiac disease, both physiological compensatory
mechanisms and therapeutic regimens have as their
goals the reduction of myocardial wall tension (and,
therefore, myocardial oxygen consumption) and the
restoration of a balance between oxygen supply and
demand, especially important in patients with im-
paired coronary blood flow. A comprehensive defini-
tion of afterload, such as that provided here, would
help students appreciate this therapeutic rationale.
The relationships among pressure, radius, and wall
thickness described above provide a clear physiolog-
ical explanation for the different patterns of hypertro-
phy and remodeling seen in response to increased
preload and increased afterload. If filling pressures,
output pressures, and stretch (factors in the numera-
tors of the equations described above) are loads im-
posed on the heart by conditions within the circula-
tory system, then a change in myocardial wall thickness
(in the denominator) can be considered as a major
myocardial response to these externally imposed pertur-
bations. For increased preload, the additional wall stress
caused by a larger chamber radius is normalized by
increasing the wall thickness enough to restore the ratio
EDR LV/wLV in the equation above for preload. Likewise,
for an increased afterload generated by a greater output
impedance requiring higher ventricular pressures dur-
ing systole, the systolic wall stress is normalized by
hypertrophy that restores the ratio SPLV/wLV.
In conclusion, the tendency clearly exists in texts, in
conversation, and even in formal lectures to use short,
simple definitions of preload and afterload. Preload is
defined variously as \u201cfilling pressure\u201d or end-diastolic
FIG. 1.
Factors determining preload: a flow diagram illustrating the various
factors within the cardiovascular system that determine preload and
therefore end-diastolic myocardial passive wall stress based on the pa-
rameters in the Law of LaPlace: chamber radius, chamber pressure, and
wall thickness.
volume; afterload is often simplified as \u201ctotal periph-
eral resistance\u201d or arterial pressure. According to the
above analysis, these are only components of preload
and afterload and don\u2019t tell the whole story. If, in the
mind of a student, afterload is defined only as aortic
pressure, then that student will not be able to appre-
ciate fully the increases in afterload (left ventricular
wall stress) and, therefore, oxygen consumption that
would accompany aortic stenosis, obstructive cardio-
myopathy, or ventricular remodeling associated with
increased chamber radius.
It is my contention that preload and afterload should
be consistently defined in terms of myocardial wall
stress (or tension) and that the definitions should
always include the major factors affecting wall ten-
sion for each, namely, chamber pressure, chamber
radius, and wall thickness. If you keep wall stress or
\u201cwall tension\u201d built into your definitions of preload
and afterload, you will be better able, in my opinion,
to help your students understand cardiovascular
pathophysiology and the therapeutic approaches to
heart disease.
The author acknowledges the students in the College of Osteo-
pathic Medicine and in Physician Assistant and Nurse Anesthesia
programs of the University of New England for many constructive
criticisms and comments regarding what really works in the class-
Address for reprint requests and other correspondence: J. M. Nor-
ton, Dept. of Physiology and Pharmacology, Univ. of New England
College of Osteopathic Medicine, 11 Hill\u2019s Beach Rd., Biddeford,
ME 04005 (E-mail:
Received 22 June 2000; accepted in final form 30 October 2000
1. Berne RM and Levy MN. Cardiovascular Physiology. St.
Louis: Mosby, 1997, p. 1\u2013324.
2. Berne RM, Levy MN, Koeppen BM, and Stanton BA. Phys-
iology. St. Louis: Mosby, 1998, p. 1\u20131131.
3. Bullock J, Boyle J, and Wang MB. Physiology. Philadelphia:
Williams & Wilkins, 1995, p. 1\u2013641.
FIG. 2.
Factors determining afterload: a flow diagram illustrating the various fac-
tors within the cardiovascular system that determine afterload and there-
fore myocardial wall tension during systole based on the parameters of the
Law of LaPlace: chamber radius, chamber pressure, and wall thickness.
4. Cheitlin MD, Sokolow M, and McIlroy MB. Clinical Cardi-
ology. Norwalk, CT: Appleton & Lange, 1993, p. 1\u2013741.
5. Costanzo LS. Physiology. Philadelphia: Saunders, 1998, p.
6. Ganong WF. Review of Medical Physiology. Stamford, CT:
Appleton & Lange, 1999, p. 1\u2013851.
7. Green JF. Fundamental Cardiovascular and Pulmonary
Physiology. Philadelphia: Lea & Febiger, 1982, p. 1\u2013347.
8. Grossman CJ. Blond\u2019s Medical Guides: Physiology. New
York: Sulzburger & Graham, 1995, p. 1\u2013439.
9. Guyton AC and Hall JE. Textbook of Medical Physiology.
Philadelphia: Saunders, 1996, p. 1\u20131148.
10. Harrison\u2019s Online., 2000.
11. Honig CR. Modern Cardiovascular Physiology. Boston: Little,
Brown and Company, 1988, p. 1\u2013317.
12. Hsu B, Tadlock CH, Assef S, and Percelay J. Physiology: A
Review with Questions and Answers. Boston: Little, Brown
and Company, 1987, p. 1\u2013249.
13. Integrated Medical Curriculum Online. http://www.imc., 2000.
14. Johnson LR. Essential Medical Physiology. Philadelphia: Lip-
pincott-Raven, 1998, p. 1\u2013858.
15. Levick JR. An Introduction to Cardiovascular Physiology.
Oxford, UK: Butterworth-Heinemann, 1995, p. 1\u2013326.
16. Lilly LS. Pathophysiology of Heart Disease. Baltimore, MD:
Williams & Wilkins, 1998, p. 1\u2013401.
17. Lingappa VR and Farey K. Physiological Medicine: A Clini-
cal Approach to Basic Medical Physiology. New York:
McGraw-Hill, 2000, p. 1\u20131008.
18. Little RC and Little WC. Physiology of the Heart and Circu-
lation. Chicago: Year Book Medical, 1989, p. 1\u2013379.
19. McPhee SJ, Lingappa VR, Ganong WF, and Lange JD. Patho-
physiology of Disease: An Introduction to Clinical Medicine.
New York: Lange Medical Books/McGraw-Hill, 2000, p. 1\u2013662.
20. Milnor WR. Cardiovascular Physiology. New York: Oxford
Univ. Press, 1990, p. 1\u2013501.
21. Moffett DF, Moffett SB, and Schauf CL. Human Physiology:
Foundations and Frontiers. St. Louis, MO: Mosby, 1993, p. 1\u2013831.
22. Mohrman DE and Heller LJ. Cardiovascular Physiology.
New York: McGraw-Hill, 1997, p. 1\u2013254.
23. Mountcastle VB. Medical Physiology. St. Louis, MO: Mosby,
1980, p. 951\u20131999.
24. Patton HD, Fuchs AF, Hille B, Scher AM, and Steiner R.
Textbook of Physiology: Circulation, Respiration, Body Flu-
ids, Metabolism, and Endocrinology. Philadelphia: Saunders,
1989, p. 771\u20131596.
25. Richardson DR, Randall DC, and Speck DF. Cardiopulmo-
nary System. Madison, CT: Fence Creek, 1999, p. 1\u2013176.
26. Schmidt RF and Thews G. Human Physiology. Berlin:
Springer-Verlag, 1983, p. 1\u2013725.
27. Sherwood L. Human Physiology: From Cells to Systems.
Belmont, CA: Wadsworth, 1997, p. 1\u2013753.
28. Smith JJ and Kampine JP. Circulatory Physiology\u2013The
Essentials. Baltimore, MD: Williams & Wilkins, 1990, p.
29. Tadlock CH. Physiology: An Illustrated Review With Ques-
tions and Explanations. Boston: Little, Brown and Company,
1996, p. 1\u2013333.
30. Thomas CL. Taber\u2019s Cyclopedic Medical Dictionary. Philadel-
phia: Davis, 1993, p. 1\u20132590.
31. West JB. Physiological Basis of Medical Practice. Baltimore,