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Circulation in muscle during acute pressor responses to emotional stress and during chronic sustained elevation of blood pressure
Annotations
Circulation responses
in muscle to emotional
sustained
elevation
during acute stress and of blood
During transient rises in blood pressure produced by an acute emotional stress, such as asking the subject to carry out simple mental arithmetic at a speed with which he is unable to cope,’ or frightening him about his state of health,2 blood is shifted from the kidneys, splanchnic region, and skin to the skeletal muscles, where a marked vasodilatation takes place. 3,4 Because of these opposite changes in vascular tone, the total peripheral vascular resistance may fall, remain unchanged, or increase, depending on the balance of vasoconstriction and vasodilatation in the various regions of the body. An increase in cardiac output is an integral part of this hemodynamic reaction. Only in those instances in which there is severe visceral vasoconstriction unbalanced by an equal increase in muscular vasodilation does total peripheral vascular resistance rise markedly and cardiac output remain unchanged or decrease, probably on the basis of reflex connections which exist between the peripheral vascular bed and the heart. A similar hemodynamic change accompanied by a rise in blood pressure has been produced in anesthetized cats and dogs by Eliasson and associates,6 who electrically stimulated a zone extending from the anterior margin of the supraoptic region posteriorly throughout the hypothalamus to the level of the mammillary bodies. Abrahams and Hilton” demonstrated the same result in unanesthetized cats with electrodes implanted into the same hypothalamic region; stimulated by a current of low intensity these animals exhibited a behavior pattern reminiscent of the orientation or “what-isit” reaction of Pavlov.7 With a current of higher intensity a typical rage reaction was produced. A similar regional hemodynamic effect can also be elicited by faradic stimulation of the motor cortex.8 Although the visceral vasoconstriction is mediated by adrenergic sympathetic nerves, Folkow and Uvnas8 have established that the vasodilatation in muscles during stimulation of the hypothalamus is potentiated by eserine and abolished by atropine, and concluded that it is mediated by sympathetic cholinergic fibers. Electrophysiologic exploration of the hypothalamus in human beings is, of course, difficult. However, the identity of the efferent pathways mediating the emotional hemodynamic response with those of the response to hypothalamic stimulation
424
pressor during
chronic
pressure
favor an identity of mechanisms of the two reactions: the renal vasoconstriction produced by anxiety can be abolished by the administration of the adrenergic blocking agent Dibenamine.10 Emotional vasodilation in muscle can be at least partly inhibited by stellate-ganglion anesthesia and by intravenous and, especially, intra-arterial atropine injected into the vessels supplying the explored forearm muscles.*Jr This, along with an almost instantaneous onset of emotional vasodilation, at least in some subjects, speaks in favor of a reflex nature and mediation by sympathetic cholinergic fibers. There seems to be, however, a humoral component involved also, judging from a delay period of as much as 35 seconds in some subjects, and also from the incomplete blocking of the vasodilation by atropine, which completely abolished the action of a dose of acetylcholine chosen to produce a vasodilatation that was similar in magnitude to that previously brought on by emotional stress. This humoral agent, probably also active in animals in which section of the sympathetic nerve supply to the muscles does not entirely abolish the vasodilation produced by stimulation of the hypothalamus, is still to be defined, but might be epinephrine, which is liberated by hypothalamic stimulation, the muscular vasodilatory effect of which is well established. Thus, it appears that during emotional stress in human beings the hemodynamic reaction mobilized is the same as that in animals during faradic stimulation of their motor cortex and of a definite zone in the hypothalamus. Moreover, the hemodynamic response bears many analogies to that which accompanies strenuous muscular exercise.‘* That this hemodynamic change is also centrally mediated is suggested by the fact that it was possible to produce the same hemodynamic pattern by verbal suggestion of a strenuous muscular action.13 It seems that the same type of hemodynamic response is elicited whenever the organism is faced with an unknown situation or stimulus which might be potentially dangerous. Under such conditions, not only does the animal explore the stimulus with his sensory organs (“orientation reflex”), but his blood pressure transiently increases, blood flow in the skin drops, and blood is apparently shifted to the muscular parts of the explored extremity.‘r
Annotations
There are, however, some important differences. LVhereas during emotional stress the increase in blood flow in muscle was found to occur simultaneously in all the regions studied, during muscular exercise this increase was limited only to the active regions’s A finding to the contrary-an increase in blood flow in inactive muscle groupslz-has its explanation in the accompanying emotional factor and can be removed by previous trainingI (Brod and Ulrych, unpublished data). Whereas in muscular exercise the enhanced supply of blood to the working muscles subserves their increased metabolic demands, and is accompanied by an increased consumption of oxygen, increased arteriovenous oxygen difference, and increased consumption of glucose, this is not so during emotional hyperemia. Here the consumption of oxygen either changes not at all or increases very slightly, probably as a consequence of the increase in tone, which can be demonstrated by electromyography.‘6 Glucose consumption also does not rise. The increase in blood flow is out of all proportion to the changes (if any) in oxygen consumption, so that the oxygen A-V difference invariably drops.‘? Th&, during emotional stress, the increase in blood flow in muscle occurs independently of any change in oxygen consumption and has obviously a different biologic basis. This is further corroborated by the fact that, whereas the extra blood during muscle exercise flows through muscle capillaries which have opened up at least partly under the influence of the accumulating vasoactive metabolites,‘8 the extra blood during emotional hyperemia seems to flow through functional bypasses excluding the capillary blood bed. This is suggested by the absence of change in the slope of the disappearance curve of K131, injected into the muscle, during the emotional stress, whereas there is a marked steepening of the slope during muscle exercise.lT Also, there is no change in the capillary filtration rate in the muscles during emotion, whereas muscle exercise is connected with an increase in this function (P?erovsk$, Ulrych, Heine, Linhart, Brod, unpublished data), which is obviously dependent, in the lirst place, on the size of the capillary surface, i.e., on the number of the patent capillaries. Although the afferent side of the regulating mechanism, effecting the shift of blood from the skin, kidneys, and splanchnic area during strenuous exercise in man, is not yet firmly established, it seems to be obvious that, with a given volume of blood, the opening of the vascular bed in the working muscles necessitates a closure of some parts of the vascular bed in other regions, if the venous return and cardiac output are to be sustained (or even increased). That this response is coordinated at the cerebral level is suggested by the abovementioned experimental work in which the same response could be elic:*.ed from the motor cortex. Mobilization of the same type of reaction during the rage reaction is-with the foregoing in mindeasily understood: in animals (cats) this reaction accompanies situations of acute threat to life, which have to be faced by tight or flight, i.e., a violent muscular action on which the preservation of life depends. Also, situations connected with the orientation reaction might prove to be threatening
425
therefore, necessitate the same muscular and, mobilization. If the greatest fraction of the cardiac output is diverted to muscle, the animal will have an advantage should the situation prove to be dangerous and should immediate action be required, in contrast to a situation in which blood is pumped to muscle only when the maximum effort has already started. It is only with the development of civilized man that the environment has lost much of its threatening character; however, the “threats to life” have moved to a different plane, and, although visible muscular action is suppressed by social inhibition, life situations which are accompanied by fear, anger, or anxiety still elicit the hemodynamic preparation for violent muscular action which accompanied such subjective feeling throughout thousands of years of phylogenesis. This reaction which prepares the circulation to an optimal efliciency, should muscular action ensue, subsides as soon as the stimulus which produced this hemodynamic response is over. In some normotensive subjects these pressor responses, however, tend to be not only exaggerated but also protracted, and fair evidence exists that these subjects later develop permanent hypertension more frequently than do the “normoreactors.“‘g Since the hemodynamic change in underlying essential hypertension is analogous to that just described during acute pressor reactions,20 the conclusion seems justifiable that the permanent hypertensive state is due to some fixation of this preparatory hemodynamic pattern for muscular action. Whether this “tixation” is due to a “wearing out” of the centralnervous-system coordinating mechanism of this response (in a way analogous to a steel spring which is eventually worn out by frequent use, this analogy applying even to the heredity factor corresponding to the quality of steel) or to some other newly acquired pathology of coordinating mechanisms of the central nervous system or of the effector in the vascular wall has to be established by further research. J. Brod, M.D., D.Sc. Institute for Cardiovascdar Research, Prague 4, Czechoslovakia REFERENCES 1. Brod, J., Fencl, V., Hejl, Z., and Jirka, J.: Circulatory changes underlying blood pressure elevation during acute emotional stress (mental arithmetic) in normotensive and hypertensive subjects, CIin. SC. 18:269, 1959. 2. Blair, D. A., Glover, W. E., Greenfield, A. D. M., and Roddie, I. C.: The activation of cholinergic vasodilator nerves in the human forearm during emotional stress, J. Physiol. (London) 147:278, 1959. 3. Wilkins, R. W., and Eichna, L. W.: Blood flow to the forearm and calf. I. Vasomotor reactions: role of the sympathetic nervous system, Bull. Johns Hopkins Hosp. 68:425, 1941. 4. Golenhofen, K., and Hildebrandt, G.: Psychische Einfliisse auf die Muskeldurchblutung, Pfliiger’s Arch. ges. Physiol. 263:637, 1957. 5. Eliasson, S., Folkow, B., Lindgren, P., and UvnBs, B.: Activation of sympathetic vaso-
426
6.
7.
8.
9.
10.
11.
12.
Am. Heart 1. Sefitember, 196.l
Annotations
dilator nerves lo the slieletal ir~usclcs in the cat by hypothalamic stimulation, Acta physiol. scandinav. 23:333, 19.51. Ahrahams, V. C., and Hilton, S. M.: Defense reactions in the cat elicited by hypothalamic stimulation, J. Physiol. (London) 140:3P, 1958. Pavlov, I. P.: Lektsii o rabote bolshikh polusharii golovnogo mozga, Moskva-Leningrad, 1927, Gosizdat. Green, H. D., and Hoff, E. C.: Effects of faradic stimulation of cerebral cortex on limb and renal volumes in cat and monkey, Am. J. Physiol. 118:641, 1937. Folkow, B., and Hvnais, B.: Do adrenergic vasodilator nerves exist? Acta physiol. scandinav. 20:329, 1950. Brod, J., Fejfar, Z., and Fejfarov& M. H.: The role of neuro-humoral factors in the genesis of renal haemodynamic changes in heart failure, Arta med. scandinav. 148:273, 1954. Barcroft, H., Brod, J., Hejl, Z., Hirsjarvi, E. A., and Kitchin, A. H.: The mechanism of the vasodilatation in the forearm muscle during stress (mental arithmetic), Clin. SC. 19:577, 1960. Fencl, V., Hejl, Z., Jirka, J., and Brod, J.: The relation of the distribution of regional vascular resistances to the level of muscular
Thoughts
concerning
spatial
The Committee on Electrocardiography and Vectorcardiography of the American Heart Association is entrusted with recommending a spatial vectorcardiographic system or systems for physicians to use in communicating their vectorcardiographic findings obtained from cardiac patients. Workers in this field appear to agree that the system(s) to be recommended should rest upon a sound biophysical foundation. At present, several systems derived along this line exist, with certain characteristics differentiating one from the other. Internists who have gained a thorough knowledge of, and had sound experience in, clinical cardiology, cardiac electrophysiology, and the biophysical foundation of vectorcardiographic systems understand that no present system (nor any future ones), no matter how laboriously derived, is clearly better than fellow systems of sound biophysical foundation, nor does any present system, by its own merits, deserve to be the spatial vectorcardiographic system for recommendation. Therefore, members of the Committee, as internists with the aforesaid qualifications, find it truly hard to recommend any system based upon the conventional criteria of selection, such as judges use to decide a *Work from
supported the National
by
U.S.P.H.S.
Heart Institute.
Research
Grant
HE-07695
13.
11.
15.
16. 17.
18.
19.
20.
exercise in healthy subjects, Car et vasa 3:106, 1960. Brad, J.: Essential hypertension. Haemodynamic observations with a bearing on its pathogenesis, Lancet 2:773, 1960. Madlafousek, J.: Orientation reaction as an introductory component of the defensive adaptative equipment of the organism (title translated). Cs. psychol. 1:39, 1957. Blair, D. A., Glover, W. E., and Roddie, J. C.: Vasomotor responses in the human arm during leg exercise, Circulation Res. 9:264, 1961. Von Eiff, A. W. : Klinische Aspekte des Muskeltonus, Med. Grundlagenforsch. 3:65, 1950. Brod, J., Hejl, Z., and Ulrych, M.: Metabolic changes in the forearm muscle and skin during emotional muscular vasodilatation, Clin. Sc. 25:1, 1963. Krogh, A.: The anatomy and physiology of the capillaries, ed. 2, New Haven, 1929, Yale University Press. Hines, E. A., Jr.: The significance of vascular hyperreaction as measured by the cold-pressor test, AM. HEART J. 19:408,1940. Brod, J., Fencl, V., Hejl, Z., Jirka, J., and TJlrych, M.: General and regional haemodynamic pattern underlying essential hypertension, Clin. SC. 23:339, 1962.
VCG systems*
contest. One fact that concerns all is that even in normal healthy man the electrical field on the thoracic wall usually assumes multipolar activity for a significantly long time during the ventricular depolarization. An alternative was to recommend several biophysically founded systems and let the individual physician select the one he preferred. It is true that among these systems there is a certain interchangeability that usually is nonexistent among intuitive systems. But such interchangeability is valid to a certain extent only with normal human subjects. With cardiac patients, however, these biophysical lead systems are practically also not interchangeable in spite of a linear transformation. Obviously, vector loops of different shapes recorded from several systems do not constitute a practical, communicative solution. After profound insight into these matters had been gained, there appeared to be no proper way to recommend any system. Yet there is definitely the need to communicate clinical vectorcardiographic findings under identical description. In true respect for our great teachers, I wish to suggest a system utilizing their famous contributions in vectorcardiography. Einthoven laid the foundation of frontal plane vectorcardiography when, in 1913, he introduced the equilateral tri-
Circulation responses
in muscle to emotional
sustained
elevation
during acute stress and of blood
During transient rises in blood pressure produced by an acute emotional stress, such as asking the subject to carry out simple mental arithmetic at a speed with which he is unable to cope,’ or frightening him about his state of health,2 blood is shifted from the kidneys, splanchnic region, and skin to the skeletal muscles, where a marked vasodilatation takes place. 3,4 Because of these opposite changes in vascular tone, the total peripheral vascular resistance may fall, remain unchanged, or increase, depending on the balance of vasoconstriction and vasodilatation in the various regions of the body. An increase in cardiac output is an integral part of this hemodynamic reaction. Only in those instances in which there is severe visceral vasoconstriction unbalanced by an equal increase in muscular vasodilation does total peripheral vascular resistance rise markedly and cardiac output remain unchanged or decrease, probably on the basis of reflex connections which exist between the peripheral vascular bed and the heart. A similar hemodynamic change accompanied by a rise in blood pressure has been produced in anesthetized cats and dogs by Eliasson and associates,6 who electrically stimulated a zone extending from the anterior margin of the supraoptic region posteriorly throughout the hypothalamus to the level of the mammillary bodies. Abrahams and Hilton” demonstrated the same result in unanesthetized cats with electrodes implanted into the same hypothalamic region; stimulated by a current of low intensity these animals exhibited a behavior pattern reminiscent of the orientation or “what-isit” reaction of Pavlov.7 With a current of higher intensity a typical rage reaction was produced. A similar regional hemodynamic effect can also be elicited by faradic stimulation of the motor cortex.8 Although the visceral vasoconstriction is mediated by adrenergic sympathetic nerves, Folkow and Uvnas8 have established that the vasodilatation in muscles during stimulation of the hypothalamus is potentiated by eserine and abolished by atropine, and concluded that it is mediated by sympathetic cholinergic fibers. Electrophysiologic exploration of the hypothalamus in human beings is, of course, difficult. However, the identity of the efferent pathways mediating the emotional hemodynamic response with those of the response to hypothalamic stimulation
424
pressor during
chronic
pressure
favor an identity of mechanisms of the two reactions: the renal vasoconstriction produced by anxiety can be abolished by the administration of the adrenergic blocking agent Dibenamine.10 Emotional vasodilation in muscle can be at least partly inhibited by stellate-ganglion anesthesia and by intravenous and, especially, intra-arterial atropine injected into the vessels supplying the explored forearm muscles.*Jr This, along with an almost instantaneous onset of emotional vasodilation, at least in some subjects, speaks in favor of a reflex nature and mediation by sympathetic cholinergic fibers. There seems to be, however, a humoral component involved also, judging from a delay period of as much as 35 seconds in some subjects, and also from the incomplete blocking of the vasodilation by atropine, which completely abolished the action of a dose of acetylcholine chosen to produce a vasodilatation that was similar in magnitude to that previously brought on by emotional stress. This humoral agent, probably also active in animals in which section of the sympathetic nerve supply to the muscles does not entirely abolish the vasodilation produced by stimulation of the hypothalamus, is still to be defined, but might be epinephrine, which is liberated by hypothalamic stimulation, the muscular vasodilatory effect of which is well established. Thus, it appears that during emotional stress in human beings the hemodynamic reaction mobilized is the same as that in animals during faradic stimulation of their motor cortex and of a definite zone in the hypothalamus. Moreover, the hemodynamic response bears many analogies to that which accompanies strenuous muscular exercise.‘* That this hemodynamic change is also centrally mediated is suggested by the fact that it was possible to produce the same hemodynamic pattern by verbal suggestion of a strenuous muscular action.13 It seems that the same type of hemodynamic response is elicited whenever the organism is faced with an unknown situation or stimulus which might be potentially dangerous. Under such conditions, not only does the animal explore the stimulus with his sensory organs (“orientation reflex”), but his blood pressure transiently increases, blood flow in the skin drops, and blood is apparently shifted to the muscular parts of the explored extremity.‘r
Annotations
There are, however, some important differences. LVhereas during emotional stress the increase in blood flow in muscle was found to occur simultaneously in all the regions studied, during muscular exercise this increase was limited only to the active regions’s A finding to the contrary-an increase in blood flow in inactive muscle groupslz-has its explanation in the accompanying emotional factor and can be removed by previous trainingI (Brod and Ulrych, unpublished data). Whereas in muscular exercise the enhanced supply of blood to the working muscles subserves their increased metabolic demands, and is accompanied by an increased consumption of oxygen, increased arteriovenous oxygen difference, and increased consumption of glucose, this is not so during emotional hyperemia. Here the consumption of oxygen either changes not at all or increases very slightly, probably as a consequence of the increase in tone, which can be demonstrated by electromyography.‘6 Glucose consumption also does not rise. The increase in blood flow is out of all proportion to the changes (if any) in oxygen consumption, so that the oxygen A-V difference invariably drops.‘? Th&, during emotional stress, the increase in blood flow in muscle occurs independently of any change in oxygen consumption and has obviously a different biologic basis. This is further corroborated by the fact that, whereas the extra blood during muscle exercise flows through muscle capillaries which have opened up at least partly under the influence of the accumulating vasoactive metabolites,‘8 the extra blood during emotional hyperemia seems to flow through functional bypasses excluding the capillary blood bed. This is suggested by the absence of change in the slope of the disappearance curve of K131, injected into the muscle, during the emotional stress, whereas there is a marked steepening of the slope during muscle exercise.lT Also, there is no change in the capillary filtration rate in the muscles during emotion, whereas muscle exercise is connected with an increase in this function (P?erovsk$, Ulrych, Heine, Linhart, Brod, unpublished data), which is obviously dependent, in the lirst place, on the size of the capillary surface, i.e., on the number of the patent capillaries. Although the afferent side of the regulating mechanism, effecting the shift of blood from the skin, kidneys, and splanchnic area during strenuous exercise in man, is not yet firmly established, it seems to be obvious that, with a given volume of blood, the opening of the vascular bed in the working muscles necessitates a closure of some parts of the vascular bed in other regions, if the venous return and cardiac output are to be sustained (or even increased). That this response is coordinated at the cerebral level is suggested by the abovementioned experimental work in which the same response could be elic:*.ed from the motor cortex. Mobilization of the same type of reaction during the rage reaction is-with the foregoing in mindeasily understood: in animals (cats) this reaction accompanies situations of acute threat to life, which have to be faced by tight or flight, i.e., a violent muscular action on which the preservation of life depends. Also, situations connected with the orientation reaction might prove to be threatening
425
therefore, necessitate the same muscular and, mobilization. If the greatest fraction of the cardiac output is diverted to muscle, the animal will have an advantage should the situation prove to be dangerous and should immediate action be required, in contrast to a situation in which blood is pumped to muscle only when the maximum effort has already started. It is only with the development of civilized man that the environment has lost much of its threatening character; however, the “threats to life” have moved to a different plane, and, although visible muscular action is suppressed by social inhibition, life situations which are accompanied by fear, anger, or anxiety still elicit the hemodynamic preparation for violent muscular action which accompanied such subjective feeling throughout thousands of years of phylogenesis. This reaction which prepares the circulation to an optimal efliciency, should muscular action ensue, subsides as soon as the stimulus which produced this hemodynamic response is over. In some normotensive subjects these pressor responses, however, tend to be not only exaggerated but also protracted, and fair evidence exists that these subjects later develop permanent hypertension more frequently than do the “normoreactors.“‘g Since the hemodynamic change in underlying essential hypertension is analogous to that just described during acute pressor reactions,20 the conclusion seems justifiable that the permanent hypertensive state is due to some fixation of this preparatory hemodynamic pattern for muscular action. Whether this “tixation” is due to a “wearing out” of the centralnervous-system coordinating mechanism of this response (in a way analogous to a steel spring which is eventually worn out by frequent use, this analogy applying even to the heredity factor corresponding to the quality of steel) or to some other newly acquired pathology of coordinating mechanisms of the central nervous system or of the effector in the vascular wall has to be established by further research. J. Brod, M.D., D.Sc. Institute for Cardiovascdar Research, Prague 4, Czechoslovakia REFERENCES 1. Brod, J., Fencl, V., Hejl, Z., and Jirka, J.: Circulatory changes underlying blood pressure elevation during acute emotional stress (mental arithmetic) in normotensive and hypertensive subjects, CIin. SC. 18:269, 1959. 2. Blair, D. A., Glover, W. E., Greenfield, A. D. M., and Roddie, I. C.: The activation of cholinergic vasodilator nerves in the human forearm during emotional stress, J. Physiol. (London) 147:278, 1959. 3. Wilkins, R. W., and Eichna, L. W.: Blood flow to the forearm and calf. I. Vasomotor reactions: role of the sympathetic nervous system, Bull. Johns Hopkins Hosp. 68:425, 1941. 4. Golenhofen, K., and Hildebrandt, G.: Psychische Einfliisse auf die Muskeldurchblutung, Pfliiger’s Arch. ges. Physiol. 263:637, 1957. 5. Eliasson, S., Folkow, B., Lindgren, P., and UvnBs, B.: Activation of sympathetic vaso-
426
6.
7.
8.
9.
10.
11.
12.
Am. Heart 1. Sefitember, 196.l
Annotations
dilator nerves lo the slieletal ir~usclcs in the cat by hypothalamic stimulation, Acta physiol. scandinav. 23:333, 19.51. Ahrahams, V. C., and Hilton, S. M.: Defense reactions in the cat elicited by hypothalamic stimulation, J. Physiol. (London) 140:3P, 1958. Pavlov, I. P.: Lektsii o rabote bolshikh polusharii golovnogo mozga, Moskva-Leningrad, 1927, Gosizdat. Green, H. D., and Hoff, E. C.: Effects of faradic stimulation of cerebral cortex on limb and renal volumes in cat and monkey, Am. J. Physiol. 118:641, 1937. Folkow, B., and Hvnais, B.: Do adrenergic vasodilator nerves exist? Acta physiol. scandinav. 20:329, 1950. Brod, J., Fejfar, Z., and Fejfarov& M. H.: The role of neuro-humoral factors in the genesis of renal haemodynamic changes in heart failure, Arta med. scandinav. 148:273, 1954. Barcroft, H., Brod, J., Hejl, Z., Hirsjarvi, E. A., and Kitchin, A. H.: The mechanism of the vasodilatation in the forearm muscle during stress (mental arithmetic), Clin. SC. 19:577, 1960. Fencl, V., Hejl, Z., Jirka, J., and Brod, J.: The relation of the distribution of regional vascular resistances to the level of muscular
Thoughts
concerning
spatial
The Committee on Electrocardiography and Vectorcardiography of the American Heart Association is entrusted with recommending a spatial vectorcardiographic system or systems for physicians to use in communicating their vectorcardiographic findings obtained from cardiac patients. Workers in this field appear to agree that the system(s) to be recommended should rest upon a sound biophysical foundation. At present, several systems derived along this line exist, with certain characteristics differentiating one from the other. Internists who have gained a thorough knowledge of, and had sound experience in, clinical cardiology, cardiac electrophysiology, and the biophysical foundation of vectorcardiographic systems understand that no present system (nor any future ones), no matter how laboriously derived, is clearly better than fellow systems of sound biophysical foundation, nor does any present system, by its own merits, deserve to be the spatial vectorcardiographic system for recommendation. Therefore, members of the Committee, as internists with the aforesaid qualifications, find it truly hard to recommend any system based upon the conventional criteria of selection, such as judges use to decide a *Work from
supported the National
by
U.S.P.H.S.
Heart Institute.
Research
Grant
HE-07695
13.
11.
15.
16. 17.
18.
19.
20.
exercise in healthy subjects, Car et vasa 3:106, 1960. Brad, J.: Essential hypertension. Haemodynamic observations with a bearing on its pathogenesis, Lancet 2:773, 1960. Madlafousek, J.: Orientation reaction as an introductory component of the defensive adaptative equipment of the organism (title translated). Cs. psychol. 1:39, 1957. Blair, D. A., Glover, W. E., and Roddie, J. C.: Vasomotor responses in the human arm during leg exercise, Circulation Res. 9:264, 1961. Von Eiff, A. W. : Klinische Aspekte des Muskeltonus, Med. Grundlagenforsch. 3:65, 1950. Brod, J., Hejl, Z., and Ulrych, M.: Metabolic changes in the forearm muscle and skin during emotional muscular vasodilatation, Clin. Sc. 25:1, 1963. Krogh, A.: The anatomy and physiology of the capillaries, ed. 2, New Haven, 1929, Yale University Press. Hines, E. A., Jr.: The significance of vascular hyperreaction as measured by the cold-pressor test, AM. HEART J. 19:408,1940. Brod, J., Fencl, V., Hejl, Z., Jirka, J., and TJlrych, M.: General and regional haemodynamic pattern underlying essential hypertension, Clin. SC. 23:339, 1962.
VCG systems*
contest. One fact that concerns all is that even in normal healthy man the electrical field on the thoracic wall usually assumes multipolar activity for a significantly long time during the ventricular depolarization. An alternative was to recommend several biophysically founded systems and let the individual physician select the one he preferred. It is true that among these systems there is a certain interchangeability that usually is nonexistent among intuitive systems. But such interchangeability is valid to a certain extent only with normal human subjects. With cardiac patients, however, these biophysical lead systems are practically also not interchangeable in spite of a linear transformation. Obviously, vector loops of different shapes recorded from several systems do not constitute a practical, communicative solution. After profound insight into these matters had been gained, there appeared to be no proper way to recommend any system. Yet there is definitely the need to communicate clinical vectorcardiographic findings under identical description. In true respect for our great teachers, I wish to suggest a system utilizing their famous contributions in vectorcardiography. Einthoven laid the foundation of frontal plane vectorcardiography when, in 1913, he introduced the equilateral tri-