- Email: [email protected]
Venous pressure responses to exercise
VENOUS
PRESSURE
RESPONSES
TO EXERCISE
T
HE main reason why measurement of the venous blood pressure is not adapted to routine clinical use is that the results obtained by the usual technique are not sufficienbly reliable to be of great clinical importance. Venous pressure readings on normal persons, as recorded by different authors, show a midc variation. The range of this variation is still greater when different methods are compared. In many casesof heart disease with decreased functional capacit,y of the cardiovascular system, the venous pressure at rest is within normal limits, and it rises only when there is clinical evidrncc of congestive heart failure. Certain American authors’ stated recently that, in their experience, venous pressure mcasut’ements have been of little diagnostic aid in borderline cases of congestive heart failure. For this reason, efforts have becm made to devise a method of measing the venous pressure during and aft,cr bodily exercise, in order to obtain a more reliable evaluation of the ~~athoph~siolo~ic events in the cardiovenous system. Venous pressure responses to exercise have been investigated by Hooker,2 Sellott,,” Villaret, and others,4, ’ Bedford and \\‘right,6 White, Rarker, and Allen,7 Schneider and Collins,s and, rcccntly, by Nienwenhuizen.!’ All these authors obscrvcd a rise of venous pressure mit,h muscular exertion which lasted usually throughout the whole period of the activity. Whitr, Ha~kcr, and Allen’ found in normal subjects that the venous pressure row a few ccntimetc~ts of water dilring csercisc. It fell to, or lwlow. the cwntrol lcvcl immediately on cessation of the exercise. Subjects with con:estivc heart failure had a high resting venous pressure, which rose considerably on exercise and did not rcturn to normal when it ceased. Nicnwenhuizen” followed the venous pressure for ten minutes aftc>r wcrciw, and arrived at the conclusion Ihat in normal subjects the x-cnous l)rrss~~re falls to its resting level within fifteen seconds after exercise. He oljserved in cases of slight rongestive heart failure that, thr restin,n value was normal, and that only the response IO exercise betrayed tho patholonic condition. This preliminary report is based ~lpon 1’22 csercise test,s on eight,y patients. The group, is small! and the ljurposc of this article is not to From the Cardiac Clinic of the Media1 Faculty of Pal’ia. Received for publication Jan. 4, 1941. 320
S%RKEI,Y
:
VENOCS
I’KIWSVKE
RESI’ONSES
TO
ESICKCISE
361
draw conclusions, but to record our observations. We believe t,hat the results we obtained may bc of interest and value for furt,hcr investigations. METHOD
We employed the air-filled system, with an aneroid manometer. This method is suitable for clinical use, and even for serial measurements lasting some minutes, when technical precautions are strictly maintainell. For details of the technique, reference shoultl he made to the works of Villaret, ant1 others,lo anI1 Bedford and Wright.” After having ascertained the resting value, the subject was tolcl to raise, successively, the right and left leg ten times each, keeping the upper part of the hotly as still as possible. The venous pressure ~VRR taken immetliately on cessation of the exercise, and then thirty seconds, and one, two, and three minutes after it ceased. In this way a venous pressure curve consisting of six readings was obtained. In some cases, the communication between manometer and vein was maintaine,d during the whole experiment, even during exercise, and the readings so taken were compared with those obtained on the same subjects when communication hall been interrupted, and restoretl only at the moment of the measurements. No differences were found. The needle, the metal nozzle, am1 the short piece of rubber tubing were syringed with 3.8 per cent sodium citrate solution just before the experiment, in order to avoid blo0.d coagulation. The bloocl usually remainetl fluid until the end of the esperimerit (four to five minutes) ; if it (lit1 not, which happenetl very rarely, the results were rejected. RESUI,TS
In eight cases, in which there was neither clinical nor electrocardiographic evidence of heart disease, the resting venous pressure was normal (from 6 to 12 cm. of water j. It rose about 2 to 5 cm. of water during exercise, and returned to the basal level wit,hin thirty seconds after exercise was stopped (see Fig. 1 j. These observations are in agreement with those of White, Barker, and ,411eq7 and Nieuwenhuizen.g
2@3
Time in minutes Fig.
l.-Normal
venous
pressure
response
to
exercise.
In thirty-eight out of fifty-four cases (70.3 per cent! in which there was clinical evidence of congestive heart failure, the resting venous
362
THE:
AMERICAS
HEART
.JOlJRSAI>
pressure was increased (above 12 cm. of water), and the response to exercise was a pathologic one, irrcspec+ivc of the nnturc of the cardiac disease. The venous pressure ~howcd a grcat,cr rise tlnring excrcisc, and it either retnrncd to t,hc initial level more slowlp than in normal subjects, or not at all (luring the period of observation. In twelve of the sixteen cases of this group in which the resting values wcrc normal, the venous pressure curve after esercise was pat,hologic in the sense mentioned above, which was in keeping with the clinical evidence of venous engorgement . In four cases, both the restin? value and that after exercise were wit,hin normal limits. Of eighteen patienis with heart disease without any clinical evidence of congestive heart failure ad with a normal ~c11011~ pressure at rest, eight exhibited a normal response to exercise. If1 the remaining ten cases, the venous pressure rose considerably during exercise and fell below the initial level after it. This fall of the venous pressure after exercise has been noted by Nieuwenhuizen,” who explained it as a regulative mechanism. He stated that this kind of response may indicate latent congestive heart failure. In our experience, auricular fibrillation, per SC, does not alter t,he In our cases of auricular fibrillation, the venous presvenous pressure. sure was increased only when the fibrillation was associated with congestive heart failure. Howcvcr, in cases of auricular flutt,er the venous pressure seemed to he rather subject to pathologic allerations. It is difficult to explain this ohserration. The question whether the mechanism of auricular flutter, per se, is able to alter one or more factors which are responsible for the maintenance of normal peripheral venous pressure requires further investigation. II 1LTXTR ,
‘ \TIVE
CASES
CASE 1.-L. p. was a man, aged 60, Who hall heart SoUnds of poor quality and a presystolic gallop rhythm. His blood pressure was I90/100. There was no evidence the left ventricle was enlarged. The of venous engorgement. Roentgenologically, The blood Wassermann reelectrocardiogram showed complete A-V heart block. The venous pressure was normal at rest, and fell below the action was negative. complete heart block, probably initial level after exerc.ise (Fig. 2). Diagnoses: caused by coronary sclerosis ; no clinical signs of congestive heart failure; venous pressure normal at rest, with a pathologic response to exercise which may have intlicatad a decrease in the functional capacity of the cardiovenous system. CASE Z.-M. S. was a woman, 40 years of age, who had the auscultatory signs of mitral stenosis and aortic incompetence. Her pulse was irregular. The blood pressure measured 110/50. There was venous engorgement in the neck, rbles were heard over the basal portions of the lungs, the liver was siightly enlarged, and there was slight edema of the lower extremities. Roent,genologic examination showed that the The electrocardiogram revealed auricular fibrillaheart was symmetrically enlarged. tion and low voltage of the QRS complexes. The venous pressure at rest was slightly above normal ; it showed a pronounced rise during exercise, and did not return to the initial level until three minutes after exercise (Fig. 3). Diagnoses: rheumatic
SZEKEI,Y mitral failure. ment.
stenosis and The venous
:
VENOUS
PRESSURE
aortic incompetence, pressure readings
and
RESPONSES
363
TO EXERCISE
with clinical signs of clinical manifestations
congestive were in
heart agree-
2a
14
$0
S in minutes
Time Fig.
Time in Fig.
2.
Pathologic response Fig. Z.-Normal venous pressure at rest. nounced rise and fall below the initial level. Fig. 3.-Slightly increased venous pressure at rest. No return Evident pathologic response to exercise. until three minutes.
minutes 3. to
exercise
to the
initial
; prolevel
Time in mlnutee Fig.
4.-Normal
venous
pressure
curve rhythm
both during fibrillation (dotted line).
(solid
line)
and
sinus
CASE 3.-J. E. was a 39-year-old man who had auricular fibrillation without any There were no signs of congestive heart failure. The evidence of a valvular lesion. Roentgenologically, the heart was normal in size and blood pressure was 120/80. shape. The electrocardiogram showed auricular fibrillation, with normal ventricular complexes. The administration of quinidine abolished the auricular fibrillation. The venous pressure curve was normal both when he ha.d fibrillation and after normal auricular fibrillation of unsinus rhythm hatl been restored (Fig. 4). Diagnoses: pertain etiology ; no calinicaal rvi~lenw of congest,ire heart failure; normal venous pressure.
(“ME i 4 .-J. G ., a 45.year-old man, tions of congestive heart failure.
bad The
auricular flutter blood pressure
and no clinical was 115/80.
manifestaRoentgeno-
364
THE
AMERICAN
HEART
JOURNAL
logically, tile heart wa,s nonwtl. An electroc~artlioglam which mas made after cessawith T-ware inversion in the tion of the auricular flutter showed sinus rhythm, standard leads. The details of the venous pressure measurements are shown in auricular flutter, probably caused by coronary Fig. 5. Diagnosis : l~aroxyswal artery disease. The venous prwsure was abnormally high at rest when flutter was present, and showed a pathologic response to exercise; after sinus rhythm became rr-established the resting value was normal, ant1 the response to exercise was nearly normal.
3
Time in minutes Fig.
S.-Pathologic normal
venous venous
pressure pressure
curve curve
during during
auricular flutter (solid sinus rhythm (dotted
line). line).
Nearly
DISCUSSION
It is well known that exercise is accompanied by an elevation of the venous pressure. It may be emphasized that the degree of this elevation and the time necessary for the venous pressure to return to its basal level after exercise seem to be important factors in evaluating the functional capacity of t,he cardiovenous system. In our normal subjects there was only a slight rise in venous pressure during exercise (about 1 to 4 cm. of water), and it reached its initial level within thirty seconds after (~scrrise and ncvt>r fell below it,. In some cases of heart cliseasr without any clinical signs of congestive heart failure, the resting value was within normal limits, but in
SZEKELY
:
VENOUS
PRESSURE
RESPONSES
TO
EXERCISE
365
the exercise experiment, after a rise oC sercral centimeters of wat,er, the venous pressure dropped below the initial lcrel. Whit.e, Barker, and Allen’ and Nieuwenhuizen” found that there was a slight fall below the basal level after exercise, not exceedin? 1.5 em. of water (Nieuwenhuizen), even in healthy young people. A greater fall below the original level was considered bp Nieuwenhuizm as a pathologic reaction, and our observations support I his view. It is open to question whether the fall of venous pressure below the initial lcrcl after exercise is due more to retrograde influences from the heart, than to temporary changes in peripheral vascular tonus. Hooker” stated that local changes in vascular tonus caused no noticeable changes in venous pressure, and he concluded that VC~OUS pressure is normally independent. of periphcral vascular resistence. The peripheral venous pressure is independent of factors affecting the peripheral vascular system or the blood flow therein, provided the heart, is fully compet,ent: as has been pointed On the other hand, it is difficult to out by lsystu and Middlcton.12 regard this fall of the venous pressure below the initial level after esercise as the result purely of’ some cardiac fador. We have observed it, however, only in cases of heart disease without, clinical evidence of congestive failure. We believe that this response of the VC~LOLLS pressure to exercise may be explained by a decrease of the venous tonus in the presence of potential cardiac insufficiency. In cases in which there was clinical evidence of congestive heart failure, the resting value was usually high, there was A considerable rise on exertion, and it took a longer time to return to the initial level than in normal subjects. SUMMARY
The venous pressure, if measured only once, with the patient at rest, gives no satisfactory clinical information. The results of measuring the venous pressure during and after exercise enable one t,o make a more reliable evaluat,ion of t,he functional capacity of the cardiovenous system. The air-filled system for measuring the venous pressure with an aneroid manometer is a sound method, and is reliable enough for routine clinical use when technical precautions are strict. The different types of venous pressure curves which were obtained in the exercise experiments are discussed. I wish to express my gratitude to Professor Laubry, for his constant help and suggestions in the preparation Rire to thank Dr. John Parkinson of London, England, script and made many suggestions for its improvement.
Head of the Cardiac Clinic, of this paper. I also dewho kindly read the nmnu-
REFERENCES
1. Lyons, R. H., Kennedy, J. H., and Pressure by the Direct Method,
Burwell, AM.
C. J.: HEART
J.
The 16:
Measurement 675,
1938.
of Venous
366
THE
AMERICAS
HEART
JOURNAT,
2. Hooker, D. H.: The Effect of Exercise Upon the Venous Blew1 Pressure, Am. J. Phvsial. 28: 23.5. 1911. 3. Schott,~ E. : Die Erhiihung ties Druckes im veniisen System hri hnstrengung als Mass fiir die Funktionstiichtigkeit des menschlichen IIerzens. Deutsches Arch. f. klin. Me,d. 108: 537, 1915: 4. Villaret, M., Saint Girons,, Fr.! and Grellety-Bosviel, P.: La. tension veineuse peripherique et ses modificatmns pathologiques, Presse m&l. 31: 318, 1923. La Pression veineuse 3. Villaret, M., Saint Girons, I+., and Justin-Besanpon, L.: peripherique, Paris. 1Iasson et Cir. 1930. 6. Bedford, D. E., and Wright, K.: Observations on the Venous Pressure in Normal Individuals, Lanret 2: 106, 1924. 7. White, H. L., Barker, P. S., ant1 Allen, D. S.: Venous Pressure Responses to Exercise in Patients With Heart Disease, &I. HF.~~T J. 1: 160, 1935. Venous Pressure Responses to Exercise, Am. 8. Schneider, E. C., and Collins, R.: J. Physiol. 121: 574, 193X. 9. Nieuwenhuizen, C. L. (1.: Der veniise Blutdruck narh Arbeitsleistung. Eine Funktionspriifung der Zirkulation, Acta Med. Scand. 103: 171, 1946. 10. Villaret,, M., Saint Girons, Fr., and Guillaume, J.: Contrihution L l’etude clinique de la tension veineuse. Technique et premiers rbsultats, Compt. rend. Sot. de biol. 84: 80, 1921. 11. Hooker, D. R.: Observations on the Venous Blootl Pressure in Man, Am. J. Physiol. 35: 73, 1914, 12. Eyster, J. A. E., and Middleton, W. S.: Clinical Studies in Venous Pressure, Arc.h. Int. Med. 34: 228, 1924. 13. Olmer, D., Jouve, A. X., and Vague, J.: Une Cpreuvr fonct,ionnelle Ile la cirrulation de retour, Pressr m&l. 2: 1233, 1938.
PRESSURE
RESPONSES
TO EXERCISE
T
HE main reason why measurement of the venous blood pressure is not adapted to routine clinical use is that the results obtained by the usual technique are not sufficienbly reliable to be of great clinical importance. Venous pressure readings on normal persons, as recorded by different authors, show a midc variation. The range of this variation is still greater when different methods are compared. In many casesof heart disease with decreased functional capacit,y of the cardiovascular system, the venous pressure at rest is within normal limits, and it rises only when there is clinical evidrncc of congestive heart failure. Certain American authors’ stated recently that, in their experience, venous pressure mcasut’ements have been of little diagnostic aid in borderline cases of congestive heart failure. For this reason, efforts have becm made to devise a method of measing the venous pressure during and aft,cr bodily exercise, in order to obtain a more reliable evaluation of the ~~athoph~siolo~ic events in the cardiovenous system. Venous pressure responses to exercise have been investigated by Hooker,2 Sellott,,” Villaret, and others,4, ’ Bedford and \\‘right,6 White, Rarker, and Allen,7 Schneider and Collins,s and, rcccntly, by Nienwenhuizen.!’ All these authors obscrvcd a rise of venous pressure mit,h muscular exertion which lasted usually throughout the whole period of the activity. Whitr, Ha~kcr, and Allen’ found in normal subjects that the venous pressure row a few ccntimetc~ts of water dilring csercisc. It fell to, or lwlow. the cwntrol lcvcl immediately on cessation of the exercise. Subjects with con:estivc heart failure had a high resting venous pressure, which rose considerably on exercise and did not rcturn to normal when it ceased. Nicnwenhuizen” followed the venous pressure for ten minutes aftc>r wcrciw, and arrived at the conclusion Ihat in normal subjects the x-cnous l)rrss~~re falls to its resting level within fifteen seconds after exercise. He oljserved in cases of slight rongestive heart failure that, thr restin,n value was normal, and that only the response IO exercise betrayed tho patholonic condition. This preliminary report is based ~lpon 1’22 csercise test,s on eight,y patients. The group, is small! and the ljurposc of this article is not to From the Cardiac Clinic of the Media1 Faculty of Pal’ia. Received for publication Jan. 4, 1941. 320
S%RKEI,Y
:
VENOCS
I’KIWSVKE
RESI’ONSES
TO
ESICKCISE
361
draw conclusions, but to record our observations. We believe t,hat the results we obtained may bc of interest and value for furt,hcr investigations. METHOD
We employed the air-filled system, with an aneroid manometer. This method is suitable for clinical use, and even for serial measurements lasting some minutes, when technical precautions are strictly maintainell. For details of the technique, reference shoultl he made to the works of Villaret, ant1 others,lo anI1 Bedford and Wright.” After having ascertained the resting value, the subject was tolcl to raise, successively, the right and left leg ten times each, keeping the upper part of the hotly as still as possible. The venous pressure ~VRR taken immetliately on cessation of the exercise, and then thirty seconds, and one, two, and three minutes after it ceased. In this way a venous pressure curve consisting of six readings was obtained. In some cases, the communication between manometer and vein was maintaine,d during the whole experiment, even during exercise, and the readings so taken were compared with those obtained on the same subjects when communication hall been interrupted, and restoretl only at the moment of the measurements. No differences were found. The needle, the metal nozzle, am1 the short piece of rubber tubing were syringed with 3.8 per cent sodium citrate solution just before the experiment, in order to avoid blo0.d coagulation. The bloocl usually remainetl fluid until the end of the esperimerit (four to five minutes) ; if it (lit1 not, which happenetl very rarely, the results were rejected. RESUI,TS
In eight cases, in which there was neither clinical nor electrocardiographic evidence of heart disease, the resting venous pressure was normal (from 6 to 12 cm. of water j. It rose about 2 to 5 cm. of water during exercise, and returned to the basal level wit,hin thirty seconds after exercise was stopped (see Fig. 1 j. These observations are in agreement with those of White, Barker, and ,411eq7 and Nieuwenhuizen.g
2@3
Time in minutes Fig.
l.-Normal
venous
pressure
response
to
exercise.
In thirty-eight out of fifty-four cases (70.3 per cent! in which there was clinical evidence of congestive heart failure, the resting venous
362
THE:
AMERICAS
HEART
.JOlJRSAI>
pressure was increased (above 12 cm. of water), and the response to exercise was a pathologic one, irrcspec+ivc of the nnturc of the cardiac disease. The venous pressure ~howcd a grcat,cr rise tlnring excrcisc, and it either retnrncd to t,hc initial level more slowlp than in normal subjects, or not at all (luring the period of observation. In twelve of the sixteen cases of this group in which the resting values wcrc normal, the venous pressure curve after esercise was pat,hologic in the sense mentioned above, which was in keeping with the clinical evidence of venous engorgement . In four cases, both the restin? value and that after exercise were wit,hin normal limits. Of eighteen patienis with heart disease without any clinical evidence of congestive heart failure ad with a normal ~c11011~ pressure at rest, eight exhibited a normal response to exercise. If1 the remaining ten cases, the venous pressure rose considerably during exercise and fell below the initial level after it. This fall of the venous pressure after exercise has been noted by Nieuwenhuizen,” who explained it as a regulative mechanism. He stated that this kind of response may indicate latent congestive heart failure. In our experience, auricular fibrillation, per SC, does not alter t,he In our cases of auricular fibrillation, the venous presvenous pressure. sure was increased only when the fibrillation was associated with congestive heart failure. Howcvcr, in cases of auricular flutt,er the venous pressure seemed to he rather subject to pathologic allerations. It is difficult to explain this ohserration. The question whether the mechanism of auricular flutter, per se, is able to alter one or more factors which are responsible for the maintenance of normal peripheral venous pressure requires further investigation. II 1LTXTR ,
‘ \TIVE
CASES
CASE 1.-L. p. was a man, aged 60, Who hall heart SoUnds of poor quality and a presystolic gallop rhythm. His blood pressure was I90/100. There was no evidence the left ventricle was enlarged. The of venous engorgement. Roentgenologically, The blood Wassermann reelectrocardiogram showed complete A-V heart block. The venous pressure was normal at rest, and fell below the action was negative. complete heart block, probably initial level after exerc.ise (Fig. 2). Diagnoses: caused by coronary sclerosis ; no clinical signs of congestive heart failure; venous pressure normal at rest, with a pathologic response to exercise which may have intlicatad a decrease in the functional capacity of the cardiovenous system. CASE Z.-M. S. was a woman, 40 years of age, who had the auscultatory signs of mitral stenosis and aortic incompetence. Her pulse was irregular. The blood pressure measured 110/50. There was venous engorgement in the neck, rbles were heard over the basal portions of the lungs, the liver was siightly enlarged, and there was slight edema of the lower extremities. Roent,genologic examination showed that the The electrocardiogram revealed auricular fibrillaheart was symmetrically enlarged. tion and low voltage of the QRS complexes. The venous pressure at rest was slightly above normal ; it showed a pronounced rise during exercise, and did not return to the initial level until three minutes after exercise (Fig. 3). Diagnoses: rheumatic
SZEKEI,Y mitral failure. ment.
stenosis and The venous
:
VENOUS
PRESSURE
aortic incompetence, pressure readings
and
RESPONSES
363
TO EXERCISE
with clinical signs of clinical manifestations
congestive were in
heart agree-
2a
14
$0
S in minutes
Time Fig.
Time in Fig.
2.
Pathologic response Fig. Z.-Normal venous pressure at rest. nounced rise and fall below the initial level. Fig. 3.-Slightly increased venous pressure at rest. No return Evident pathologic response to exercise. until three minutes.
minutes 3. to
exercise
to the
initial
; prolevel
Time in mlnutee Fig.
4.-Normal
venous
pressure
curve rhythm
both during fibrillation (dotted line).
(solid
line)
and
sinus
CASE 3.-J. E. was a 39-year-old man who had auricular fibrillation without any There were no signs of congestive heart failure. The evidence of a valvular lesion. Roentgenologically, the heart was normal in size and blood pressure was 120/80. shape. The electrocardiogram showed auricular fibrillation, with normal ventricular complexes. The administration of quinidine abolished the auricular fibrillation. The venous pressure curve was normal both when he ha.d fibrillation and after normal auricular fibrillation of unsinus rhythm hatl been restored (Fig. 4). Diagnoses: pertain etiology ; no calinicaal rvi~lenw of congest,ire heart failure; normal venous pressure.
(“ME i 4 .-J. G ., a 45.year-old man, tions of congestive heart failure.
bad The
auricular flutter blood pressure
and no clinical was 115/80.
manifestaRoentgeno-
364
THE
AMERICAN
HEART
JOURNAL
logically, tile heart wa,s nonwtl. An electroc~artlioglam which mas made after cessawith T-ware inversion in the tion of the auricular flutter showed sinus rhythm, standard leads. The details of the venous pressure measurements are shown in auricular flutter, probably caused by coronary Fig. 5. Diagnosis : l~aroxyswal artery disease. The venous prwsure was abnormally high at rest when flutter was present, and showed a pathologic response to exercise; after sinus rhythm became rr-established the resting value was normal, ant1 the response to exercise was nearly normal.
3
Time in minutes Fig.
S.-Pathologic normal
venous venous
pressure pressure
curve curve
during during
auricular flutter (solid sinus rhythm (dotted
line). line).
Nearly
DISCUSSION
It is well known that exercise is accompanied by an elevation of the venous pressure. It may be emphasized that the degree of this elevation and the time necessary for the venous pressure to return to its basal level after exercise seem to be important factors in evaluating the functional capacity of t,he cardiovenous system. In our normal subjects there was only a slight rise in venous pressure during exercise (about 1 to 4 cm. of water), and it reached its initial level within thirty seconds after (~scrrise and ncvt>r fell below it,. In some cases of heart cliseasr without any clinical signs of congestive heart failure, the resting value was within normal limits, but in
SZEKELY
:
VENOUS
PRESSURE
RESPONSES
TO
EXERCISE
365
the exercise experiment, after a rise oC sercral centimeters of wat,er, the venous pressure dropped below the initial lcrel. Whit.e, Barker, and Allen’ and Nieuwenhuizen” found that there was a slight fall below the basal level after exercise, not exceedin? 1.5 em. of water (Nieuwenhuizen), even in healthy young people. A greater fall below the original level was considered bp Nieuwenhuizm as a pathologic reaction, and our observations support I his view. It is open to question whether the fall of venous pressure below the initial lcrcl after exercise is due more to retrograde influences from the heart, than to temporary changes in peripheral vascular tonus. Hooker” stated that local changes in vascular tonus caused no noticeable changes in venous pressure, and he concluded that VC~OUS pressure is normally independent. of periphcral vascular resistence. The peripheral venous pressure is independent of factors affecting the peripheral vascular system or the blood flow therein, provided the heart, is fully compet,ent: as has been pointed On the other hand, it is difficult to out by lsystu and Middlcton.12 regard this fall of the venous pressure below the initial level after esercise as the result purely of’ some cardiac fador. We have observed it, however, only in cases of heart disease without, clinical evidence of congestive failure. We believe that this response of the VC~LOLLS pressure to exercise may be explained by a decrease of the venous tonus in the presence of potential cardiac insufficiency. In cases in which there was clinical evidence of congestive heart failure, the resting value was usually high, there was A considerable rise on exertion, and it took a longer time to return to the initial level than in normal subjects. SUMMARY
The venous pressure, if measured only once, with the patient at rest, gives no satisfactory clinical information. The results of measuring the venous pressure during and after exercise enable one t,o make a more reliable evaluat,ion of t,he functional capacity of the cardiovenous system. The air-filled system for measuring the venous pressure with an aneroid manometer is a sound method, and is reliable enough for routine clinical use when technical precautions are strict. The different types of venous pressure curves which were obtained in the exercise experiments are discussed. I wish to express my gratitude to Professor Laubry, for his constant help and suggestions in the preparation Rire to thank Dr. John Parkinson of London, England, script and made many suggestions for its improvement.
Head of the Cardiac Clinic, of this paper. I also dewho kindly read the nmnu-
REFERENCES
1. Lyons, R. H., Kennedy, J. H., and Pressure by the Direct Method,
Burwell, AM.
C. J.: HEART
J.
The 16:
Measurement 675,
1938.
of Venous
366
THE
AMERICAS
HEART
JOURNAT,
2. Hooker, D. H.: The Effect of Exercise Upon the Venous Blew1 Pressure, Am. J. Phvsial. 28: 23.5. 1911. 3. Schott,~ E. : Die Erhiihung ties Druckes im veniisen System hri hnstrengung als Mass fiir die Funktionstiichtigkeit des menschlichen IIerzens. Deutsches Arch. f. klin. Me,d. 108: 537, 1915: 4. Villaret, M., Saint Girons,, Fr.! and Grellety-Bosviel, P.: La. tension veineuse peripherique et ses modificatmns pathologiques, Presse m&l. 31: 318, 1923. La Pression veineuse 3. Villaret, M., Saint Girons, I+., and Justin-Besanpon, L.: peripherique, Paris. 1Iasson et Cir. 1930. 6. Bedford, D. E., and Wright, K.: Observations on the Venous Pressure in Normal Individuals, Lanret 2: 106, 1924. 7. White, H. L., Barker, P. S., ant1 Allen, D. S.: Venous Pressure Responses to Exercise in Patients With Heart Disease, &I. HF.~~T J. 1: 160, 1935. Venous Pressure Responses to Exercise, Am. 8. Schneider, E. C., and Collins, R.: J. Physiol. 121: 574, 193X. 9. Nieuwenhuizen, C. L. (1.: Der veniise Blutdruck narh Arbeitsleistung. Eine Funktionspriifung der Zirkulation, Acta Med. Scand. 103: 171, 1946. 10. Villaret,, M., Saint Girons, Fr., and Guillaume, J.: Contrihution L l’etude clinique de la tension veineuse. Technique et premiers rbsultats, Compt. rend. Sot. de biol. 84: 80, 1921. 11. Hooker, D. R.: Observations on the Venous Blootl Pressure in Man, Am. J. Physiol. 35: 73, 1914, 12. Eyster, J. A. E., and Middleton, W. S.: Clinical Studies in Venous Pressure, Arc.h. Int. Med. 34: 228, 1924. 13. Olmer, D., Jouve, A. X., and Vague, J.: Une Cpreuvr fonct,ionnelle Ile la cirrulation de retour, Pressr m&l. 2: 1233, 1938.