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Blood flow in the internal mammary artery
Annotations
Theoretic considerations of the “dip” of constrictive pericarditis
Following its original description in 1946,’ various explanations have been offered for the presence of the post-systolic “dip” (Fig. 1) seen in pressure tracings recorded from the cavity of the right ventricle of patients with chronic constrictive pericarditis. It has been suggested that the “dip” is an artifact produced by a low frequency recording apparatus,2 but the pattern has been found consistently in patients with constrictive pericarditis since high frequency recording equipment has become available. Another explanation for the presence of the diastolic “dip” is that it represents an actual cardiodynamic eventsId-i.e., because the ventricles are completely empty at the end of systole and the atria1 pressure is high, rapid ventricular filling takes place which is abruptly terminated by the thickened pericardium. However, this theory does not explain why the ventricular relaxation is not isometric with time. Although the possibility of elastic recoil of the thickened pericardium and chest wall has been mentioned by some,5 a precise mechanism has not been offered. We believe that a sudden to rather abrupt elastic recoil of the distorted (during systole) thickened pericardium when the ventricle rather suddenly relaxes is responsible for the diastolic “dip” in constrictive pericarditis and we, therefore, offer the following hypothesis. The heart in constrictive pericarditis is encased in a thick shell of fibrous connective tissue, with or without calcium, which is fixed to and, therefore, a part of the ventricular wall. Thus, when the ventricle contracts, work is performed on this thick wall which deforms in much the same manner as when one “loads” a spring. Following termination of myocardial contraction and with the sudden “unloading” of the distorted fibrous pericardium with the onset of diastole, the ventricular wall abruptly springs back into “place,” suddenly reducing intracavitary pressure, thereby literally “sucking” blood from the atrium into the ventricle. This recoil of the ventricular wall results in the rapid fall in ventricular pressure which is responsible for the ventricular diastolic “dip” recorded in the intracavitary pressure tracing. The ventricle fills rapidly and therefore an early plateau of the right ventricular pressure tracing is seen (Fig. 1). Supporting evidence for this concept is seen in experimental cardiac tamponade produced with air or fluid. In such a situation the fluid or air in the pericardinl cavity is not fixed to the myocardial wall even though diastolic filling of the ventricle is re-
post-systolic
Fig. 1. Time course showing post-systolic
of right ventricular pressure dip in constrictive pericarditis.
stricted. Thus, during systole there is no “physiologic spring” to “load,” nor is there one to suddenly “unload” during the early phase of diastole. Under such circumstances, therefore, the characteristic “dip ‘I6 in right ventricular pressure is not expected nor recorded.’ Parenthetically, it may be noted that the work performed in deforming the pericardium in constrictive pericarditis is not useful work and therefore myocardial contraction is less efficient and work and energy are wasted “loading a physiologic spring.” This wasted work must contribute in part to the extra work of the heart which, in turn, contributes to early myocardial failure observed in patients with constrictive pericarditis. A possible comparison can be made between the heart in constrictive pericarditis and a heart with myocardial fibrosis in which the myocnrdium has been partially replaced by fibrous connective tissue. In the latter heart, the amount of contractile element has been reduced and/or the remainder diseased, and, in addition, unnecessary work by an injured myocardium is required to deform the interstitial fibrous connective tissue. The “spring-load” concept is reflected in the right ventricular pressure
569
trxcin~s from pltients with such hc,lrt\, which ‘ire similar to the trarinxs recorded from patients xvith constrictive pericarditis. R The same conrepth ap1)11to hearts with endornrdial fibrosis and thirkeuilly.
Tulane
4.
5.
G. E. Rurch, M.D. 1‘. D. Giles, M.D. Department of Medicine University School of Medicine 1330 Tulane Ave. New Orleans, La. 70112
6.
REFERENCES
7.
1. Bloomfield, R. A., Lauson, H. D., Cournand, A., Breed, E. S., and Richards, D. \i’., Jr.: Recording of right heart pressures in normal subjects and in patients with chronic pulmonary disease and various types of cardio-circulatory disease, J. Clin. Invest. 25:639, 1946. 2. Wiggers, C. J.: Physiology in health and disease, Philadelphia, 1949, Lea & Febiger, p, 648. 3. McKusick, V. A.: Chronic constrictive pericarditis, Bull. Johns Hopkins Hosp. 905, 1952.
Blood
flow
in the
8.
internal
mammary
Use of the internal mammary artery (IMA) as a coronary bypass graft has been criticized on the basis of its small caliber and limited flow capacity. However, a late failure rate as high as 30 per cent has been reported for saphenous vein in the first yeart, in contrast to three per cent for the IMA. Therefore, in the past 10 months the IMA has been used 78 times for coronary bypass grafting. In most instances free graft flow was measured by a volumetric timed collection immediately prior to making the nnastomosis. After discontinuation of cardiopulmonary bypass, IMA flow was measured using an electromagnetic flow probe. Observations were made of basal flow, of reactive hyperemia flow
Table I. Flow data for internal coronary bypass grafts
mammary
Variables Number of grafts Free flow (ml./min.) Mean arterial pressure Basal flow Reactive hyperemia Peak flow (papaverine) *Abbreviations: graft.
IMA
= internal
Right
(mm.
mammary
86 84 68 68 79
Hg)
artery
graft;
RCA
Ilansen, A. T., Eskildsen, I’., ,nld Gijtxxhe. H.: Pressure curves from the tripht :turicle and the right ventricle in chronic constrictive pericarditis, Circulation 3:881, 1951. Harvey, Ii. M., Ferrer, M. I., Cathrart. Ii. ‘I‘., Richards, 11. \V., and Cournnnd, A.: Mechanic-al and myocardial factors in chronic constrictive pericarditis, Circulation 8:695, 1953. E’u, 1’. N. G.. I,ovejoy, F. \Y., Jr., Joos, 1-I. A., Nye, R. E., Jr., and Mahoney, E. B.: Right auricular and ventricular pressure patterns in constrictive pericarditis, Circulation 7:102, 19.53. Fowler, N. O., Shabetai, R., and Braunstein, J. R.: Transmural ventricular pressures in experimental cardiac tamponade, Circ. Res. 7:733, 1959. Somers, K., Brenton, I). I’., D’:irbeln, I’. G., Fowler, J. M., Kanyerezi, B. Ii., and Sood, N. K.: Haemodynamic features of severe endomyocardial fibrosis of right ventricle, including comparison with constrictive pericarditis, Br. Heart J. 30:322, 1968.
artery
after a 30 second graft occlusion, and of peak flow after injection of 15 mg. of papaverine into the graft. (Papaverine injection was performed in the first 34 grafts and then discontinued.) This data is compared with flow data obtained in the standardized manner from a much larger series of saphenous vein coronary bypass grafts. Free flow was not measured in the vein grafts (see Table I). It is apparent that basal graft flows are similar for the IMA and saphenous vein whether to the right coronary artery (RCA) or to the left anterior descending artery (LAD). Both reactix-e hyperemia flow and peak flow are significantly less for the IMA. These observations indicate that the flow
artery
IMA* 17 32 + * * *
bypass grafts
Left
9 4 9 9 7
= right
98 93 56 59 97
cmcmary
IMA 51 * + * f f
artery
compared
Vein
to saphenous vein
RCA
Vein LAD
185 6 3 4 4 9
61 + 4 86 + 4 174+ 8
graft;
IAD
= left anterior
213 57 * 7.5 * 155
descen&ng
f
3 4 7
aitery
Theoretic considerations of the “dip” of constrictive pericarditis
Following its original description in 1946,’ various explanations have been offered for the presence of the post-systolic “dip” (Fig. 1) seen in pressure tracings recorded from the cavity of the right ventricle of patients with chronic constrictive pericarditis. It has been suggested that the “dip” is an artifact produced by a low frequency recording apparatus,2 but the pattern has been found consistently in patients with constrictive pericarditis since high frequency recording equipment has become available. Another explanation for the presence of the diastolic “dip” is that it represents an actual cardiodynamic eventsId-i.e., because the ventricles are completely empty at the end of systole and the atria1 pressure is high, rapid ventricular filling takes place which is abruptly terminated by the thickened pericardium. However, this theory does not explain why the ventricular relaxation is not isometric with time. Although the possibility of elastic recoil of the thickened pericardium and chest wall has been mentioned by some,5 a precise mechanism has not been offered. We believe that a sudden to rather abrupt elastic recoil of the distorted (during systole) thickened pericardium when the ventricle rather suddenly relaxes is responsible for the diastolic “dip” in constrictive pericarditis and we, therefore, offer the following hypothesis. The heart in constrictive pericarditis is encased in a thick shell of fibrous connective tissue, with or without calcium, which is fixed to and, therefore, a part of the ventricular wall. Thus, when the ventricle contracts, work is performed on this thick wall which deforms in much the same manner as when one “loads” a spring. Following termination of myocardial contraction and with the sudden “unloading” of the distorted fibrous pericardium with the onset of diastole, the ventricular wall abruptly springs back into “place,” suddenly reducing intracavitary pressure, thereby literally “sucking” blood from the atrium into the ventricle. This recoil of the ventricular wall results in the rapid fall in ventricular pressure which is responsible for the ventricular diastolic “dip” recorded in the intracavitary pressure tracing. The ventricle fills rapidly and therefore an early plateau of the right ventricular pressure tracing is seen (Fig. 1). Supporting evidence for this concept is seen in experimental cardiac tamponade produced with air or fluid. In such a situation the fluid or air in the pericardinl cavity is not fixed to the myocardial wall even though diastolic filling of the ventricle is re-
post-systolic
Fig. 1. Time course showing post-systolic
of right ventricular pressure dip in constrictive pericarditis.
stricted. Thus, during systole there is no “physiologic spring” to “load,” nor is there one to suddenly “unload” during the early phase of diastole. Under such circumstances, therefore, the characteristic “dip ‘I6 in right ventricular pressure is not expected nor recorded.’ Parenthetically, it may be noted that the work performed in deforming the pericardium in constrictive pericarditis is not useful work and therefore myocardial contraction is less efficient and work and energy are wasted “loading a physiologic spring.” This wasted work must contribute in part to the extra work of the heart which, in turn, contributes to early myocardial failure observed in patients with constrictive pericarditis. A possible comparison can be made between the heart in constrictive pericarditis and a heart with myocardial fibrosis in which the myocnrdium has been partially replaced by fibrous connective tissue. In the latter heart, the amount of contractile element has been reduced and/or the remainder diseased, and, in addition, unnecessary work by an injured myocardium is required to deform the interstitial fibrous connective tissue. The “spring-load” concept is reflected in the right ventricular pressure
569
trxcin~s from pltients with such hc,lrt\, which ‘ire similar to the trarinxs recorded from patients xvith constrictive pericarditis. R The same conrepth ap1)11to hearts with endornrdial fibrosis and thirkeuilly.
Tulane
4.
5.
G. E. Rurch, M.D. 1‘. D. Giles, M.D. Department of Medicine University School of Medicine 1330 Tulane Ave. New Orleans, La. 70112
6.
REFERENCES
7.
1. Bloomfield, R. A., Lauson, H. D., Cournand, A., Breed, E. S., and Richards, D. \i’., Jr.: Recording of right heart pressures in normal subjects and in patients with chronic pulmonary disease and various types of cardio-circulatory disease, J. Clin. Invest. 25:639, 1946. 2. Wiggers, C. J.: Physiology in health and disease, Philadelphia, 1949, Lea & Febiger, p, 648. 3. McKusick, V. A.: Chronic constrictive pericarditis, Bull. Johns Hopkins Hosp. 905, 1952.
Blood
flow
in the
8.
internal
mammary
Use of the internal mammary artery (IMA) as a coronary bypass graft has been criticized on the basis of its small caliber and limited flow capacity. However, a late failure rate as high as 30 per cent has been reported for saphenous vein in the first yeart, in contrast to three per cent for the IMA. Therefore, in the past 10 months the IMA has been used 78 times for coronary bypass grafting. In most instances free graft flow was measured by a volumetric timed collection immediately prior to making the nnastomosis. After discontinuation of cardiopulmonary bypass, IMA flow was measured using an electromagnetic flow probe. Observations were made of basal flow, of reactive hyperemia flow
Table I. Flow data for internal coronary bypass grafts
mammary
Variables Number of grafts Free flow (ml./min.) Mean arterial pressure Basal flow Reactive hyperemia Peak flow (papaverine) *Abbreviations: graft.
IMA
= internal
Right
(mm.
mammary
86 84 68 68 79
Hg)
artery
graft;
RCA
Ilansen, A. T., Eskildsen, I’., ,nld Gijtxxhe. H.: Pressure curves from the tripht :turicle and the right ventricle in chronic constrictive pericarditis, Circulation 3:881, 1951. Harvey, Ii. M., Ferrer, M. I., Cathrart. Ii. ‘I‘., Richards, 11. \V., and Cournnnd, A.: Mechanic-al and myocardial factors in chronic constrictive pericarditis, Circulation 8:695, 1953. E’u, 1’. N. G.. I,ovejoy, F. \Y., Jr., Joos, 1-I. A., Nye, R. E., Jr., and Mahoney, E. B.: Right auricular and ventricular pressure patterns in constrictive pericarditis, Circulation 7:102, 19.53. Fowler, N. O., Shabetai, R., and Braunstein, J. R.: Transmural ventricular pressures in experimental cardiac tamponade, Circ. Res. 7:733, 1959. Somers, K., Brenton, I). I’., D’:irbeln, I’. G., Fowler, J. M., Kanyerezi, B. Ii., and Sood, N. K.: Haemodynamic features of severe endomyocardial fibrosis of right ventricle, including comparison with constrictive pericarditis, Br. Heart J. 30:322, 1968.
artery
after a 30 second graft occlusion, and of peak flow after injection of 15 mg. of papaverine into the graft. (Papaverine injection was performed in the first 34 grafts and then discontinued.) This data is compared with flow data obtained in the standardized manner from a much larger series of saphenous vein coronary bypass grafts. Free flow was not measured in the vein grafts (see Table I). It is apparent that basal graft flows are similar for the IMA and saphenous vein whether to the right coronary artery (RCA) or to the left anterior descending artery (LAD). Both reactix-e hyperemia flow and peak flow are significantly less for the IMA. These observations indicate that the flow
artery
IMA* 17 32 + * * *
bypass grafts
Left
9 4 9 9 7
= right
98 93 56 59 97
cmcmary
IMA 51 * + * f f
artery
compared
Vein
to saphenous vein
RCA
Vein LAD
185 6 3 4 4 9
61 + 4 86 + 4 174+ 8
graft;
IAD
= left anterior
213 57 * 7.5 * 155
descen&ng
f
3 4 7
aitery