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Disturbed blood flow in the carotid artery: Its physiological and clinical significance
Disturbed blood Its physiological
flow and
in the carotid artery: clinical significance
Isaac Starr, M.D.* Christophe Ambrosi, M.D.* Joel H. Manchester, M.D.** James C. Shelburne, M.D.** Philadelphia, Pa.
E
lasticity in the rubber membranes, rubber tubing, and air transmission systems used in the early clinical studies of the pulse prevented the proper recording of its high frequency (HF) components, so one cannot expect to find evidence of HF abnormalities in this literature. We know of no mention of such abnormalities before 1955, when Smith,’ after improving his apparatus by greatly diminishing the size of his air transmission system, described an HF abnormality in the carotid pulse of a case of aortic stenosis. Smith also performed a very illuminating experiment on this patient: after he increased the size of his air transmission system until it resembled the apparatus used in early work on the pulse, the HF abnormality disappeared and was replaced by the “bisferiens” type of pulse, so often described as characteristic of aortic stenosis in the older literature.2 Soon after Smith’s study, the use of rigid apparatus, in conjunction with electrical
methods of transmission and recording, provided records in which the HF components of the pulse were much better recorded, and Smith’s finding was soon confirmed in several laboratories.3-7 In this laboratory increasing interest in the cardiac forces and in incoordination of the cardiac contraction led to continued efforts to improve our knowledge of the HF components of the pulse. Thus, since 1959, the pulse derivative has been recorded routinely to bring out HF information and, in 1964, the sensor was shifted from the brachial to the carotid artery to minimize the loss of HF information which occurs as the wave travels down the artery. Since that time, pulse records, containing far more HF information than has been recorded in most other clinical studies of the pulse, have been secured in over 1,000 subjects, both patients and healthy persons. Certain of these patients exhibited an HF abnormality of the carotid pulse so
From the Department of Therapeutic Ressrch and the Department of Medicine, Cardiovascular-Pulmonary Division, School of Medicine, University of Pennsylvania. Philadelphia, Pa. Received for publication Dec. 21, 1972. Reprint requests to: Dr. Isaac Starr, University of Pennsylvania. 851 Gates Memorial Pavilion, Philadelphia, Pa. 19104. *Drs. Starr and Ambroei were supported by grant No. HE 625 CVB from the United States Public Health Service, National Institutes of Health. **Drs. Manchester and Shelbume were supported by grant No. HL 8805 from the United States Public Health Service. National Institutes of Health.
644
American
Heart
Journal
November,
1973
Vol.
86, No.
5, pp. 644-650
I’olwnr Nfcmbcr
86 5
striking tha.t our curiosity was aroused. This study has enabled us to define its physiological and clinical significance. Methods
We used a capacitance Brecht and Bouche transducer having a frequency response flat to 200 Hz.~ The transducer was attached to a short rod which projected 1.5 cm. beyond a metal circle which surrounded it. ‘The tip of this rod, placed over a point where maximal pulsation in the carotid had been palpated, was pushed down until the circle was in contact with the skin, and then it was held firmly in place with a strap around the neck. A standard differentiating circuit and two channels of a Sanborn Twin-beam recorder were used to record the pulse and its derivative simultaneously. The methods of calibrating the pulse derivative (I’D) and of measuring the maximum rate of pressure rise (PD max) have been described.4 Such records were always taken after the supine subjects had rested comfortably for at least. 15 minutes. Several positions of the transducer lrvere tried in each subject, that producing the largest record-i.e., the record requiring the least amplification, being preferred. ULF force ballistocardiograms, taken simultaneously with the pulse records, play a very minor part in this study. When right and left heart catheterizations were performed, they \vere done a day or two before or after the pulse records were taken. Pressuresobtained at catheterization were inscribed by an Electronics-for-lIeditine DR12 polybeam photographic recorder using a Statham P23 DB transducer. The transvalvular aortic gradient was measured during pullback from the left ventricle, the systolic mean gradient being recorded. We used the conventional 20 mm. Hg as the upper limit of normal for the aortic valve gradient. Subjects
The pati’ents studied were adults who had, or were suspected of having, serious cardiac disease. All were inpatients in the University Hospital, and all were ambulatory. One hundred-eighty patients were subjected to cardiac catheterization. Since the
Disturbed
blood jlow in carotid artery
645
composition of this group was biased by the ordinary criteria for selecting patients for this test, a larger and a more representative group of cardiac patients was secured by adding the last 169 cardiac patients studied who had not been catheterized, records of their pulse derivatives having been taken in conjunction with ballistocardiographic studies. The final hospital diagnosis, used to classify each case, was made by a doctor without knowledge of our findings in the pulse. Results
What we have called the carotid high frequency abnormality, illustrated in Figs. 1 and 2, consists of a brief burst of high frequency distortion superimposed on the basic pattern of the pulse derivative for part of the cardiac cycle. Usually of 15 Hz or faster, the burst starts at, or shortly after, the main wave’s peak, and usually lasts from 0.1 to 0.4 second. By its regular position at this part of the cardiac cycle, the abnormality can be easily distinguished from electrical “noise.” As shown in Figs. 1 and 2, when the abnormality was present and the rhythm regular, the general pattern was repeated with every heart beat, but there was often some variation in the HF details of the burst. Such small differences are probably due to artefacts, for slight changes in the exact positioning of the sensor on the artery and in the pressure applied often caused similar changes in the record, probably by altering the transmission of the HF vibrations from arterial lumen to sensor. No similar bursts of HF distortion have ever been encountered in pulse derivatives secured on healthy persons, so the abnormality can be recognized at a glance (Fig. 1). Duplicate runs, made on the same day or on different days, give excellent agreement of the general pattern of the abnormality, despite some differences in the HF details. \‘ery conspicuous in the pulse derivative, the HF abnormality can sometimes be recognized in the conventional pulse, but only if one examines the record very carefully (Fig. 1); in the majority of cases it would certainly be overlooked. Table I was compiled from data secured from the 180 patients catheterized. There
646
Starr
Pt
ni.
Calcilic aortic stenosis Aortic stenosis (non-calcific) Subaortic stenosis Aortic stenosis and insufficiency Aortic insufficiency without stenosis Mitral valve disease Coronary artery disease Congenital septal defect or patent ductus Cardiomyopath) Hypertensive heart disease Congenital pulmonary stenosis Other cardiac lesions No cardiac diagnosis
15
1
11 7 1
13 27 57
0 0 0
12 6 5
0 0 0
3 3 9
is a highly significant relationship betwen the presence and absence of the carotid HF abnormality and the normality and ahnormality of the gradient; chi square = 63. The relations between the presence and absence of the HF abnormalities and the final clinical diagnoses in the group catheterized are shown in Table I. In the enlarged group of 349 patients the HF abnormality was present in 89 per cent of 3.5 cases diagnosed aortic stenosis; in 48 per cent of 29 cases diagnosed aortic regurgitation n-ithout stenosis; and in less than 1 per cent of 285 cases diagnosed cardiac disease without aortic valve involvement. It has not been seen in any healthy person. Obviously there is a highly significant relation between the carotid HF abnormality and aortic valve disease. Discussion Relation to the thrill. The genesis of the HF abnormality demonstrated in our patients is surely related to that of the thrill palpable in so many cases of nortic stenosis, but our modern methods detect the abnormality in many cases in \\.hich no thrill was discovered at routine examination. E\-i-
clcntly \ve ha\-c a more delicate test than palpation provides. Genesis of the carotid HP abnormality. AA~1 array of clinical evidence indicates that an a~aatomical factor, associated with the aortic valve, is of prime importance in the genesis of this abnormality. It \vas very seldom encountered in patients without manifest aortic valve disease. In all four cases in which an aortic valve prosthesis \vas inserted into a previously stenotic orifice, the HF abnormality disappeared (Fig. 2j or II-as greatly ameliorated, although lower frequency abnormalities often remained in the pulse record. But our evidence also points to the importance of a physiological factor in its causation. In all cases the HF distortion occurred in only one part of the cardiac cycle, at and after the time of the normal peak of the pulse derivative, when ejection velocity would be at its highest (Figs. 1 and 2). In some cases in which the heart beats differed in strength (Fig. l), the abnormality was present whenever the pulse was large, and absent when it was small. In one case (Fig. 3) the HF abnormality disappeared after coronary bypass surgery, to reappear after the heart had recovered from the immediate effects of the operation. Such differences are certainly not due to structural changes in an aortic lesion; a physiological factor, such as differences in flow I-elocity, must be invoked to account for the findings. One patient, later demonstrated at operation to have a tight aortic stenosis, never exhibited the carotid HF abnormality. Before operation his PL> max was one of the smallest encountered in this study and his cardiac output (dye method) was calculated to be only 1.4 liters min./N.” Apparently his blood velocity was too small to generate the HF abnormality, despite the presence of the aortic lesion. Several cases of wide-open aortic regurgitation, nhose ejection acceleration must have been \-ery great to account for their large force ballistocardiograms and huge PIN> max’s (Fig. 3), showed no trace of the carotid HF abnormality. Evidently neither a tight stenosis of itself, nor a high ejection velocity of itself, is sufficient to produce the abnormality. So our evidence leads to a theory which is consistent n-ith well-known
Disturbed
blood $0~ in carotid artery
647
E. High frequency abnormalities in the carotid pulse. Arrows point to features of interest. Fig. 1, A through A, .L\ normal record for comparison. PD max = 680 mm. Hg per second. B, Enlarged carotid pulse (left) and pulse derivatil-e (right). Patient Ii. N., age 18 , gradient 32 mm. Hg. Congenital aortic stenosis, aortic insufficiency, Grade 2. Note conspicuous HF abnormalities in PD and that they can also be seen in the enlarged conventional pulse. PD max = 477 mm. Hg per second. C, Same records of patient F. U., age 54, gradient 57 mm. Hg. Aortic stenosis, aortic insufficiency, Grade 3. Note conspicuous abnormality in PD; it is present but almost unrecognizable in the enlarged conventional carotid pulse. PD max = 324 mm. Hg per second. D, Carotid PD Iof patient T. R., age 23. RHD, severe aortic and mitral regurgitation, atrial fibrillation, gradient variable, minimum 10 mm. Hg. Note HF abnormality in large beats, its absence from smaller. E, Carotid PD (left) and brachial PD (right) of D. C., age 33. Aortic stenosis and aortic insufficiency, Grade 4. Gradient 80 mm. Hg, PD’ max = 248 mm. Hg per second. Note maximum HF abnormality in carotid PD, its almost complete disappearance by the time the brachial was reached.
physical facts: both a distorted aortic lumen and a :flow velocity which exceeds a critical level are needed to produce the bursts of disturbed flow we detect in our patients. Classic physical experiments indicate that similar factors are concerned in the genesis of disturbed flows in tubes.g Roughness of the wall and irregularities in the shape of the tubes, such as narrowing and widening, will promote the appearance of turbulence wlhenever flow velocity exceeds a critical level. Nevertheless, turbulence, as usually defined today, is a phenomenon of much higher jfrequency than our methods of recording the pulse would detect9 Thus, while evidence secured by Doppler techniques1° indicates that blood turbulence does indeed accompany some cases of
aortic stenosis, our studies provide no evidence for or against its presence in our cases. So our data suggest that the carotid high frequency abnormality found in our patients is due to a disturbance of flow profile in which normal streamlined flow is interrupted by eddies, vortices, and jets. This abnormality should not be called “turbulence” but, if sufficiently intense, it would probably be accompanied by turbulence. Such a physiologic abnormality would, like turbulence, handicap the heart by increasing the impedance to ejection. So we have demonstrated that a physiological abnormality of blood flow, which handicaps cardiac performance, is present in most cases of aortic stenosis. Relation of disturbed aortic flow to ab-
I;i;r. 2, .1 through D. Effect of the inqertion of a prosthetic cnxed ball valve into a btenotic aortic orilice. :l :cnd R, Carotid PD of N. LT., age 68. Ltretic aortic steno& and insufficiency. ‘-1, Before operation, gadient 17 mm. Hg, I’D mnx = 411 mm. Hx l,er second. A. After oper;Ltion, PD max = 817. Note di
normal aortic valve gradients. The disturbed flow indicated by the HF abnormalit!. in the pulse is accompanied by an abnormal gradient in almost all our cases. Theoretically the two are related in several \\.ays. Velocity being constant, abnormal pressure drops across the aortic orifice might conceivably be due to impedance caused 1,~ narrowing alone, or by disturbed flo\v alone. In the great majority of our cases the increased gradient was prohahly due to l,oth factors, how much each contributed Ijeing unknown. Impedance due to disturbed flo\\ alone may be larger than most doctors realize. Schultz and colleagues” perfused normal and arteriosclerotic abdominal aortas secured at necropsy \vith a fluid of the same viscosity as blood; in normal vessels the gradient at a velocity of 40 C.C. per second was 2 to 3 mm. Hg. But in one sclerotic aorta with a maximum narro\\-ing of only 6 per cent, a gradient of 12 mm. Hg was found. Since this amount of narro\\-ing would not cause a detectable gradient increase if produced experimentally in a normal vessel, this fourfold increase of gradient must be attributed to the impedance of a
flo\\. disturbed by roughening and distortion oi the I-essei ~~11s. Oh\~iouslj: the disturbed AOXV pattern demonstrated in our patients may be an important factor in their disability. From the physiological viewpoint, both gradient and flow disturbance are influenced l)y blood velocity, but in a different \vay. j.enturi’s principle describes the relation of narrowing to the gradient; in this formula \*elocity appears as a continuous function. In equations describing the relations of turbulence and disturbed flows, velocity is a step function---i.e., the phenomenon appears when velocity exceeds a critical level. So it is easy to see w-hy an abnormal gradient and a disturbed flow are usually associated in our patients, and also that they need not always be associated. Our clinical data on the latter situation are of interest. Discussion of unr~sztal jindings. In 17 cases the H F abnormality \vas present, but the pressure gradient across the aortic val\,-e was not abnormally increased. 1Iost of these were cases of aortic valve disease in which regurgitation predominated. Evi-
Disturbed
blood jlow in carotid artery
649
Fig. 3. Left, panels A, B and C. Factors in the presence or absence of the carotid HF abnormality. Carotid pulse derivative of B. T., age 54, diagnosed coronary heart disease. A, Before operation, note HF abnormalities. B, Twelve days after coronary bypass operation; note disappearance of HF abnormalities. C, Two months postoperative; note return of HF abnormality. PD max was 300, 276, and 300 mm. Hg per second in the three records. Iii& p,zneZ, Carotid pulse derivative over force BCG of N. R., age 23, wide open aortic regurgitation, PD max = 4,500 mm. Hg per second, which is record breaking. Calibration of force BCG, 13 small divisions = 275 (103) dynes. So this record is also huge. The aortic valve gradient was normal. Note that, in the presence of what must have been a very great blood velocity, HF abnormalities in the carotid PD are absent.
dently, a roughening without narrowing of the orifice may produce a disturbed flow causing too little impedance to produce gradient abnormality. In five cases the gradient was found to be abnormally increased, but no disturbed flow was detected. Such findings might have been due to an artefact for which we were on the lookout; should any patient be more excited at catheterization than when the pulse derivative was taken, such fmdings might well result. However, the pulse rates recorded at the t\vo tests lvere so similar in each of these five patients that it is hard to believe that differences in excitement jvere the cause of our findings. It is easier to believe that the increased impedance in these cases was due to aortic narrowing alone, the lesion having so little roughness that a disturbed flop- did not accompany it. The possibility that disturbed flojl- in the carotid might be created lvithout an aortic lesion should also be discussed, for we ha\-e five cases in which the HF abnormality Ii-as present without any clinical evidence of aortic valve disease. All these were cases of advanced rheumatic heart disease \I-ith several mitral valvulitis. To account for murmurs heard in the aortic area \I-hen that valve is normal, it has been suggested12
that, when blood regurgitates through a deficient mitral valve in sufficient amount, the jet strikes the atria1 wall adjacent to the aortic arch; such a jet might not only produce an audible murmur but might also set up vibrations in the aortic blood which our sensor would detect. While one should not forget that an aortic lesion, so common in advanced cases of RHD, might have been present in these five cases, though undiagnosed, those doing the catheterization were convinced that this valve \vas normal. It is also conceivable that small elements of a myocardium nhich had lost the coordination of its contraction might beat such a rapid tattoo on the ventricular blood that rapid fluctuation of the rate of change of pressure would appear in the carotid. High frequency distortions are often superimposed on undamped ventricular pressure records, and perhaps too often dismissed as artefacts. But II-e found no evidence of HF distortion in the contour of the ballistocardiograms of an)- of these cases. The common types of cardiac incoordination produce distortions of these records of a lo\\-er frequency than those encountered in the carotid HF abnormality. While other possibilities cannot be ruled out at this time, the genesis of disturbed
flop\- in the carotid artery is clearly related to a lesion of the aortic valve in the great majority of our cases. Conclusions
Records of the carotid pulse and its first time derivative have been taken, under standard resting conditions, in 349 cardiac patients, 180 of whom were subjected to cardiac catheterization. These results have been analyzed to throw light on an abnormality of pulse contour, conspicuous in the pulse derivative, a burst of high frequency distortion occurring at and after the peak of the main wave. The presence of this abnormality is closely related to the presence of aortic valve lesions, diagnosed either by the aortic valve gradient, or by conventional clinical evidence. While such a lesion must be a prime factor in its genesisin most cases, the evidence also indicates that a second factor must be present before the abnormality is produced, sufficient velocity of the ejected blood. This theory is satisfactory in 98 per cent of our cases, the few discrepancies are discussed. Such rapid fluctuations in the carotid pulse derivative indicate a disturbance of blood flow in which its normal streamlined character is broken up by vortices, jets, and eddies. Such a disturbance should not be called turbulence, because turbulence is defined today as a phenomenon of much higher frequency than our methods would detect. The eddies and whorls of such disturbed flows must increase the impedance to cardiac ejection and, like turbulence, make the heart’s task more difficult. This handicap is very common in aortic valve disease.
REFERENCES 1. Smith, J. E.: :I technique for recordins rxotid artery pulsations with special reference to aortic >tenosis, AM. HEART J. 49:428, 1955. 2. Corm, H. I.., Jr., and Horwitz. 0.: Cardiac and vascular diseases, Philadelphia, 1971, I.ea 8r Febiger, Publishers. 3. Starr, I., and Ogawa, 5.: On taking the first derivative of the pulse and its relations to the ballistocardiogram, Fed. Proc. 19:106, 1960. 4. Starr, I., and Ogawa, S.: A clinical study of the first derivative of the brachial pulse. Normal standards and abnormalities encountered in heart disease, A&f. HEART J. 65:482, 1963. 5. Mason, D. T., Braunwald, E., Ross, J., Jr., and Morrow, A. G.: Diagnostic value of first and second derivatives of the arterial pressure pulse in aortic valve disease and hypertrophic subaortic stenosis, Circulation 30:90, 1964. 6. Boiteau, G. M., and Allenstein, B. J.: Hypertrophic sub-aortic stenosis, Am. J. Cardiol. 8:614, 1961. 7. Braunwald, E., Goldblatt, A., Aygen, M. M., Rockoff. S. D.. and Morrow. A. G.: Concrenital aortic s;enosis[ clinical and hemodynami: findings in 100 patients, Circulation 27:426, 1963. 8. Brecht, K., and Bouche, H. L.: Zut Abnahme des Arterienpulses am Menshen mit den Infraton-?vliktophon, Pfluegers Arch. 257:490, 1953. 9. Ettinger, E. 0.: Flow patterns and vascular geometry, in Ettinger, c. O., editor: Pulsatile blood flow. New York. 1964, McGraw-Hill Book Company, Inc. ’ 10. Side, C. D., and Gosling, R. G.: Non-surgical assessment of cardiac function, Nature 232:335, 1971. 11. Schultz, R. D., Hokanson, D. E., and Strandness, D. E., Jr.: Pressure-flow and stress-strain measurements of normal and diseased aortoiliac segments, Surg. Gynecol. Obstet. 124:1267, 1967. 12. Mercer, E. N., and l%.alters, $1. B.: hlitral regurgitation simulating aortic stenosis, Can. Med. Assoc. J. 93:413, 1965.
flow and
in the carotid artery: clinical significance
Isaac Starr, M.D.* Christophe Ambrosi, M.D.* Joel H. Manchester, M.D.** James C. Shelburne, M.D.** Philadelphia, Pa.
E
lasticity in the rubber membranes, rubber tubing, and air transmission systems used in the early clinical studies of the pulse prevented the proper recording of its high frequency (HF) components, so one cannot expect to find evidence of HF abnormalities in this literature. We know of no mention of such abnormalities before 1955, when Smith,’ after improving his apparatus by greatly diminishing the size of his air transmission system, described an HF abnormality in the carotid pulse of a case of aortic stenosis. Smith also performed a very illuminating experiment on this patient: after he increased the size of his air transmission system until it resembled the apparatus used in early work on the pulse, the HF abnormality disappeared and was replaced by the “bisferiens” type of pulse, so often described as characteristic of aortic stenosis in the older literature.2 Soon after Smith’s study, the use of rigid apparatus, in conjunction with electrical
methods of transmission and recording, provided records in which the HF components of the pulse were much better recorded, and Smith’s finding was soon confirmed in several laboratories.3-7 In this laboratory increasing interest in the cardiac forces and in incoordination of the cardiac contraction led to continued efforts to improve our knowledge of the HF components of the pulse. Thus, since 1959, the pulse derivative has been recorded routinely to bring out HF information and, in 1964, the sensor was shifted from the brachial to the carotid artery to minimize the loss of HF information which occurs as the wave travels down the artery. Since that time, pulse records, containing far more HF information than has been recorded in most other clinical studies of the pulse, have been secured in over 1,000 subjects, both patients and healthy persons. Certain of these patients exhibited an HF abnormality of the carotid pulse so
From the Department of Therapeutic Ressrch and the Department of Medicine, Cardiovascular-Pulmonary Division, School of Medicine, University of Pennsylvania. Philadelphia, Pa. Received for publication Dec. 21, 1972. Reprint requests to: Dr. Isaac Starr, University of Pennsylvania. 851 Gates Memorial Pavilion, Philadelphia, Pa. 19104. *Drs. Starr and Ambroei were supported by grant No. HE 625 CVB from the United States Public Health Service, National Institutes of Health. **Drs. Manchester and Shelbume were supported by grant No. HL 8805 from the United States Public Health Service. National Institutes of Health.
644
American
Heart
Journal
November,
1973
Vol.
86, No.
5, pp. 644-650
I’olwnr Nfcmbcr
86 5
striking tha.t our curiosity was aroused. This study has enabled us to define its physiological and clinical significance. Methods
We used a capacitance Brecht and Bouche transducer having a frequency response flat to 200 Hz.~ The transducer was attached to a short rod which projected 1.5 cm. beyond a metal circle which surrounded it. ‘The tip of this rod, placed over a point where maximal pulsation in the carotid had been palpated, was pushed down until the circle was in contact with the skin, and then it was held firmly in place with a strap around the neck. A standard differentiating circuit and two channels of a Sanborn Twin-beam recorder were used to record the pulse and its derivative simultaneously. The methods of calibrating the pulse derivative (I’D) and of measuring the maximum rate of pressure rise (PD max) have been described.4 Such records were always taken after the supine subjects had rested comfortably for at least. 15 minutes. Several positions of the transducer lrvere tried in each subject, that producing the largest record-i.e., the record requiring the least amplification, being preferred. ULF force ballistocardiograms, taken simultaneously with the pulse records, play a very minor part in this study. When right and left heart catheterizations were performed, they \vere done a day or two before or after the pulse records were taken. Pressuresobtained at catheterization were inscribed by an Electronics-for-lIeditine DR12 polybeam photographic recorder using a Statham P23 DB transducer. The transvalvular aortic gradient was measured during pullback from the left ventricle, the systolic mean gradient being recorded. We used the conventional 20 mm. Hg as the upper limit of normal for the aortic valve gradient. Subjects
The pati’ents studied were adults who had, or were suspected of having, serious cardiac disease. All were inpatients in the University Hospital, and all were ambulatory. One hundred-eighty patients were subjected to cardiac catheterization. Since the
Disturbed
blood jlow in carotid artery
645
composition of this group was biased by the ordinary criteria for selecting patients for this test, a larger and a more representative group of cardiac patients was secured by adding the last 169 cardiac patients studied who had not been catheterized, records of their pulse derivatives having been taken in conjunction with ballistocardiographic studies. The final hospital diagnosis, used to classify each case, was made by a doctor without knowledge of our findings in the pulse. Results
What we have called the carotid high frequency abnormality, illustrated in Figs. 1 and 2, consists of a brief burst of high frequency distortion superimposed on the basic pattern of the pulse derivative for part of the cardiac cycle. Usually of 15 Hz or faster, the burst starts at, or shortly after, the main wave’s peak, and usually lasts from 0.1 to 0.4 second. By its regular position at this part of the cardiac cycle, the abnormality can be easily distinguished from electrical “noise.” As shown in Figs. 1 and 2, when the abnormality was present and the rhythm regular, the general pattern was repeated with every heart beat, but there was often some variation in the HF details of the burst. Such small differences are probably due to artefacts, for slight changes in the exact positioning of the sensor on the artery and in the pressure applied often caused similar changes in the record, probably by altering the transmission of the HF vibrations from arterial lumen to sensor. No similar bursts of HF distortion have ever been encountered in pulse derivatives secured on healthy persons, so the abnormality can be recognized at a glance (Fig. 1). Duplicate runs, made on the same day or on different days, give excellent agreement of the general pattern of the abnormality, despite some differences in the HF details. \‘ery conspicuous in the pulse derivative, the HF abnormality can sometimes be recognized in the conventional pulse, but only if one examines the record very carefully (Fig. 1); in the majority of cases it would certainly be overlooked. Table I was compiled from data secured from the 180 patients catheterized. There
646
Starr
Pt
ni.
Calcilic aortic stenosis Aortic stenosis (non-calcific) Subaortic stenosis Aortic stenosis and insufficiency Aortic insufficiency without stenosis Mitral valve disease Coronary artery disease Congenital septal defect or patent ductus Cardiomyopath) Hypertensive heart disease Congenital pulmonary stenosis Other cardiac lesions No cardiac diagnosis
15
1
11 7 1
13 27 57
0 0 0
12 6 5
0 0 0
3 3 9
is a highly significant relationship betwen the presence and absence of the carotid HF abnormality and the normality and ahnormality of the gradient; chi square = 63. The relations between the presence and absence of the HF abnormalities and the final clinical diagnoses in the group catheterized are shown in Table I. In the enlarged group of 349 patients the HF abnormality was present in 89 per cent of 3.5 cases diagnosed aortic stenosis; in 48 per cent of 29 cases diagnosed aortic regurgitation n-ithout stenosis; and in less than 1 per cent of 285 cases diagnosed cardiac disease without aortic valve involvement. It has not been seen in any healthy person. Obviously there is a highly significant relation between the carotid HF abnormality and aortic valve disease. Discussion Relation to the thrill. The genesis of the HF abnormality demonstrated in our patients is surely related to that of the thrill palpable in so many cases of nortic stenosis, but our modern methods detect the abnormality in many cases in \\.hich no thrill was discovered at routine examination. E\-i-
clcntly \ve ha\-c a more delicate test than palpation provides. Genesis of the carotid HP abnormality. AA~1 array of clinical evidence indicates that an a~aatomical factor, associated with the aortic valve, is of prime importance in the genesis of this abnormality. It \vas very seldom encountered in patients without manifest aortic valve disease. In all four cases in which an aortic valve prosthesis \vas inserted into a previously stenotic orifice, the HF abnormality disappeared (Fig. 2j or II-as greatly ameliorated, although lower frequency abnormalities often remained in the pulse record. But our evidence also points to the importance of a physiological factor in its causation. In all cases the HF distortion occurred in only one part of the cardiac cycle, at and after the time of the normal peak of the pulse derivative, when ejection velocity would be at its highest (Figs. 1 and 2). In some cases in which the heart beats differed in strength (Fig. l), the abnormality was present whenever the pulse was large, and absent when it was small. In one case (Fig. 3) the HF abnormality disappeared after coronary bypass surgery, to reappear after the heart had recovered from the immediate effects of the operation. Such differences are certainly not due to structural changes in an aortic lesion; a physiological factor, such as differences in flow I-elocity, must be invoked to account for the findings. One patient, later demonstrated at operation to have a tight aortic stenosis, never exhibited the carotid HF abnormality. Before operation his PL> max was one of the smallest encountered in this study and his cardiac output (dye method) was calculated to be only 1.4 liters min./N.” Apparently his blood velocity was too small to generate the HF abnormality, despite the presence of the aortic lesion. Several cases of wide-open aortic regurgitation, nhose ejection acceleration must have been \-ery great to account for their large force ballistocardiograms and huge PIN> max’s (Fig. 3), showed no trace of the carotid HF abnormality. Evidently neither a tight stenosis of itself, nor a high ejection velocity of itself, is sufficient to produce the abnormality. So our evidence leads to a theory which is consistent n-ith well-known
Disturbed
blood $0~ in carotid artery
647
E. High frequency abnormalities in the carotid pulse. Arrows point to features of interest. Fig. 1, A through A, .L\ normal record for comparison. PD max = 680 mm. Hg per second. B, Enlarged carotid pulse (left) and pulse derivatil-e (right). Patient Ii. N., age 18 , gradient 32 mm. Hg. Congenital aortic stenosis, aortic insufficiency, Grade 2. Note conspicuous HF abnormalities in PD and that they can also be seen in the enlarged conventional pulse. PD max = 477 mm. Hg per second. C, Same records of patient F. U., age 54, gradient 57 mm. Hg. Aortic stenosis, aortic insufficiency, Grade 3. Note conspicuous abnormality in PD; it is present but almost unrecognizable in the enlarged conventional carotid pulse. PD max = 324 mm. Hg per second. D, Carotid PD Iof patient T. R., age 23. RHD, severe aortic and mitral regurgitation, atrial fibrillation, gradient variable, minimum 10 mm. Hg. Note HF abnormality in large beats, its absence from smaller. E, Carotid PD (left) and brachial PD (right) of D. C., age 33. Aortic stenosis and aortic insufficiency, Grade 4. Gradient 80 mm. Hg, PD’ max = 248 mm. Hg per second. Note maximum HF abnormality in carotid PD, its almost complete disappearance by the time the brachial was reached.
physical facts: both a distorted aortic lumen and a :flow velocity which exceeds a critical level are needed to produce the bursts of disturbed flow we detect in our patients. Classic physical experiments indicate that similar factors are concerned in the genesis of disturbed flows in tubes.g Roughness of the wall and irregularities in the shape of the tubes, such as narrowing and widening, will promote the appearance of turbulence wlhenever flow velocity exceeds a critical level. Nevertheless, turbulence, as usually defined today, is a phenomenon of much higher jfrequency than our methods of recording the pulse would detect9 Thus, while evidence secured by Doppler techniques1° indicates that blood turbulence does indeed accompany some cases of
aortic stenosis, our studies provide no evidence for or against its presence in our cases. So our data suggest that the carotid high frequency abnormality found in our patients is due to a disturbance of flow profile in which normal streamlined flow is interrupted by eddies, vortices, and jets. This abnormality should not be called “turbulence” but, if sufficiently intense, it would probably be accompanied by turbulence. Such a physiologic abnormality would, like turbulence, handicap the heart by increasing the impedance to ejection. So we have demonstrated that a physiological abnormality of blood flow, which handicaps cardiac performance, is present in most cases of aortic stenosis. Relation of disturbed aortic flow to ab-
I;i;r. 2, .1 through D. Effect of the inqertion of a prosthetic cnxed ball valve into a btenotic aortic orilice. :l :cnd R, Carotid PD of N. LT., age 68. Ltretic aortic steno& and insufficiency. ‘-1, Before operation, gadient 17 mm. Hg, I’D mnx = 411 mm. Hx l,er second. A. After oper;Ltion, PD max = 817. Note di
normal aortic valve gradients. The disturbed flow indicated by the HF abnormalit!. in the pulse is accompanied by an abnormal gradient in almost all our cases. Theoretically the two are related in several \\.ays. Velocity being constant, abnormal pressure drops across the aortic orifice might conceivably be due to impedance caused 1,~ narrowing alone, or by disturbed flo\v alone. In the great majority of our cases the increased gradient was prohahly due to l,oth factors, how much each contributed Ijeing unknown. Impedance due to disturbed flo\\ alone may be larger than most doctors realize. Schultz and colleagues” perfused normal and arteriosclerotic abdominal aortas secured at necropsy \vith a fluid of the same viscosity as blood; in normal vessels the gradient at a velocity of 40 C.C. per second was 2 to 3 mm. Hg. But in one sclerotic aorta with a maximum narro\\-ing of only 6 per cent, a gradient of 12 mm. Hg was found. Since this amount of narro\\-ing would not cause a detectable gradient increase if produced experimentally in a normal vessel, this fourfold increase of gradient must be attributed to the impedance of a
flo\\. disturbed by roughening and distortion oi the I-essei ~~11s. Oh\~iouslj: the disturbed AOXV pattern demonstrated in our patients may be an important factor in their disability. From the physiological viewpoint, both gradient and flow disturbance are influenced l)y blood velocity, but in a different \vay. j.enturi’s principle describes the relation of narrowing to the gradient; in this formula \*elocity appears as a continuous function. In equations describing the relations of turbulence and disturbed flows, velocity is a step function---i.e., the phenomenon appears when velocity exceeds a critical level. So it is easy to see w-hy an abnormal gradient and a disturbed flow are usually associated in our patients, and also that they need not always be associated. Our clinical data on the latter situation are of interest. Discussion of unr~sztal jindings. In 17 cases the H F abnormality \vas present, but the pressure gradient across the aortic val\,-e was not abnormally increased. 1Iost of these were cases of aortic valve disease in which regurgitation predominated. Evi-
Disturbed
blood jlow in carotid artery
649
Fig. 3. Left, panels A, B and C. Factors in the presence or absence of the carotid HF abnormality. Carotid pulse derivative of B. T., age 54, diagnosed coronary heart disease. A, Before operation, note HF abnormalities. B, Twelve days after coronary bypass operation; note disappearance of HF abnormalities. C, Two months postoperative; note return of HF abnormality. PD max was 300, 276, and 300 mm. Hg per second in the three records. Iii& p,zneZ, Carotid pulse derivative over force BCG of N. R., age 23, wide open aortic regurgitation, PD max = 4,500 mm. Hg per second, which is record breaking. Calibration of force BCG, 13 small divisions = 275 (103) dynes. So this record is also huge. The aortic valve gradient was normal. Note that, in the presence of what must have been a very great blood velocity, HF abnormalities in the carotid PD are absent.
dently, a roughening without narrowing of the orifice may produce a disturbed flow causing too little impedance to produce gradient abnormality. In five cases the gradient was found to be abnormally increased, but no disturbed flow was detected. Such findings might have been due to an artefact for which we were on the lookout; should any patient be more excited at catheterization than when the pulse derivative was taken, such fmdings might well result. However, the pulse rates recorded at the t\vo tests lvere so similar in each of these five patients that it is hard to believe that differences in excitement jvere the cause of our findings. It is easier to believe that the increased impedance in these cases was due to aortic narrowing alone, the lesion having so little roughness that a disturbed flop- did not accompany it. The possibility that disturbed flojl- in the carotid might be created lvithout an aortic lesion should also be discussed, for we ha\-e five cases in which the HF abnormality Ii-as present without any clinical evidence of aortic valve disease. All these were cases of advanced rheumatic heart disease \I-ith several mitral valvulitis. To account for murmurs heard in the aortic area \I-hen that valve is normal, it has been suggested12
that, when blood regurgitates through a deficient mitral valve in sufficient amount, the jet strikes the atria1 wall adjacent to the aortic arch; such a jet might not only produce an audible murmur but might also set up vibrations in the aortic blood which our sensor would detect. While one should not forget that an aortic lesion, so common in advanced cases of RHD, might have been present in these five cases, though undiagnosed, those doing the catheterization were convinced that this valve \vas normal. It is also conceivable that small elements of a myocardium nhich had lost the coordination of its contraction might beat such a rapid tattoo on the ventricular blood that rapid fluctuation of the rate of change of pressure would appear in the carotid. High frequency distortions are often superimposed on undamped ventricular pressure records, and perhaps too often dismissed as artefacts. But II-e found no evidence of HF distortion in the contour of the ballistocardiograms of an)- of these cases. The common types of cardiac incoordination produce distortions of these records of a lo\\-er frequency than those encountered in the carotid HF abnormality. While other possibilities cannot be ruled out at this time, the genesis of disturbed
flop\- in the carotid artery is clearly related to a lesion of the aortic valve in the great majority of our cases. Conclusions
Records of the carotid pulse and its first time derivative have been taken, under standard resting conditions, in 349 cardiac patients, 180 of whom were subjected to cardiac catheterization. These results have been analyzed to throw light on an abnormality of pulse contour, conspicuous in the pulse derivative, a burst of high frequency distortion occurring at and after the peak of the main wave. The presence of this abnormality is closely related to the presence of aortic valve lesions, diagnosed either by the aortic valve gradient, or by conventional clinical evidence. While such a lesion must be a prime factor in its genesisin most cases, the evidence also indicates that a second factor must be present before the abnormality is produced, sufficient velocity of the ejected blood. This theory is satisfactory in 98 per cent of our cases, the few discrepancies are discussed. Such rapid fluctuations in the carotid pulse derivative indicate a disturbance of blood flow in which its normal streamlined character is broken up by vortices, jets, and eddies. Such a disturbance should not be called turbulence, because turbulence is defined today as a phenomenon of much higher frequency than our methods would detect. The eddies and whorls of such disturbed flows must increase the impedance to cardiac ejection and, like turbulence, make the heart’s task more difficult. This handicap is very common in aortic valve disease.
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