Seminar on Clinical Application
of Techniques to Measure Blood Flow in Man. Part IV ALBERT0
BENCHIMOL,
MD, FACC, Guest Editor
Clinical Application of the Doppler Ultrasonic Flowmeter
ALBERT0 KENNETH Phoenix,
BENCHIMOL, 8. DESSER,
MD, MD
FACC
Arizona
instantaneous and continuous measurement of phasic blood flow velocity was obtained with the Doppler ultrasonic flowmeter system in over 700 patients. Using transcutaneous and implanted probes, flow velocity was recorded from arteries in normal subjects and patients with aortic valvular and subvalvular disease, arrhythmias, myocardial infarction and congestive heart failure. Catheter probe recordings were obtained from the superior vena cava, right atrium, right ventricle, aorta, carotid arteries and coronary arteries in patients with a variety of clinical disorders. Ventricular diastolic and atrial systolic flow in atrial septal defect, compensatory diastolic flow acceleration in tricuspid insufficiency, peak flow velocity variations dependent on previous cycle length in arrhythmias, small atrial contribution to ventricular systolic flow, diagnostic recognition of aortic valvular disease, and other flow velocity relations are stressed.
The purpose of this report is to review our experience with the Doppler ultrasonic flowmeter. This technique has permitted both noninvasive and invasive study of phasic flow velocity within the cardiovascular system. The analysis of wave forms obtained with this device has elucidated phasic flow characteristics of normal subjects and patients with cardiovascular abnormalities.
Materials and Methods
for Cardiovascular DisHospital, Phoenix, Ariz. This investigation was supported in part by the Nichol’s Memorial Fund. Address for reprints: Albert0 Benchimol, MD, Good Samaritan Hospital, 1033 E. McDowell Rd., Phoenix, Ariz. 85006. From the
eases,
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institute
Good Samaritan
For the past G years, we have used this technique in over 700 patients with a variety of cardiovascular disorders. Normal subjects and patients with heart disease were studied utilizing. 3 methods of recording phasie flow velocity: transcutaneous probe, implanted probe and catheter probe. These probes are connected to a Doppler ultrasonic flowmeter. This technique of measuring flow velocity and the instrumentation and principles were originally described by Franklin et al.‘,’ Two lead zirconate piezoelectric hemidiscoid crystals are afixed to the probe being utilized. High frequency sound (‘7 to 10 mHz1 from 1 crystal hemidise is coupled to blood passing through the vessel lumen or cardiac chamber under study. A portion of the emitted sound is backscattered by the blood cells and detected by the other crystal hemidisc. The reflected signal differs in frequency from the incident signal by an amount proportional to the velocity of the blood cells. Thus, the frequency of the backscattered sound is proportional to blood velocity. Zero flow velocity is obtained by briefly disconnecting the input signal to the frequency meter, since zero frequency shift corresponds to zero velocity. continuous determination of As with the electromagnetic sensor, blood flow velocity with a high frequency response is possible with this approach. The Doppler sensing devices do not have to be calibrated individually since they are calibrated by the Doppler equation. Electromagnetic flowmeter sensing devices need to be calibrated individually.:’
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The majority of wave forms described in this review were obtained with a Doppler unit that did not distinguish between forward and reverse flow velocity but inscribed both as an upright deflection on the record. A bidirectional Doppler unit is currently being utilized for further investigation of phasic blood flow velocity in man, and a few observations relevant to this technique will be discussed. The crystals are mounted Transcutaneous probe: on a plastic unit placed 45’ to the skin surface over the course of an underlying .vessel. Using commercially available gel, the transducer is filled. Gluing of the probe to the skin over the blood vessel is accomplished with pressure adhesive. Maximal pulsatile excursion of the vessel to be probed is the optimal site of application. Motion of the patient causes negligible disturbance in monitoring. Implanted probe: A variety of probes are available for surgical implantation around the blood vessels. Our studies in man using this technique have been restricted to femoral and brachial arterial flow velocity measurements in which 4, 5 or 6 mm cuff probes were used. Catheter probes : The 2 hemidiscs of crystal, measuring 1.5 mm in diameter, are mounted on the end of a standard no. 6, 7 or 8 woven Dacron@ cardiac catheter.4 Mounting of the hemidiscs on a “double lumen” catheter has allowed measurement of flow velocity (from tip of catheter) and pressure from near the site in the vascular bed where flow is being measured. The flow meter signals from each probing method are recorded on a multichannel tape recorder (Sanborn model 3900) and on a light beam oscillographic recorder (Electronics for Medicine, Model DR 12). Simultaneous recordings of the electrocardiogram, phonocardiogram and intracardiac pressures during right and left heart catheterization are frequently performed. In addition, simultaneous measurements using 2 techniques, that is, transcutaneous probe and implanted probe, have been carried out.
Results
and Comments
Transcutaneous and Implanted Probes5-7 Normal
Femoral, brachial, radial and dorsalis pedis arterial flow velocity analog records consisted of a major systolic wave related to ventricular systole. This wave represented forward flow and correlated well in timing with intraarterial pressure curves obtained from the same sites. A secondary wave followed the primary or antegrade wave. It occurred in early diastole and coincided in time with the dicrotic notch of a simultaneous arterial pressure curve. The probable source for this wave is centrally directed arterial retrograde flow, although part of this velocity pattern may represent forward flow. The wave forms of the flow velocity curves obtained with the transcutaneous and implanted probe techniques were similar in amplitude and contour in both normal and abnormal subjects.
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Figure 1. Simultaneous lead II of the electrocardiogram femoral arterial (FA) flow (implanted probe) recording 50 year old man with aortic stenosis and rate-related bundle branch block (LBBB). Note the characteristic rise of the systolic flow wave seen with aortic stenosis.
and i,n a left slow
Abnormal
Aortic valvular and subvalvular disease : Aortic stenosis resulted in a decreased peak flow velocity.; slow rise of the ascending limb of the antegrade wave, prolonged and rounded peak, and diminished peak flow velocity of the secondary wave (Fig. 1). A different pattern was noted in patients with idiopathic hypertrophic subaortic stenosis. The ascending limb was inscribed rapidly, and there was a sharp and early peak flow velocity. Administration of isoproterenol resulted in exaggeration of these findings. Patients with aortic insufficiency manifested a rapid ascending limb, sharp peak, rapid fall-off. and increased area under the curve. A large secondary wave with a slow fall-off was common. In the presence of combined aortic stenosis and insufficiency, a large secondary wave indicated that aortic insufficiency was a significant hemodynamic lesion.” Thus, the Doppler technique is a useful modality for the noninvasive recognition of aortic valvular and subvalvular disease. Acute myocardial infarction-coronary care unit: Dorsalis pedis arterial blood flow velocity was determined in the coronary care unit in 15 patients with acute myocardial infarction. A portable frequency-modulation tuner allowed the nurse to detect abnormalities of flow velocity by audible monitoring. Despite electrocardiographic evidence of normal sinus rhythm, pulsus alternans developed in 2 patients 30 to 60 minutes before the onset of acute left ventricular failure.? This technique may play an important role in coronary care, specifically of patients with myocardial infarction. It is a useful adjunct to electrocardiographic monitoring because, in addition to monitoring of heart rate, it provides information on qualitative and quantitative flow. Arrhythmias : The transcutaneous method offers a simple noninvasive technique for monitoring peripheral blood flow during arrhythmias. A trial arrhythmias : Atria1 and atrioventricular (A-V) junctional premature beats caused a variable peak flow velocity, dependent on the preceding diastolic interval (Fig. 2). Extrasystoles occurring 0.36 second or less after the previous sinus beat usually did not result in measurable flow velocity. In the majority of cases, the post-
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Lead II of the electrocardiogram and simultaFigure 2. and implanted prolbe recordings of neous transcutaneous brachial arterial (BA) flow velocity from a 51 year old man with an old inferior wall myocardial infarction and extra. systoles. The arrows mark 2 junctional premature beats. Note the qualitative similarity of the wave forms recorded with the 2 techniques. The extrasystoles result in diminished peak flow velocity.
extrasystolic beat manifested higher peak t-low velocity; the longer the diastolic cycle length, the greater the peak flow of the subsequent beat. However, this correlation was more apparent in patients with rapid ventricular rates. Length of the R-R interval had less significance at slower rates. Conversion of atria1 fibrillation to sinus rhythm resulted in significantly greater peak flows in those patients who had atria1 fibrillation with ventricular rates greater than 120/min. It appears that improvement in flow after electroconversion is more dependent on the subsequent ventricular rate than on a properly coordinated atria1 eontraction. Ventricular arrhythmias: Ventricular premature beats resulted in a small peak flow velocity. Shorter extrasystolic intervals caused lesser peak flows, and postextrasystolic increase in flow velocity was common. Ventricular tachyeardia resulted in reduced peak flow velocity with increase in the diastolic flow component (Fig. 3). Fifty percent of the “regular beats” occurring during pacemaker-induced bursts of ventricular tachycardia resulted in no measurable arterial flow velocity. The focus of ventricular stimulation did not ap-
Figure 3. Simultaneous lead II of the electrocardiogram and dorsalis pedis arterial pulse and transcutaneous flow velocity recordings from a 60 year old man with acute anterior wall myocardial infarction, left anterior hemiblock and recurrent ventricular tachycardia. Note the decreased peak systolic and increased diastolic flow velocities during the tachyarrhythmia. After each paroxysm of tachycardia, there is a diastolic pause and an increase in the flow velocity associated with the succeeding sinus beat.
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pear to influence the degree of peripheral perfusion. In all arrhythmias with rapid heart rates, the peak flow velocity of the last beat usually had a higher value than other beats during the tachyarrhythmia. The explanation of this observation is not apparent.” Ventricular fibrillation predictably resulted in a marked decrease of flow velocity as long as the arrhythmia lasted. Greater peak flow veComplete heart block: locities were observed with beats associated with a P-R interval between 80 and 160 msec. Further prolongation resulted in a decrease in flow velocity. The lowest peak flow velocity occurred when atria1 contraction took place during ventricular systole. Catheter Studies Normal
Superior vena cava-right atrium*: There was no significant difference in flow velocity wave forms recorded from the superior vena cava and right atrium. Three distinct waves were recorded. An S wave, the predominant wave, followed the QRS complex and peaked at mid or late ventricular systole. The D wave was inscribed during ventricular diastole and coincided with the Y descent of the right atria1 pressure curve. An A wave was seen in half of the patients. It usually was represented by a notch in the ascending limb of the following S wave. It coincided with the downslope of the a wave of the right atria1 or superior vena caval pressure recording. Inspiration caused an increase in amplitude of all flow velocity records and, conversely, expiration reversed these changes. The Valsalva maneuver resulted in a sharp decline in flow velocity to nearly zero. Upon cessation of the maneuver, flow velocity increased sharply with a significant overshoot. The flow velocity records in the superior vena cava and right atrium exhibit an inverse relation with the pressures recorded in those areas. The A wave represents minimal retrograde flow from atria1 contraction, and this has been confirmed with use of the bidirectional Doppler technique. The S wave results from flow increase in the superior vena cava and right atrium due to atria1 relaxation. Maximal acceleration of blood toward the right heart chambers during the middle of ventricular diastole causes peaking of the D wave. Right ventricle9 : Records obtained from the right ventricular outflow tract revealed a systolic wave related to ventricular systole and occurring during the ascending limb of the right ventricular pressure curve. This wave represents acceleration of blood from right ventricular ejection toward the pulmonary artery. The onset of this wave followed the QRS complex of the electrocardiogram by 50 to 100 msec. Inspiration, expiration and the Valsalva
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maneuver altered the phasic flow velocity in a manner similar to that of the superior vena cavaright atria1 records. AortalO: The aortic flow velocity curve was recorded as a major systolic wave related to ventricular systole. The onset of this wave followed the QRS complex of the electrocardiogram by 50 msec, and the wave peaked during the ascending limb of the T wave. Peak flow resulted in a short, sharp frequency shift and was followed by a rapid downward slope. The downslope was interrupted by a sharp notch occurring at the time of the second heart sound and dicrotic notch of simultaneous phonocardiographic and aortic pressure recordings. This notch appears to represent the end of mechanical systole. Peripherally directed forward aortic flow velocity resulted in the primary wave. A secondary wave followed the primary wave. This wave may represent centrally directed retrograde flow (Fig. 4). In general, the configuration of the wave resembled that recorded from the femoral artery. Carotid artery” : The carotid arterial flow velocity pattern contour is different from that of the ascending aorta primarily because flow velocity in this vascular bed never returns to zero velocity, indicating that flow to the brain is continuous throughout the entire cardiac cycle. Inspiratory records revealed a decrease in both systolic and diastolic flow velocities ; expiration caused the reverse. With the onset of the Valsalva maneuver, carotid arterial flow velocity decreased and, upon cessation, returned to the control values with a slight overshoot. Coronary artery12 : Phasic coronary arterial flow velocity wave forms were characterized by a major diastolic wave representing maximal acceleration of blood during ventricular diastole. The systolic fraction of coronary blood velocity was less than 15 percent of the diastolic component. This predominant diastolic fraction was not found in any other vessel studied in man and is unique for coronary arterial flow velocity. However, large fractions of diastolic flow do occur in other vascular beds such as the renal and carotid arteries.
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Figure 4. Simultaneous lead II of the electrocardiogram and mean pulmonary arterial pressure, sot-tic pressure and aortic flow velocity recordings from a 39 year old man with coronary artery disease. During performance of a Valsalva maneuver there is a rise followed by a decrease in systolic and diastolic aortic flow velocities and pressure. On termination of the maneuver there is a marked “overshoot” phenomenon. The records subsequently return to control levels. Note the pri. mary and secondary aortic flow velocity waves.
Tricuspid insufficiency*“: The major abnormalities in patients with permanent tricuspid insufficiency studied with catheters in the superior vena cava and right atrium were a diminished S wave and a large increase in the diastolic D wave. The amplitude of the S wave was inversely proportional to the systolic regurgitant wave of the right atria1 pressure curve. The peak of the D wave occurred during the maximal decline in right atria1 pressure. Patients with a severe degree of tricuspid insufficiency had the largest D waves. Velocity of flow in patients with tricuspid insufficiency decreases during ventricular systole with compensatory acceleration occurring during ventricular diastole. Two opposite streams of blood flowing during ventricular systole result in a diminished superior vena caval flow: first, the regurgitant stream from the right ventricle to the right atrium and superior vena cava ; second, that from the superior vena cava toward the right atrium. The acceleration of diastolic flow velocity in these patients was also recorded in the inferior vena cava, LII
Abnormal
Atria1 septal defect13 : Six patients with a secundum type of atria1 septal defect were studied with a flow catheter in the right atrium. There was an increase in the amplitude of the A and D waves, but the S wave remained normal in size. It appears that a large fraction of the left to right shunt in patients with atria1 septal defect occurs during atria1 contraction and early ventricular diastole. This finding may explain the mid-diastolic murmurs, with or without atria1 systolic components frequently heard or recorded in patients with atria1 septal defect (Fig. 5).
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Figure 5. Simultaneous lead II of the electrocardiogram, tricuspid area phonocardiogram (TA), right atrial pressure (RA PRESS.), left atrial pressure (LA PRESS.) and left atrial flow. velocity (VEL) recordings from a 31 year old woman with atrial septal defect. Note the large diastolic flow component (D) which probably represents reverse flow velocity toward the right atrium.
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Figure 6. Simultaneous lead II of the electrocardiogram and aortic pressure, mean right atrial pressure and aortic flow velocity recordings from a 59 year old man with no evidence of heart disease. Note the right atrial pacemaker artifact (PAC. ART.) discharging at a rate of 140/min. There is progressive increase of the P-R interval until an atria! beat is blocked (no. 5) and Wenckebach periods of second degree atrioventricular block then occur. The first beat of each subsequent cycle manifests a large aortic peak flow velocity with a corresponding increase in aortic pressure, dependent on preceding diastolic cycle length.
Figure 7. Simultaneous lead II of the electrocardiogram, right ventricular (RV) pressure and right coronary arterial blood flow velocity recorded from a normal 19 year old girl. Note the large diastolic fraction of coronary arterial flow velocity during sinus rhythm. During a burst of catheter-induced ventricular tachycardia (VT), coronary artery blood flow velocity falls to almost zero base line values despite measureable right ventricular pressure. Upon termination of the tachyarrhythmia there is an abrupt increase in coronary arterial blo,od flow velocity to levels greater than pretachycardia values.
hepatic vein and jugular vein, thus confirming the well known clinical findings of a pulsatile liver and distended jugular vein observed in this condition. Arrhythmias-extrasystoles: Right atria1 and superior vena caval flow patterns recorded during atria1 and ventricular premature beats revealed biphasic curves with small S and large D waves.H Postextrasystolic S wave increase was present after both types of premature beats, In patients with atria1 extrasystoles, if atria1 contraction occurred at a time when the tricuspid valve was still closed, the S wave was small and the D wave was large. This latter finding is compatible with transient episodes of tricuspid insufficiency during extrasystoles.14 Premature contractions occurring early in the cardiac cycle (less than 300 msec after the preceding beat) resulted in practically no right
ventricular flow velocity.” Greater postextrasystolic peak flow velocity of the right ventricle was observed with (1) smaller peak velocity of the extrasystolic beat, (2) longer compensatory pauses, and (3) ventricular origin of the premature beat. Flow velocity was affected in the aorta and carotid artery much the same as in the right ventricle by extrasystoles. Atria1 fibrillation : During atria1 fibrillation, the A wave was absent from the right atria1 flow velocity record. The flow contour was biphasic with a large D wave and a large S wave. After cardioversion, the A wave reappeared, thus confirming that this wave probably represents a small retrograde flow from atria1 contraction.R Right ventricular, aortic and carotid arterial flow responses to atria1 fibrillation were similar.“ml’ Peak flow velocity variations were directly proportional to the preceding cycle length and inversely proportional to the peak flow velocity of the preceding beat; these variations were more pronounced at ventricular rates greater than 130/min. These beat to beat changes in flow velocity were also seen during pacemaker-induced atria1 tachycardia with block (Fig. 6). Ventricular tachycardia: In right atria1 records, the peak flow velocity decreased by 20 to 30 percent with the onset of this arrhythmia. The short diastolic periods during ventricular tachycardia increase the diastolic fraction of the flow velocity.8 Right ventricular blood velocity fell rapidly to zero despite measurable right ventricular pressuresy With the onset of ventricular tachycardia, aortic peak flow velocity decreased and, when the tachyarrhythmia lasted more than a few minutes, the peak flow velocity rose slightly. Arterial pressure curves revealed pulsus alternans in many patients when the rate was greater than 150/min. Flow velocity “alternans” similarly occurred. This “flow alternans” may be explained on the basis of
Simultaneous lead II ,of the electrocardiogram, Figure 8. tricuspid area phonocardiogram (TA), bidirectional aortic flow velocity (VELDC.), aortic pressure and right atrial pressure recordings from a 38 year old man with aortic insufficiency. Note the characteristic bifid systolic forward flow velocity recording of aortic incompetence. The shaded area beneath zero base line represents retrograde flow velocity. A third forward flow velocity wave is recorded during early diastole, followed by a small but appreciable intermittent reverse flow velocity component. 1 = 1st heart sound, 2 = 2nd heart sound, SM z systolic murmur, DM = diastolic murmur.
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alternating increases and decreases in ventricular volume.l” During supraventricular and ventricular tachycardia, cycle lengths with very short intervals resulted in reduced yet measurable flow. Muscular potentiation of some form may explain this phenomenon. In contrast, an extrasystole occurring after a diastolic interval of 350 msec or less caused no measurable flow velocity. Carotid arterial flow recordings were similar to those of the aorta. Approximately 50 percent of the beats resulted in no measurable carotid flow velocity. This finding provides evidence for the observation that patients with ventricular tachycardia frequently have syncopal episodes that are related to decreased cerebral perfusion11 Ventricular tachycardia resulted in a marked diminution of coronary arterial blood flow velocity, and at times zero flow velocity was recorded (Fig. 7). Heart block : Velocity recordings from the right atrium revealed that in patients with first degree A-V block, the A-S wave interval in the flow curve was prolonged in proportion to the P-R interval of the electrocardiogram. The A waves correlated well with P waves of the electrocardiogram during second and third degree A-V block.R Subjects with complete heart block manifested variations in the amplitude of the S and D waves as a function of the P-R interval. The morphologic aspects of the records were similar to those described for tricus-
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pid insufficiency. When the P wave was inscribed during ventricular systole, tricuspid insufficiency probably occurred.‘4 Aortic flow velocity records during complete heart block were similar in variation to those from the right atrium, suggesting that effective atria1 contraction can increase stroke volume by a small but appreciable amount.10 Bidirectional
Flow Velocity Studies
Development of a directional blood flow velocity sensorlo and its application to a Doppler flowmeter catheter has permitted further characterization of phasic flow velocity dynamics in normal subjects and patients with cardiovascular disease. Bidirectional flow velocity records obtained from the aorta revealed marked retrograde flow during ventricular extrasystoles and tachycardia, not unlike that seen with organic aortic valvular insufficiency (Fig. 8). Conclusion
This technique is valuable in the invasive and noninvasive study of flow velocity dynamics within the cardiovascular system. Instantaneous and continuous measurement of phasic blood flow velocity in normal subjects and patients with a variety of cardiovascular abnormalities appears to be its major advantage.
References 1. Franklin DL, Schlegel W, Rushmer RF: Blood flow measured by Doppler frequency shift of back-scattered ultrasound. Science 134564-565, 1961 2. Franklin D, Schlegel W, Watson NW: Ultrasonic Doppler shift blood flowmeter: circuitry and practical applications. Biomed Sci Iristrum 1:309-315, 1963 3. Wexler L, Bergel DH, Gabe IT, et al: Velocity of blood flow in normal venae cavae. Circ Res 23:349-359, 1963 4. Stegall HF, Stone HW, Bishop VS, et al: A catheter tip pressure and velocity sensor (abstr). Proc 20th Ann Conf Eng Med Biol 27:4, 1967 5. Benchimol A, Maia IG, Gartlan JL, et al: Telemetry of arterial flow in man with a Doppler ultrasonic flowmeter. Amer J Cardiol22:75-84, 1968 6. Benchimol A, Maroko P, Gartlan J, et al: Continuous measurement of arterial flow in man during atrial and ventricular arrhythmias. Amer J Med 46:52-63, 1969 7. Benchimol A, Pedraza A, Brenner L, et al: Transcutaneous measurement of arterial flow velocity with a Doppler flowmeter in normal subjects and patients with cardiac dysfunction. Chest 57:69-78, 1970 8. Benchimol A, Stegall HF, Gartlan JL, et ak Right atrium and superi,or vena cava flow velocity in man measured with the Doppler catheter flowmeter telemetry system Amer J Med 48:303-308, 1970
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9. Benchimol A, Tio S, Gartlan J: Radiotelemetry of right ventricular blood velocity in man. Amer J Cardiol 25: 649-654, 1970 10. Benchimol A, Stegall HF, Maroko PR, et al: Aortic flow velocity in man during cardiac arrhythmias measured with the Doppler catheter-flowmeter system. Amer Heart J 78:649-659, 1969 11. Benchimol A, Barreto EC, Goldstein MR, et al: Measurement of phasic carotid artery flow velocity in man. Amer J Med 49:170-174, 1970 12. Benchimol A, Stegall HF, Gartlan JL: New method to measure phasic coronary blood flow velocity in man. Amer Heart J 81:93-101,197l 13. Benchimol A, Barreto EC, Garilan JL: Right atrial flow velocity in patients with atrial septal defect. Amer J Cardiol 25:381-386, 1970 14. Benchimol A, Barreto EC, Tio S: Phasic right atrium and superior vena cava flow in patients with tricuspid insufficiency. Amer Heart J 79:603-612, 1970 15. Benchimol A, Desser KB, Gartlan JL: Bidirectional blood flow velocity in the cardiac chambers and great vessels studied with the Doppler ultrasonic flowmeter. Amer J Med, in press 16. McLeod FD Jr: Directional Doppler demodulation (abstr). Proc 20th Ann Conf Eng Med Biol 27:1, 1967
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