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Doppler measurement of phasic continuous left ventricular blood flow velocity during ventricular arrhythmias
Doppler measurement of phasic continuous left ventricular blood flow velocity during ventricular arrhythmias Albert0 Benchimol, M.D. Kenneth B. Desser, M.D. Ting Fu Wang, M.D. Phoeniz, Ark
Introduction of a Doppler flowmeter catheter into the left ventricle of man has provided new information regarding phasic, continuous, and instantaneous blood flow velocity.1 We describe here the measurement of left ventricular blood velocity during selected ventricular arrhythmias in conscious human subjects. Material
and method
Sixty-eight patients comprised the study group. There were 61 men and 7 women whose ages ranged from 22 to 70 with a mean of 46 years. Fifty subjects had coronary artery disease, 6 had valvular heart disease, 8 had primary myocardial or pericardial heart disease, and 4 had no evidence of cardiac abnormality. Normal subjects were studied because of the presence of chest pain or systolic murmurs originally thought to represent heart disease. All diagnoses were established on the basis of complete rightand left-heart catheterization, selective coronary cineangiography, and indicator dilution curves. All patients were studied in the postabsorptive nonsedated state in the supine position. Phasic instantaneous left ventricular blood flow velocity was measured by radiotelemetry utilizing the Doppler ultrasonic flowmeter catheter. Details concerning this technique have recently been described’ and are summarized as follows: using local anesthesia with 1 per cent lidocaine, the Doppler flowmeter catheter was introduced into From the Institute for Cardiovascular Diseases, Good Samaritan Hospital, Phoenix. Supported in Part by the Nichols Memorial Fund Received for publication March 6, 1974. Reprint requests: Dr. Alhertn Benchimol, Good Samaritan Hospital, P. 0. Box 2989, Phoenix, Ark 85062.
742
a brachial arterial incision and passed in a retrograde fashion across the aortic valve into the left ventricle. A No. 7 or 8 Zucker bipolar catheter connected to a Statham P23 Db-strain gauge was passed to the right heart via a medial antecubital vein cutdown for the purpose of obtaining right atria1 or ventricular pressures. All catheter movement was monitored by constant fluoroscopic image intensification. Phasic left ventricular blood velocities, right-heart pressures, along with Lead II of ‘the electrocardiogram and at times phonocardiograms, apexcardiograms, or external carotid pulse tracings were simultaneously recorded in an Electronics for Medicine DR-12 oscilloscopic photographic recorder. Ventricular arrhythmias were either spontaneous in origin, evoked by right ventricular catheter motion or, in a single case, induced by performance of a Valsalva maneuver. The blood velocity waveforms described in this paper represent those recorded from left ventricular outflow tract or in a few cases, the midcavity position. In the absence of aortic valvular regurgitation, outflow tract blood velocity patterns are characterized by a large systolic ejection wave followed by a smaller diastolic fraction. Left ventricular midcavity wave contours are usually triphasic, with atrial, systolic ejection, and diastolic components.’ Reslllts Left ventricular blood flow velocity was monitored during ventricular extrasystoles in 53 subjects. Premature depolarizations reduced peak outflow tract blood velocities in direct relation to their coupling intervals; when the latter were less Ventricular
premature
beats.
December, 1974, Vol. 88,
NO.
6, pp. 742-747
Doppler measurement of’L V blood flow velocity
1. Simultaneously recorded Lead II (L II1 of the electrocardiogram, tricuspid area (TA) phonocardiogram, external carotid artery pulse tracing (CT), and left ventricular outflow tract blood velocity in a 48-year-old man with coronary artery disease. Ventricular premature beats reduce peak left ventricular blood flow velocity in relation to their coupling intervals. The last extrasystole (QRS complex No. 151, with a preceding R-R interval longer than 0.5 second, produces a minimal decline of peak blood velocity. The first salvo of premature depolarizations is followed by a five-beat period of high-low blood velocity “alternans” (beats Nos. 7 through 11). Note that the changes in peak blood velocity are paralleled by similar variation in the amplitude of the external carotid arterial pulse tracing. Fig.
Fig. 2. Simultaneously recorded Lead II (L II) of the electrocardiogram, tricuspid area (TA) phonocardiogram, right ventricular (RF’) pressure, apexcardiogram (ACG), and phasic left ventricular midcavity blood flow velocity in a 44-year-old man with coronary artery disease. Catheter-induced ventricular premature beats result in a shortened preceding diastolic blood flow velocity time and a decline of subsequent peak systolic and diastolic blood velocities. Note that the small left ventricular systolic blood velocities are associated wi1.h minimal amplitude on the simultaneously recorded apexcardiogram.
than 0.5 second, the diminution of blood velocity was most manifest. Variations of peak outflow tract blood velocity were accompanied by similar alterations in the amplitude of deflection on simultaneously recorded external carotid pulse tracings. Periods of postextrasystolic left ventricular blood velocity alternation were observed in four subjects (Fig. 1). Peak left ventricular midcavity systolic blood velocity declined in relation to the degree of QRS complex prematurity as described above for out-
American Heart Journal
flow tract records. In addition, ventricular extrasystoles reduced preceding diastolic blood velocity times and effected a diminution of subsequent peak diastolic blood flow velocities. The reduction of peak systolic left ventricular blood velocity induced by premature beats was paralleled by a decrease in the total deflection of the simultaneously recorded apexcardiogram (Fig. 2). In two patients with aortic insufficiency, peak systolic blood velocities were diminished by premature ventricular contractions, yet left ven-
743
Benchimol, Desser, and Wang
E O-LCONTROL
I’
3. Simultaneously recorded Lead II (L II) of the electrocardiogram, tricuspid area (TA) phonocardiogram, external carotid arterial pulse tracing (CT), left ventricular outflow tract blood velocity, and right ventricular (RV) pressure in a 49-year-old man with aortic insufliciency. Compared with sinus beat No. 5, and ventricular fusion beat No. 1, ventricular premature beats Nos. 2 and 3 along with an escape beat (No. 41 are associated with lower peak systolic blood velocities. Peak diastolic blood velocity remains relatively stable throughout the record
tricular diastolic blood velocities remained stable (Fig. 3). Ventricular tachycardia. A total of 24 episodes of ventricular tachycardia were recorded in 18 subjects. These tachyarrhythmias produced a 62 per cent average decline of peak left ventricular blood velocity for the study group (Fig. 4). The most profound decrease of phasic blood velocity was observed in a 44-year-old man with coronary artery disease. In this latter subject, only one of nine QRS complexes recorded during ventricular tachycardia generated a phasic systolic blood velocity wave (Fig. 5). In three patients, phasic left ventricular blood velocity rapidly returned to control levels after an initial decline during ventricular tachycardia (Fig. 6). A 54-year-old woman with no catheterization evidence of heart disease presented with a history of syncopal-like episodes during straining at stool. Voluntary execution of the Valsalva maneuver produced bursts of ventricular tachycardia. These tachyarrhythmias reduced peak left ventricular outflow tract blood velocity by an average of 50 per cent (Fig. 7).
744
ENT. TACHYC.
N=18 P
”
Fig.
5
Fig. 4 Mean values (& 1 standard deviation) for peak left ventricular blood velocity during control rhythm and ventricular tachycardia in 18 subjects: control = 46 f 10 cm. per second, ventricular tachycardia = 17 f I1 cm. per second, P < 0.001.
Discussion
The findings described here demonstrate the unfavorable influence of ventricular arrhythmias on phasic left ventricular blood flow velocity in conscious man. Reductions of left ventricular pressure, stroke output, and other indices of left ventricular performance have previously been described in human subjects during ventricular tachycardia. These observations have been generally based on phasic left ventricular pressure measurement and indicator-dilution curves obtained during elective ventricular pacing.2-5 Diminution of the diastolic filling time, reduced coronary blood flow and in turn, less forceful left ventricular contraction produced the decline of blood cell velocity observed in the course of ventricular arrhythmias. Shortened diastolic left ventricular blood velocities noted at midcavity sites indicate the adverse effects of tachyarrhythmias on left ventricular filling. On the other hand, maintenance of peak diastolic blood velocities in subjects with ventricular arrhythmias and aortic valvular regurgitation can be ascribed to retrograde directional blood flow from the aorta to the left ventricular cavity. Enhanced reverse aortic blood velocity has been noted to occur in some patients during ventricular arrhythmias and may be secondary to imcomplete aortic
December,
19;4,
Vol. 88, No. 6
Doppler
measurement
of L V blood flow velocity
Fig. 5. Simultaneously
recorded Lead II (L II) of the electrocardiogram, tricuspid area (TA) phonocardiogram. continuous pulmonary artery (PA), and right ventricular (RV) pressures and left ventricular outflow tract blood velocity in a 44-year-old man with coronary artery disease. A paroxysm of ventricular tachycardia effects a marked decline of left ventricular blood velocity and only a single small systolic flow velocity wave is recorded during the arrhythmia.
Fig. 6. Simultaneously
recorded Lead II CL II) of the electrocardiogram, right ventricular (RV) pressure, and left ventricular outflow tract blood velocity in a 59-year-old man with coronary artery disease. An episode of ventricular tachycardia produces an initial 80 per cent decline of peak flow velocity. Subsequent left ventricular blood velocities return to control levels, The alterations of phasic left ventricular blood velocity are generally paralleled by concordant changes in phasic right ventricular pressure.
American
Heart Journal
746
Benchimol,
Demer, and Wang
BRA
PRESS.
Fig. 7. Simultaneously recorded Lead II CL II) of the electrocardiogram, mean right atria1 (RA) pressure, and phasic left ventricular outflow tract blood velocity in a 54-year-old woman with no catheterization evidence of heart disease. Straining against a closed glottis results in a rise of mean right atria1 pressure and two episodes of ventricular tachycardia. The tachycardias reduce peak blood flow velocity by an average of 50 per cent.
valvular closure during such rhythm disturhances.6 Of interest was the recording of postextrasystolic left ventricular blood velocity alternation in four subjects. To our knowledge, this represents the first description of blood velocity alternans within the left ventricle of man. Such highlow alternation of peak blood velocity is probably the underlying basis for documented aortic flow alternation and may be due to beat-to-beat changes of end-diastolic myocardial fiber length and ventricular contractility.’ In three patients, peak left ventricular blood velocities rapidly returned to near control levels after an initial decline during ventricular tachycardia. This latter observation can be attributed to cardiac potentiation, possibly mediated via the sympathoadrenal system.*pg Particularly noteworthy was the marked reduction of peak left ventricular blood velocity observed in a subject with paroxysmal ventricular tachycardia during performance of a Valsalva maneuver. Straining against a closed glottis has been demonstrated to result in a diminution of coronary blood velocity which is related to the degree of concomitant right atriai pressure rise.lO It is possible that the myocardium of this patient with normal coro-
746
nary arteries was particularly sensitive to reduced coronary perfusion produced by straining. The limitations and advantages of Doppler catheter measurement of left ventricular blood velocity have been previously described in detail.lDespite the fact that the crystal-tipped catheter senses the velocity of blood cells in a chamber with rapidly changing dimensions, this technique is currently the only method which can instantaneously measure phasic left ventricular blood velocities on a continuous basis. Previous studies have demonstrated the untoward influence of ventricular tachycardia on aortic,” along with coronary,12 carotid l3 rena1,14 superior mesenteric,16 and peripheral arterial blood velocities.16 It is apparent that the decline of flow velocities in these ‘regional circulations can be linked to the basic left ventricular abnormalities noted in this study Summary
Phasic instantaneous left ventricular blood velocity was continuously measured by means of the Doppler ultrasonic flowmeter catheter radiotelemetry system in 68 patients with ventricular arrhythmias. Ventricular premature
December,1974, Vol. 88, No. 6
Doppler measurement of LV blood flow velocity
depolarizations reduced peak left ventricular blood velocities in relation to their respective coupling intervals, with R-R intervals less than 0.5 second producing the greatest decline. Ventricular tachycardia in 18 subjects produced a 62 per cent mean decrease in left ventricular blood velocity. In a single subject, performance of the Valsalva maneuver effected ventricular tachycardia and a concomitant marked diminution of phasic left ventricular blood velocity. These findings demonstrate the untoward influence of ventricular extrasystoles and tachycardia on left ventricular blood velocity and provide the underlying basis for reductions of blood velocity previously demonstrated in the regional circulations of man during similar arrhythmias. REFERENCES
1. Benchimol, A., Desser, K. B., and Gartian, J. L., Jr.: Left ventricular blood flow velocity in man studied with the Doppler ultrasonic flowmeter, Ate. HEART J. 86:294, 1973. 2. Ferrer, M. I., and Harvey, R. M.: Some hemodynamic aspects of cardiac arrhythmias in man; a clinicophysiologic correlation, AM. HEART J. 88~153.1964. 3. Same& P., Bern&in, W. H., Levine,‘S., and Lopes, A.: Hemodynamic effects of tachycardias produced by atria1 and ventricular pacing, Am, J. Med. 38906, 1965. 4. Benchimol, A., Ellis, J. G., Dimond, E. G., and Wu, T. L.: Hemodynamic consequences of atria1 and ventricular arrhythmias in man, AM. HEART J. 70:774 1966. 6. Benchimol, A., and Liggett, M. S.: Cardiac hemodynamits during stimulation of the right atrium, right ventri-
American Heart Journal
6.
7.
8.
9.
10.
11.
12.
13. 14. 15.
16.
cle, and left ventricle in normal and abnormal hearts. Circulation 33:933,1966. Benchimol, A., Desser, K. B., and Gartlan, J. L., Jr.: Bidirectional blood flow velocity in the cardiac chambers and great vessels studied with the Doppler ultrasonic flowmeter, Am. J. Med. 52:467,1972. Benchimol, A., Barreto, E. C., and Tio, S. T. W.: Phasic aortic flow velocity in patients with pulsus alternans, Br. Heart J. 32:696,1970. Nakano, J.: Effects of atria1 and ventricular tachycardias on the cardiovascular dynamics, Am. J. Physiol. 206:547,1964. Nakano, J.: Effects of atria1 and ventricular tachycardia on the cardiovascular dynamics in reserpinized dogs, Am. J. Cardiol. 14:89, 1964. Benchimol, A., Wang, T. F., Deaser, K. B., and Gartlan, J. L., Jr.: The Valsalva maneuver and coronary arterial blood flow velocity. Studies in man, Ann. Intern. Med. 77:357, 1972. Benchimol, A., Stegall, H. F., Maroko, P. R., Gartlan, J. L., and Brener, L.: Aortic flow velocity in man during cardiac arrhythmias measured with the Doppler catheter-fiowmeter system, AM.HEART J.78:649,1969. Benchimol, A., Matsuo, S., Desser, K. B., Wang, T. F., and Gartlan, J. L., Jr.: Coronary artery blood flow velocity during ventricular tachycardia in man, Am. J. Med. Sci. 264:277,1972. Benchimol, A., Barreto, E. C., Goldstein, M. R., and Gartlan, J. L., Jr.: Measurement of phasic carotid artery flow velocity in man, Am. J. Med. 48~170, 1970. Benchimol. A.. and Desser. K. B.: Phasic renal arterv blood flow velocity in man during cardiac arrhythmias, Am. J. Med. Sci. 261:161, 1971. Benchimol, A., Desser, K. B., and Gartlan, J. L., Jr.: Superior meaenteric artery blood velocity in man during cardiac arrhythmias, Gastroenterology 62:950, 1972. Benchimol, A., Maroko, P., Gartlan, J. L., Jr., and Franklin, D.: Continuous measurements of arterial flow in man during atria1 and ventricular arrhythmias, Am. J. Med. 4652, 1969.
747
Introduction of a Doppler flowmeter catheter into the left ventricle of man has provided new information regarding phasic, continuous, and instantaneous blood flow velocity.1 We describe here the measurement of left ventricular blood velocity during selected ventricular arrhythmias in conscious human subjects. Material
and method
Sixty-eight patients comprised the study group. There were 61 men and 7 women whose ages ranged from 22 to 70 with a mean of 46 years. Fifty subjects had coronary artery disease, 6 had valvular heart disease, 8 had primary myocardial or pericardial heart disease, and 4 had no evidence of cardiac abnormality. Normal subjects were studied because of the presence of chest pain or systolic murmurs originally thought to represent heart disease. All diagnoses were established on the basis of complete rightand left-heart catheterization, selective coronary cineangiography, and indicator dilution curves. All patients were studied in the postabsorptive nonsedated state in the supine position. Phasic instantaneous left ventricular blood flow velocity was measured by radiotelemetry utilizing the Doppler ultrasonic flowmeter catheter. Details concerning this technique have recently been described’ and are summarized as follows: using local anesthesia with 1 per cent lidocaine, the Doppler flowmeter catheter was introduced into From the Institute for Cardiovascular Diseases, Good Samaritan Hospital, Phoenix. Supported in Part by the Nichols Memorial Fund Received for publication March 6, 1974. Reprint requests: Dr. Alhertn Benchimol, Good Samaritan Hospital, P. 0. Box 2989, Phoenix, Ark 85062.
742
a brachial arterial incision and passed in a retrograde fashion across the aortic valve into the left ventricle. A No. 7 or 8 Zucker bipolar catheter connected to a Statham P23 Db-strain gauge was passed to the right heart via a medial antecubital vein cutdown for the purpose of obtaining right atria1 or ventricular pressures. All catheter movement was monitored by constant fluoroscopic image intensification. Phasic left ventricular blood velocities, right-heart pressures, along with Lead II of ‘the electrocardiogram and at times phonocardiograms, apexcardiograms, or external carotid pulse tracings were simultaneously recorded in an Electronics for Medicine DR-12 oscilloscopic photographic recorder. Ventricular arrhythmias were either spontaneous in origin, evoked by right ventricular catheter motion or, in a single case, induced by performance of a Valsalva maneuver. The blood velocity waveforms described in this paper represent those recorded from left ventricular outflow tract or in a few cases, the midcavity position. In the absence of aortic valvular regurgitation, outflow tract blood velocity patterns are characterized by a large systolic ejection wave followed by a smaller diastolic fraction. Left ventricular midcavity wave contours are usually triphasic, with atrial, systolic ejection, and diastolic components.’ Reslllts Left ventricular blood flow velocity was monitored during ventricular extrasystoles in 53 subjects. Premature depolarizations reduced peak outflow tract blood velocities in direct relation to their coupling intervals; when the latter were less Ventricular
premature
beats.
December, 1974, Vol. 88,
NO.
6, pp. 742-747
Doppler measurement of’L V blood flow velocity
1. Simultaneously recorded Lead II (L II1 of the electrocardiogram, tricuspid area (TA) phonocardiogram, external carotid artery pulse tracing (CT), and left ventricular outflow tract blood velocity in a 48-year-old man with coronary artery disease. Ventricular premature beats reduce peak left ventricular blood flow velocity in relation to their coupling intervals. The last extrasystole (QRS complex No. 151, with a preceding R-R interval longer than 0.5 second, produces a minimal decline of peak blood velocity. The first salvo of premature depolarizations is followed by a five-beat period of high-low blood velocity “alternans” (beats Nos. 7 through 11). Note that the changes in peak blood velocity are paralleled by similar variation in the amplitude of the external carotid arterial pulse tracing. Fig.
Fig. 2. Simultaneously recorded Lead II (L II) of the electrocardiogram, tricuspid area (TA) phonocardiogram, right ventricular (RF’) pressure, apexcardiogram (ACG), and phasic left ventricular midcavity blood flow velocity in a 44-year-old man with coronary artery disease. Catheter-induced ventricular premature beats result in a shortened preceding diastolic blood flow velocity time and a decline of subsequent peak systolic and diastolic blood velocities. Note that the small left ventricular systolic blood velocities are associated wi1.h minimal amplitude on the simultaneously recorded apexcardiogram.
than 0.5 second, the diminution of blood velocity was most manifest. Variations of peak outflow tract blood velocity were accompanied by similar alterations in the amplitude of deflection on simultaneously recorded external carotid pulse tracings. Periods of postextrasystolic left ventricular blood velocity alternation were observed in four subjects (Fig. 1). Peak left ventricular midcavity systolic blood velocity declined in relation to the degree of QRS complex prematurity as described above for out-
American Heart Journal
flow tract records. In addition, ventricular extrasystoles reduced preceding diastolic blood velocity times and effected a diminution of subsequent peak diastolic blood flow velocities. The reduction of peak systolic left ventricular blood velocity induced by premature beats was paralleled by a decrease in the total deflection of the simultaneously recorded apexcardiogram (Fig. 2). In two patients with aortic insufficiency, peak systolic blood velocities were diminished by premature ventricular contractions, yet left ven-
743
Benchimol, Desser, and Wang
E O-LCONTROL
I’
3. Simultaneously recorded Lead II (L II) of the electrocardiogram, tricuspid area (TA) phonocardiogram, external carotid arterial pulse tracing (CT), left ventricular outflow tract blood velocity, and right ventricular (RV) pressure in a 49-year-old man with aortic insufliciency. Compared with sinus beat No. 5, and ventricular fusion beat No. 1, ventricular premature beats Nos. 2 and 3 along with an escape beat (No. 41 are associated with lower peak systolic blood velocities. Peak diastolic blood velocity remains relatively stable throughout the record
tricular diastolic blood velocities remained stable (Fig. 3). Ventricular tachycardia. A total of 24 episodes of ventricular tachycardia were recorded in 18 subjects. These tachyarrhythmias produced a 62 per cent average decline of peak left ventricular blood velocity for the study group (Fig. 4). The most profound decrease of phasic blood velocity was observed in a 44-year-old man with coronary artery disease. In this latter subject, only one of nine QRS complexes recorded during ventricular tachycardia generated a phasic systolic blood velocity wave (Fig. 5). In three patients, phasic left ventricular blood velocity rapidly returned to control levels after an initial decline during ventricular tachycardia (Fig. 6). A 54-year-old woman with no catheterization evidence of heart disease presented with a history of syncopal-like episodes during straining at stool. Voluntary execution of the Valsalva maneuver produced bursts of ventricular tachycardia. These tachyarrhythmias reduced peak left ventricular outflow tract blood velocity by an average of 50 per cent (Fig. 7).
744
ENT. TACHYC.
N=18 P
”
Fig.
5
Fig. 4 Mean values (& 1 standard deviation) for peak left ventricular blood velocity during control rhythm and ventricular tachycardia in 18 subjects: control = 46 f 10 cm. per second, ventricular tachycardia = 17 f I1 cm. per second, P < 0.001.
Discussion
The findings described here demonstrate the unfavorable influence of ventricular arrhythmias on phasic left ventricular blood flow velocity in conscious man. Reductions of left ventricular pressure, stroke output, and other indices of left ventricular performance have previously been described in human subjects during ventricular tachycardia. These observations have been generally based on phasic left ventricular pressure measurement and indicator-dilution curves obtained during elective ventricular pacing.2-5 Diminution of the diastolic filling time, reduced coronary blood flow and in turn, less forceful left ventricular contraction produced the decline of blood cell velocity observed in the course of ventricular arrhythmias. Shortened diastolic left ventricular blood velocities noted at midcavity sites indicate the adverse effects of tachyarrhythmias on left ventricular filling. On the other hand, maintenance of peak diastolic blood velocities in subjects with ventricular arrhythmias and aortic valvular regurgitation can be ascribed to retrograde directional blood flow from the aorta to the left ventricular cavity. Enhanced reverse aortic blood velocity has been noted to occur in some patients during ventricular arrhythmias and may be secondary to imcomplete aortic
December,
19;4,
Vol. 88, No. 6
Doppler
measurement
of L V blood flow velocity
Fig. 5. Simultaneously
recorded Lead II (L II) of the electrocardiogram, tricuspid area (TA) phonocardiogram. continuous pulmonary artery (PA), and right ventricular (RV) pressures and left ventricular outflow tract blood velocity in a 44-year-old man with coronary artery disease. A paroxysm of ventricular tachycardia effects a marked decline of left ventricular blood velocity and only a single small systolic flow velocity wave is recorded during the arrhythmia.
Fig. 6. Simultaneously
recorded Lead II CL II) of the electrocardiogram, right ventricular (RV) pressure, and left ventricular outflow tract blood velocity in a 59-year-old man with coronary artery disease. An episode of ventricular tachycardia produces an initial 80 per cent decline of peak flow velocity. Subsequent left ventricular blood velocities return to control levels, The alterations of phasic left ventricular blood velocity are generally paralleled by concordant changes in phasic right ventricular pressure.
American
Heart Journal
746
Benchimol,
Demer, and Wang
BRA
PRESS.
Fig. 7. Simultaneously recorded Lead II CL II) of the electrocardiogram, mean right atria1 (RA) pressure, and phasic left ventricular outflow tract blood velocity in a 54-year-old woman with no catheterization evidence of heart disease. Straining against a closed glottis results in a rise of mean right atria1 pressure and two episodes of ventricular tachycardia. The tachycardias reduce peak blood flow velocity by an average of 50 per cent.
valvular closure during such rhythm disturhances.6 Of interest was the recording of postextrasystolic left ventricular blood velocity alternation in four subjects. To our knowledge, this represents the first description of blood velocity alternans within the left ventricle of man. Such highlow alternation of peak blood velocity is probably the underlying basis for documented aortic flow alternation and may be due to beat-to-beat changes of end-diastolic myocardial fiber length and ventricular contractility.’ In three patients, peak left ventricular blood velocities rapidly returned to near control levels after an initial decline during ventricular tachycardia. This latter observation can be attributed to cardiac potentiation, possibly mediated via the sympathoadrenal system.*pg Particularly noteworthy was the marked reduction of peak left ventricular blood velocity observed in a subject with paroxysmal ventricular tachycardia during performance of a Valsalva maneuver. Straining against a closed glottis has been demonstrated to result in a diminution of coronary blood velocity which is related to the degree of concomitant right atriai pressure rise.lO It is possible that the myocardium of this patient with normal coro-
746
nary arteries was particularly sensitive to reduced coronary perfusion produced by straining. The limitations and advantages of Doppler catheter measurement of left ventricular blood velocity have been previously described in detail.lDespite the fact that the crystal-tipped catheter senses the velocity of blood cells in a chamber with rapidly changing dimensions, this technique is currently the only method which can instantaneously measure phasic left ventricular blood velocities on a continuous basis. Previous studies have demonstrated the untoward influence of ventricular tachycardia on aortic,” along with coronary,12 carotid l3 rena1,14 superior mesenteric,16 and peripheral arterial blood velocities.16 It is apparent that the decline of flow velocities in these ‘regional circulations can be linked to the basic left ventricular abnormalities noted in this study Summary
Phasic instantaneous left ventricular blood velocity was continuously measured by means of the Doppler ultrasonic flowmeter catheter radiotelemetry system in 68 patients with ventricular arrhythmias. Ventricular premature
December,1974, Vol. 88, No. 6
Doppler measurement of LV blood flow velocity
depolarizations reduced peak left ventricular blood velocities in relation to their respective coupling intervals, with R-R intervals less than 0.5 second producing the greatest decline. Ventricular tachycardia in 18 subjects produced a 62 per cent mean decrease in left ventricular blood velocity. In a single subject, performance of the Valsalva maneuver effected ventricular tachycardia and a concomitant marked diminution of phasic left ventricular blood velocity. These findings demonstrate the untoward influence of ventricular extrasystoles and tachycardia on left ventricular blood velocity and provide the underlying basis for reductions of blood velocity previously demonstrated in the regional circulations of man during similar arrhythmias. REFERENCES
1. Benchimol, A., Desser, K. B., and Gartian, J. L., Jr.: Left ventricular blood flow velocity in man studied with the Doppler ultrasonic flowmeter, Ate. HEART J. 86:294, 1973. 2. Ferrer, M. I., and Harvey, R. M.: Some hemodynamic aspects of cardiac arrhythmias in man; a clinicophysiologic correlation, AM. HEART J. 88~153.1964. 3. Same& P., Bern&in, W. H., Levine,‘S., and Lopes, A.: Hemodynamic effects of tachycardias produced by atria1 and ventricular pacing, Am, J. Med. 38906, 1965. 4. Benchimol, A., Ellis, J. G., Dimond, E. G., and Wu, T. L.: Hemodynamic consequences of atria1 and ventricular arrhythmias in man, AM. HEART J. 70:774 1966. 6. Benchimol, A., and Liggett, M. S.: Cardiac hemodynamits during stimulation of the right atrium, right ventri-
American Heart Journal
6.
7.
8.
9.
10.
11.
12.
13. 14. 15.
16.
cle, and left ventricle in normal and abnormal hearts. Circulation 33:933,1966. Benchimol, A., Desser, K. B., and Gartlan, J. L., Jr.: Bidirectional blood flow velocity in the cardiac chambers and great vessels studied with the Doppler ultrasonic flowmeter, Am. J. Med. 52:467,1972. Benchimol, A., Barreto, E. C., and Tio, S. T. W.: Phasic aortic flow velocity in patients with pulsus alternans, Br. Heart J. 32:696,1970. Nakano, J.: Effects of atria1 and ventricular tachycardias on the cardiovascular dynamics, Am. J. Physiol. 206:547,1964. Nakano, J.: Effects of atria1 and ventricular tachycardia on the cardiovascular dynamics in reserpinized dogs, Am. J. Cardiol. 14:89, 1964. Benchimol, A., Wang, T. F., Deaser, K. B., and Gartlan, J. L., Jr.: The Valsalva maneuver and coronary arterial blood flow velocity. Studies in man, Ann. Intern. Med. 77:357, 1972. Benchimol, A., Stegall, H. F., Maroko, P. R., Gartlan, J. L., and Brener, L.: Aortic flow velocity in man during cardiac arrhythmias measured with the Doppler catheter-fiowmeter system, AM.HEART J.78:649,1969. Benchimol, A., Matsuo, S., Desser, K. B., Wang, T. F., and Gartlan, J. L., Jr.: Coronary artery blood flow velocity during ventricular tachycardia in man, Am. J. Med. Sci. 264:277,1972. Benchimol, A., Barreto, E. C., Goldstein, M. R., and Gartlan, J. L., Jr.: Measurement of phasic carotid artery flow velocity in man, Am. J. Med. 48~170, 1970. Benchimol. A.. and Desser. K. B.: Phasic renal arterv blood flow velocity in man during cardiac arrhythmias, Am. J. Med. Sci. 261:161, 1971. Benchimol, A., Desser, K. B., and Gartlan, J. L., Jr.: Superior meaenteric artery blood velocity in man during cardiac arrhythmias, Gastroenterology 62:950, 1972. Benchimol, A., Maroko, P., Gartlan, J. L., Jr., and Franklin, D.: Continuous measurements of arterial flow in man during atria1 and ventricular arrhythmias, Am. J. Med. 4652, 1969.
747