Measurement of cardiac output in man with a nonrecirculating indicator.

The present investigation was undertaken to evaluate the utility of constant-rate injection of a nonrecirculating indicator (H(2)) for the measurement of cardiac output in man. 42 patients were studied during cardiac catheterization and 8 during acute complications of arteriosclerotic heart disease, including acute myocardial infarction. Pulmonary (or systemic) arterial H(2) concentration was measured chromatographically from 2.0 ml blood samples drawn during constant-rate injection of dissolved H(2) into the systemic venous circulation (or left heart). The chromatograph was a thermal conductivity unit housed in a constant-temperature water bath to achieve an improved signal-to-noise ratio. Intrapulmonary H(2) elimination from mixed venous blood was measured directly in 14 patients and averaged 98 +/-1.5% (SD). Reproducibility of output measurements was evaluated using triplicate determinations obtained over 45-60 sec in 25 consecutive patients. Coefficients of variation (SD/Mean x 100) averaged 3.4 +/-2.0%, making it possible to evaluate relatively small changes in measured output with conventional statistical tests. Individual measurements could be repeated at 10-15 sec intervals. Comparisons of H(2) and direct Fick measurements were made in 14 patients; H(2) outputs averaged 106 +/-4% (SEM) of Fick outputs (P > 0.1). Comparisons of H(2) and dye dilution measurements were performed in an additional 24 patients. Seven had angiographically-negligible valvular regurgitation and dye outputs averaged 106 +/-3% of H(2) outputs (P > 0.1). 17 had moderate-to-severe regurigation and dye outputs averaged 91 +/-4% of H(2) outputs (P < 0.05), suggesting a small but systematic error due to undetected recirculation of dye. The H(2) technique appears advantageous for rapidly repeated determinations of output, for quantitation of small changes in output, and for situations in which recirculation of conventional indicators is a potentially significant problem.

Turbulent blood flow in the ascending aorta of dogs.

A conical hot film anemometer probe was used to measure instantaneous velocities in the ascending aorta of anaesthetised, open-chest dogs. The probe was mounted on a saddle which allowed traversal of the aorta in 1 mm increments 4 cm above the aortic valve. From these point measurements, the radial distribution of velocity was obtained by averaging ten cardiac cycles. The contractile state of the heart was increased by sequential intravenous infusions of isoprenaline. The absolute peak centreline velocity in the baseline state ranged from 28 to 56 cm x s-1 and, in 20 micrograms x min-1 isoprenaline infusion, from 39 to 112 cm x s-1. Two major effects of isoprenaline on blood flow were noted: 1) isoprenaline dramatically increased peak centreline velocity, and 2) disturbances resembling turbulence appeared as peak velocity increased. With isoprenaline infusion disturbances existed throughout the deceleration portion of the aortic blood flow. Analysis of the frequency components of the velocity wave was performed, and significantly higher frequency components up to 100 Hertz were found in the turbulent cases compared to the laminar ones. Turbulent flow or disturbed flow is found when the ratio of Reynolds number to Womersley number is above 200. In general the hot film measurements showed that both laminar and disturbed velocity profiles tended to be flat throughout the cardiac cycle, with the sharp velocity gradient confined to the region of the wall. Turbulent normal stress during the deceleration portion of aortic blood flow were found in the orders of 15 to 30 dynes x cm-2 and the wall shear stresses were found to be from 10 dynes x cm-2 at the baseline condition to 50 dynes x cm-2 during the 20 micrograms x min-1 isoprenaline infusion.

Mitral valve prolapse in coronary artery disease.

Mitral valve motion, left ventricular segmental contraction and severity of arterial stenosis were analyzed in 92 patients with coronary artery disease and 28 patients with "atypical chest pain" and normal coronary arterio-rams. Mitral valve motion was evaluated for the presence or absence of leaflet prolapse. Segmental contraction was evaluated by calculating the percent shortening of six chords of the left ventricle measured from right anterior oblique ventriculograms. The severity of disease in each coronary vessel (left anterior descending, left circumflex and right coronary) was graded on a scale of 1 (0 to 30 percent stenosis) to 5 (complete occlusion). Mitral valve prolapse was not suspected clinically but observed angiographically in 15 of 92 patients with coronary artery disease and in 5 of 28 patients with normal coronary arteriograms. In nine patients with coronary artery disease, the prolapse was restricted to the posterior leaflet, in five it was in both the anterior and the posterior leaflets and in one patient in the anterior leaflet only. Mitral regurgitation was noted in seven patients with coronary artery disease; it was mild in six and moderate in one. Among the patients with coronary artery disease, 12 of the 15 (80 percent) with mitral valve prolapse had left ventricular asynergy compared with 63 of the 77 (82 percent) without valve prolapse. The mean scores for severity of disease in the left anterior descending, circumflex and right coronary arteries were, respectively, 4.2, 2.5 and 3.2 in the patients with valve prolapse and 4.2, 2.2 and 3.5 in those without prolapse. In summary, there was no significant correlation between mitral valve prolapse and distribution of coronary arterial obstructions or abnormal patterns of left ventricular segmental contraction. There was a high frequency of mitral valve prolapse in patients with severe coronary artery disease and in those with normal coronary arteriograms and atypical chest pain.

Coronary artery aneurysm. A review of the literature with a report of 11 new cases.

In a prospective study, 11 (1.5 percent) of 742 patients had angiographically proven coronary artery aneurysms. The clinical picture was similar to that of patients with severe coronary artery disease. The coronary artery aneurysms were multiple and were associated with extensive coronary atherosclerosis in ten of the 11 patients. Left ventricular function was impaired when measured by end-diastolic pressure, end-diastolic volume, and ejection fraction. Segmental left ventricular contraction was severely abnormal. The abnormality of segmental contraction, distribution of coronary artery obstructions, an presence of collateral circulation were not different from other patients with severe occlusive coronary atherosclerosis. These 11 cases plus the 23 previously reported ante mortem form the total reported in world literature. The etiology of cornonary artery aneurysms is most commonly atherosclerosis (17/34, or 50 percent). The natural history of this condition is not known. Because of the severe atherosclerosis and poor distal-vessel run-off, most patients are not considered good surgical condidates; however, 15 patients have had coronary arterial surgery, and 13 have survived the immediate postoperative period with some improvement of symptoms.

Effect of valve orientation on flow development past aortic valve prostheses in a model human aorta.

The effect of valve orientation on flow development in a model human aorta was studied by means of a qualitative flow visualization technique. The model replicated the geometry of the human aorta and the experiment simulated a physiologically realistic pulsatile flow. The following valves were studied: Starr-Edwards Stellite, Starr-Edwards silicone, Björk-Shiley spherical disc, Björk-Shiley convexo-concave disc, and Hall-Kaster tilting disc. All the valves had a tissue anulus diameter of 27 mm. With the ball-in-cage valves, the flow in the ascending aorta was predominantly axial and uniform throughout systole, while vortex formation was observed downstream from the ball. With the tilting disc valves, the flow development in the aorta was a function of the orientation of the valves. With the major flow orifice directed toward the commissure between the right and noncoronary cusps, the fluid motion was predominantly in the axial direction through early systole. A vortex developed along the wall of lesser curvature of the aorta with the progression of systole. In early diastole, a well-defined flow reversal was observed along the lesser curvature of the aorta. With the major flow orifice directed toward the left coronary cusp, the fluid motion, although predominantly axial, was not uniform in the ascending aorta. Regions of relative stasis present near the wall of greater curvature subsequently developed into a trapped vortex throughout the cardiac cycle. With the major flow orifice directed more posteriorly, an improved fluid dynamic characteristic was observed, and there was no trapped vortex present near the wall of greater curvature. The flow visualization study in the model human aorta suggests that, from a fluid dynamic point of view, orientation of the major flow orifice of the tilting disc valve toward the wall of lesser curvature is not advisable.

Hematological Variations After Endurance Running With Hard-and Soft-Soled Running Shoes.

In brief: Blood measurements were taken in 23 marathon runners to investigate whether the hardness of the sole of the running shoe would affect RBC indexes. Runners were randomly assigned to a group with either a firm-sole running shoe or an air-cushion shoe. Measurements before and after the 15-mile run included complete blood count, serum haptoglobin, plasma hemoglobin, and venous hemoglobin. Runners wearing air-cushion shoes demonstrated smaller hematological effects after strenuous exercise than did runners wearing firm-sole shoes. This study indicates that (1) material property of the running shoes may be correlated with physiological measurements, and (2) appropriate cushioning in running shoes may reduce the RBC abnormalities experienced in long-distance running.

Retrograde coronary artery flow in aortic valve disease.

Retrograde coronary artery flow was observed angiographically in 43 patients with aortic stenosis and/or regurgitation. In the 24 patients with pure or predominant aortic stenosis, retrograde flow was seen in all 24 during end-systole. In the eight patients with pure aortic regurgitation, retrograde flow was seen mainly during end-diastole (6/8). Among the 11 patients with stenosis and regurgitation, retrograde flow was both end-systolic and enddiastolic. Dominant left coronary arteries were seen in 13 patients; 13 showed retrograde flow in the dominant arteries. Dominant right coronary arteries were seen in 25 patients: all 25 showed retrograde flow equally in the right and left coronary. Five of the 43 patients could not be evaluated for dominance because of coronary artery occlusions. The severity of retrograde flow did not correlate with usual clinical, hemodynamic or tension-stress parameters: angina, electrocardiographic abnormality, end-diastolic pressure or volume, end-systolic pressure or volume, ejection fraction, severity of aortic regurgitation, peak or mean valve gradient, aortic valve area, myocardial tension and stress calculations, or DPTI:SPTI. In summary, retrograde coronary artery flow was seen in all 43 patients with severe aortic valve disease. The time in the cardiac cycle when retrograde flow occurred was related to the type of valve disease. Retrograde flow was seen mainly in the coronary arteries supplying the left ventricle and may result from increased regional myocardial stresses.

Temporal heterogeneity of myocardial blood flow in anesthetized dogs.

Temporal variation in perfusion to small segments of the myocardium was studied in 19 opened-chest dogs. In six control dogs, three or four differently labeled 7-10 mu microspheres were injected simultaneously into the left atrium to assess the variability in measured myocardial perfusion due to the microsphere technique. In 13 other dogs, microspheres were injected four times at 5 minute intervals while various hemodynamics parameters (mean aortic pressure, peak systolic pressure, heart rate, left ventricular end-diastolic pressure, and Vmax) were stable (less than 10% variation in any one parameter). The left ventricles were divided into 96 segments, the mean weight+/- SD of each segment was 0.95+/-0.17 grams. The flow to each segment was expressed as a percent of the mean flow of the three or four measured flows to that segment, and the difference between the largest and the smallest percent of each segment was taken as a measure of the variability of flow to that segment. The average variability of segmental flow (mean +/-SD) when the three to four differently labeled microspheres were injected was 14.0+/-4.7; and the variability when differently labeled microspheres injected sequentially was 31.0+/-10.8% (P less than 0.001). Furthermore, in the sequentially injected animals the magnitude of temporal variation was similar in various subdivisions of the ventricle (layers, walls, apex to base). The mean and standard deviation of the variability of flow to the endo, mid, and epicardial layers were 28.7+/-10.2, 30.0+/-11.3 and 34.5+/-12.4%, respectively. These changes may reflect either spontaneous or local autoregulatory changes in precapillary sphincters or arterioles.

The effect of acute aortic regurgitation on the transthoracic impedance cardiogram.

In nine anesthetized dogs, recordings of the first derivative of the transthoracic impedance cardiogram (ICG) were made during varying grades of acute aortic regurgitation. Acute aortic regurgitation was induced using a specially designed umbrella catheter, passed retrograde across the aortic valve into the left ventricle. The RFA (representing the fraction of the aortic reverse flow to the aortic forward flow) was computed using an electromagnetic flow probe implanted around the ascending aorta. Both the peak of the scalar ICG, dz/dtmax, which occurs at peak systolic ejection, and the nadir of the scalar ICG, X, which marks the closing of the aortic valve, increased with aortic regurgitation. The planimetered areas of the ICG during systole (S), and in early-diastole (X) increased during aortic regurgitation. These areas, S and X, correlated with the electromagnetic normalized aortic stroke volume (r = 0.90) and the regurgitant volume (r = 0.78), respectively. The ICG ratio X/S was correlated directly with the electromagnetic aortic regurgitant fraction (r = 0.86). This study demonstrates that the ICG waveform is consistently modified by experimental aortic regurgitation. Furthermore, these changes can be quantitatively related to the degree of aortic regurgitation.