Doppler puts pressure on our hemodynamic thinking.
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Biomedical subjects
Publications and source records attributed to G R Marx.
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The prenatal diagnosis of fetal cardiac disease has become increasingly accurate as the technology of ultrasound has improved. Although two-dimensional real-time ultrasound remains the primary method of diagnosis, Doppler blood flow velocity estimates can provide valuable pathophysiologic information to support the anatomic diagnosis. We present six cases in which Doppler studies contributed to the accuracy of the diagnosis of fetal heart disease, including tetralogy of Fallot, right and left ventricular hypoplasia, atrioventricular canal defect, double-outlet right ventricle, and pulmonic stenosis. Velocities in these cases are compared with those in normal fetuses. If Doppler flow velocities are not consistent with the observed morphologic changes, further observations are indicated. Inasmuch as most anatomical heart lesions result in altered flow patterns, Doppler investigations of intracardiac and extracardiac flow should be a routine component of the fetal echocardiogram when structural abnormalities are found.
Two-dimensional Doppler echocardiography was used to diagnose congestive heart failure in a fetus with a large sacrococcygeal teratoma. Ultrasound performed for size-date inconsistency revealed a 27.5-week fetus with hydrops and a large solid and cystic mass in the sacral region. Fetal echocardiography showed dilated ventricles and a pericardial effusion; Doppler ultrasound demonstrated increased velocities and volume flows, along with tricuspid and mitral regurgitation. At delivery, the mass was bleeding actively, the amniotic fluid was markedly bloody, and the neonatal hematocrit was 10%. We postulate that intrauterine hemorrhage from the teratoma led to anemia and high-output cardiac failure confirmed by Doppler echocardiography, and suggest that all fetuses with sacrococcygeal teratomas be evaluated by two-dimensional Doppler echocardiography to detect the presence of congestive heart failure, in order to allow well-timed therapeutic interventions.
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Cardiac output (CO), as measured by Doppler, is computed by multiplying vessel area by mean velocity. One unresolved problem is the magnitude of vessel area change during the cardiac cycle. Prior estimates have ranged from 2% to 30% area change during the cardiac cycle. The purpose of this study was to measure cyclic dimensional changes in the aorta and pulmonary artery of dogs by a very sensitive technique, mercury strain gauge plethysmography. Gauges were fixed around the pulmonary artery and the aorta and changes in vessel circumference were recorded under the following conditions: increased preload, increased afterload, decreased preload, and during administration of dobutamine, 5 and 10 micrograms/kg/min. Percent change in circumference of the aorta at baseline was small (mean circumference change = 4%, SD = 1%, SEE = 0.5). Percent change in the pulmonary artery at baseline was slightly larger (mean circumference change = 6%, SD = 5%, SEE = 2%). Mean aortic area change was 9% (SD = 2%) and for the pulmonary artery it was 12% (SD = 10%). No experimental manipulation significantly altered the percent cyclic change in vessel size from baseline except for clamping the inferior vena cava, in which mean percent change in aortic circumference decreased to 1% (SD = 1%, SEE = 5%) (p less than 0.05). Percent change in the aorta correlated only weakly with heart rate (r = 0.48), blood pressure (r = 0.4), and CO (r = 0.46). Similar values were obtained for the pulmonary artery. These data demonstrate a small but definite cyclic change in pulmonary artery area, and to a lesser extent in aortic area.
The hypothesis tested was that transducers of different types and shapes would produce different peak and mean ascending aortic (AAo) velocities. Additionally, we sought to determine if mean and peak velocity recorded from the descending aorta (DAo) were similar to velocities in the AAo. Twenty-eight consecutive individuals who had normal hearts were studied. AAo velocities were measured with four transducers including a nonimaging device that transmitted Doppler at right angles to the transducer handle, a 30-degree angled continuous wave transducer, an imaging transducer that transmitted Doppler in line with the transducer handle, and a second imaging transducer that sectored at 25 degrees to the transducer handle. DAo was studied with a standard in-line imaging transducer. Results showed that mean and peak AAo velocities recorded by transducers that transmitted off the axis of the transducer handle were similar, but the transducer that imaged along the transducer handle axis produced significantly lower peak and mean velocities. The problem that caused lower velocity for the on-axis transducer was inability to image the area immediately posterior to the sternum to permit alignment in the azimuthal dimension. The continuous wave transducer provided a wide spectral dispersion. Mean DAo velocity was similar to mean AAo velocity, but variability was large.
To evaluate the qualitative and quantitative changes in Doppler velocities in the normal fetus and newborn, 61 echo Doppler studies were performed in 18 neonates, nine of whom were also studied as fetuses. Four studies were inadequate in fetuses (one pulmonary artery, two mitral, and one tricuspid) and some post natal studies were inadequate due to inability to separate atrioventricular valve E and A velocity component waveforms (one tricuspid, three mitral). Heart rates for fetuses and newborns more than 24 hours of age and less than 24 hours of age were similar. Pulmonary artery diastolic velocities consistent with patent ductus arteriosus were present in 11 of 12 examinations at less than 6 hours of age, in 5 of 13 examined at 6 to 24 hours of age, and in 2 of 27 examined after 24 hours of age. Pulmonary artery times to peak velocity were similar in fetuses, m = 46, SD = 3 msec, and in neonates less than 6 hours of age, m = 51, SD = 13 msec, but lengthened significantly, p less than 0.05, at 6 to 24 hours (m = 69, SD = 14 msec). These changes are probably due to the dramatic changes in pulmonary vascular pressure that occur after birth. Data from 6 to 24 hours and greater than 24 hours (m = 78, SD = 13 msec) were similar. Significant differences existed for transmitral valve E/A ratios, which increased from m = 0.85 in utero to m = 1.17 (p less than 0.05) after birth, with no significant change thereafter.(ABSTRACT TRUNCATED AT 250 WORDS)
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The association of congenital heart block with maternal connective tissue disease and autoimmunity has been recently reported. Two cases of heart block were diagnosed in utero at 23 and 24 weeks' gestation. Both mothers had extensive workups for connective tissue disease that were negative. Two-dimensional and Doppler echocardiography were performed in utero and both infants had left atrial isomerism, atrioventricular canal defects, and severe hydrops in addition to heart block. Review of the recent literature identifies a subset of congenital heart block in which the mothers have no evidence for connective tissue disease, and the fetus or neonate has complex cardiac malformations and hydrops. The common features in these babies are atrioventricular canal defects and isomerism. No reports of congenital heart disease among the children of mothers with connective tissue disease fit this description. Our recent experience and literature review emphasize the previously known association between congenital heart block and congenital heart disease. This association is especially important in light of the poor prognosis for this group of fetuses and neonates.
The purposes of this study were to determine the ability of pulsed Doppler echocardiography to consistently and accurately measure cardiac output during exercise, and to measure the exercise factor by Doppler methodology when oxygen consumption was simultaneously measured. Thirty-four healthy young adolescent male volunteers (mean age 13 years) were recruited. Submaximal exercise was performed by supine bicycle ergometry. Cardiac output was calculated as mean velocity X cross-sectional area. Successful rest and exercise determinations of cardiac output were obtained in 81% (n = 52) of the studies. Mean cardiac output increased from 4.6 to 8.9 liters/min (p less than 0.001) during exercise and mean oxygen consumption increased from 212 to 899 ml/min (p less than 0.001). Doppler-estimated rest and exercise cardiac outputs correlated well with simultaneously measured oxygen consumption (r = 0.89, SEE = 1.2 liters/min; y = 0.006 X 3.2 liters/min). Mean exercise factor was 6.4 (1.2 SD). Twenty-six pairs of rest and exercise cardiac output determinations by Doppler technique and indirect Fick method were simultaneously compared in a subset population (r = 0.86, SEE = 1.4 liters/min; slope = 0.93, y intercept = 1.4 liters/min). Results of this study demonstrate that cardiac output and exercise factor can be estimated by pulsed Doppler echocardiography during exercise.
Eighty-six fetuses of 21-41 weeks' gestation with arrhythmias were studied with ultrasound and heart rate monitoring. The type of arrhythmia was identified by M-mode studies and was confirmed by postnatal electrocardiogram in 70 infants. The most common arrhythmia was premature atrial contractions (76), followed by premature ventricular contractions (five), paroxysmal supraventricular tachycardia (four), and atrial fibrillation/flutter (one). Doppler echocardiography was performed in 54 fetuses to measure flow velocities across the atrioventricular and semilunar valves. After isolated premature atrial and ventricular contractions, post-extrasystolic potentiation was demonstrated by an increase in fractional shortening (N = 32) of 49 +/- 6% in the right ventricle and 64 +/- 7% in the left ventricle. When post-extrasystolic beats were compared with normal beats, Doppler-determined time-velocity integrals increased 43% across the tricuspid valve, 41% across the mitral valve, 34% across the pulmonary valve, and 38% across the aortic valve. Mean velocity increased significantly after conversion to normal sinus rhythm in the five fetuses with supraventricular tachycardia (P less than .05). By studying the physiologic consequences of fetal arrhythmias using two-dimensional Doppler and M-mode ultrasound, we have documented the presence of post-extrasystolic potentiation after premature contractions, the existence of the Frank-Starling mechanism, and an increase in mean velocity (and therefore in cardiac output) after conversion of fetal tachyarrhythmias to normal sinus rhythm.
The origin of Still's innocent murmur, first described in 1909, is obscure. Seventy normal children and young adults, 29 with Still's murmur and 41 with no murmur, were studied. Pulsed Doppler and 2-dimensional echocardiography were used to evaluate possible causes, including tricuspid regurgitation, left ventricular bands, ascending and descending aortic and pulmonary velocities, ascending aortic diameter, and magnitude of spectral widths. Mean ascending aortic diameter relative to body surface area was significantly smaller for the group with Still's murmur (p less than 0.001). Since cardiac output was similar for the 2 groups, the average peak ascending velocity (133 cm/s) and average peak descending aortic velocity (118 cm/s) were significantly higher in the innocent murmur group as compared to similar respective means in the control group without the murmur (107 and 104 cm/s, respectively) (p less than 0.001 and p less than 0.01, respectively). No significant differences were found when the 2 groups were compared with respect to mean peak pulmonary artery velocity adjusted for body size, spectral widths in the ascending and descending aorta and in the pulmonary artery, and the presence of tricuspid regurgitation or ventricular bands. These observations suggest that the origin of Still's murmur is related to a small ascending aortic diameter with concomitant high aortic blood flow velocity.
Eleven patients with coarctation of the aorta (C of A) underwent balloon dilation angioplasty at the University of Arizona from November 1983 to January 1985. Eight had previously undergone surgery and 3 had native C of A. Two operations were considered unsuccessful: 1 in a patient who underwent tube graft--descending aortic anastomosis narrowing and 1 in a patient with a native wedge type of C of A. Overall mean gradient fell from 47 to 13 mm Hg immediately after the procedure. Mean gradient at repeat catheterization in 7 patients (mean 8 months after angioplasty) was 6 mm Hg. Five patients showed a transient increase in the gradient measured on the day after angioplasty, with 3 showing a fairly marked increase. Values returned to levels equal to or less than gradients measured immediately after the procedure. Angiographic findings at follow-up catheterization in 7 patients showed no evidence of aneurysm formation in either the operative group or in the 2 patients with native C of A who had a membrane type of deformity. Mean C of A to ascending aortic diameter ratios increased from 0.44 to 0.80. At repeat angiography, the mean ratio was 0.76 in the 7 patients studied. Further longitudinal studies in these patients are necessary before reaching conclusions about the advantage of this procedure over surgery, but these early longitudinal results are encouraging for the populations studied: postoperative patients and patients with native membrane types of C of A.
Although Doppler echocardiography has been demonstrated to accurately predict the pressure drop across the pulmonary valve in patients with pulmonary valve stenosis, prior reports have stressed the need to correct for beam-flow intercept angles, to use simultaneous imaging, and to utilize the subcostal approach. The purpose of this study was to determine the accuracy of estimating the pressure drop in pulmonary stenosis patients by means of nonimaging Doppler applied without angle correction from precordial examination. Pressure drop estimated by Doppler was compared to that measured by strain gauge manometry at catheterization. Data for 39 patients (21 simultaneous measurements; 18 nonsimultaneous) were evaluated. Results for the entire group showed a good correlation (r = 0.94; SEE = 7.9 mm Hg). The correlation for simultaneous measurement improved somewhat (r = 0.95; SEE = 5.9), but the difference was not significant. Comparison of the slope and intercept of data of this study to those of prior studies, which advocated more complex methodology, indicated that results were essentially similar and that use of the additional steps did not confer a significantly improved result. We conclude that the simplified methodology utilized in this study provides accurate Doppler estimates of pressure gradient in patients with pulmonary stenosis.
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Although the pressure gradient in aortic coarctation can usually be obtained by comparison of upper and lower limb blood pressures measured by sphygmomanometry, some patients may have upper or lower limb arterial compromise as a result of prior procedures or anomalous origin of the subclavian arteries, either of which may preclude accurate gradient measurement. To determine whether Doppler echocardiography could predict the pressure gradient, the Doppler method was used to predict transcoarctation gradients in 35 studies and the data were compared with the gradients measured at catheterization. Jet velocities were not adequately obtained by Doppler recording in three neonates with coarctation and patent ductus arteriosus, leaving 32 studies for analysis. The mean age of the study patients was 6 +/- 5.8 years. The mean Doppler-estimated gradient, calculated using only jet velocities distal to the obstruction (V2) in the modified Bernoulli equation, was 44 +/- 17 mm Hg, and the mean catheterization gradient was 36 +/- 21 mm Hg (p = NS; r = 0.91, SEE = 7.0 mm Hg; slope = 0.75, y = 17.3 mm Hg). The mean Doppler-estimated gradient using both the pre- and postcoarctation velocities (V1 and V2) in the modified Bernoulli equation (n = 26) was 36 +/- 20 mm Hg, and the mean catheterization gradient was 36 +/- 21 mm Hg (p = NS; r = 0.98, SEE = 4.2 mm Hg; slope = 0.91, y = 2.8 mm Hg). Doppler echocardiography closely estimated the pressure gradient in aortic coarctation, and estimation of the gradient improved when the velocities proximal as well as distal to the obstruction were included in the modified Bernoulli equation.
The objective of this study was to determine if the pressure drop across various types of aortic-pulmonary shunts could be accurately estimated by Doppler echocardiography, and if systolic pulmonary pressure could be estimated by referencing the pressure drop across the aortic-pulmonary shunt to systolic systemic arterial pressure measured by cuff sphygmomanometry. This was done in 22 patients and Doppler results were compared with pulmonary artery pressure measured directly by strain gauge manometry. Adequate Doppler waveforms were obtained in 21 of 22 patients; 3 had a Waterston shunt, 10 had a Blalock-Taussig shunt, 1 had a left pulmonary artery-aortic anastomosis, 6 had a patent ductus arteriosus and 1 had an aortic-pulmonary window. Systolic pulmonary artery pressure estimated by Doppler echocardiography ranged from 12 to 90 mm Hg (mean 41.3 +/- 21.4 [SD] ), and measured by strain gauge manometry ranged from 20 to 90 mm Hg (mean 44.7 +/- 20.7) (p = NS, r = 0.94, SEE = 7.4 mm Hg; slope = 0.90, y intercept = 7.4 mm Hg). Systolic pulmonary artery to aortic pressure ratios predicted by Doppler recording ranged from 0.1 to 1.0 (mean 0.4 +/- 0.2 [SD] ); when calculated from direct measurement it ranged from 0.2 to 1.0 (mean 0.4 +/- 0.2) (p = NS, r = 0.92; SEE = 0.08, slope = 0.80, y intercept = 0.09). This study demonstrates that Doppler echocardiography provides an estimation of pressure drop across aortic-pulmonary shunts, and that the data can be used to estimate systolic pulmonary artery pressure by subtracting the estimated pressure drop from the systolic systemic arterial pressure.