Pulmonary Artery Flow Velocity Research Articles

Effects of pacing tachycardia and balloon valvuloplasty on pulmonary artery impedance and hydraulic power in mitral stenosis.

Mitral stenosis is characterized by progressive pulmonary hypertension and eventual right ventricular failure. However, the correlation between right ventricular failure and the level of pulmonary hypertension is poor, suggesting that factors other than those recognized from nonpulsatile hemodynamic parameters may contribute to impaired right ventricular performance in this condition. We studied 16 patients with severe mitral stenosis (mean valve area, 1.0 +/- 0.2 cm2) at supine rest and during pacing tachycardia using high-fidelity catheter recordings of pulmonary artery (PA) pressure and flow velocity. Pulmonary impedance spectra, wave reflection properties, and hydraulic power data were derived from Fourier analysis of signal-averaged data. Pacing tachycardia (baseline heart rate, 81 +/- 11 beats per minute; pacing, 132 +/- 11 beats per minute) significantly raised pulmonary wedge and mean PA pressures. There was no change in pulmonary vascular resistance (209 +/- 144 to 232 +/- 164 dyne-sec/cm5) or PA characteristic impedance (62 +/- 25 to 55 +/- 28 dyne-sec/cm5). However, first harmonic impedance (Z1) significantly decreased (134 +/- 71 to 100 +/- 68 dyne-sec/cm5; p < 0.001). Accordingly, oscillatory and total dissipated hydraulic power per unit forward flow (WT/CO) fell during tachycardia (2.6 +/- 1.6 to 2.3 +/- 1.4 mW/ml.sec-1; p = 0.06) despite acute pulmonary hypertension. Reflected pressure waves returned earlier to the proximal PA, suggesting increased vessel stiffness. Immediately after percutaneous balloon mitral valvuloplasty (PBV) in eight of the patients, baseline and pacing data were again recorded. Compared with the pre-PBV baseline state, post-PBV resting data demonstrated no change in resistance or characteristic impedance, but there was a significant fall in Z1 (166 +/- 75 to 103 +/- 45 dyne-sec/cm5; p < 0.05) and in the magnitude of pulmonary wave reflections. WT/CO tended to decrease after PBV, and pacing after PBV produced a further decrease in WT/CO, again in association with lower Z1. These data demonstrate that 1) increased pulmonary characteristic impedance, although a feature of mitral stenosis, is not exacerbated by the acute effects of increased distending pressure; 2) pacing tachycardia in mitral stenosis causes little change in the pulmonary impedance spectrum except at low frequencies, where decreased impedance lowers power requirements per unit flow; and 3) relief of mitral stenosis produces immediate improvement in low-frequency impedance and in hydraulic power requirements. These findings suggest that although characteristic impedance may be a measure of the long-term effects of pulmonary hypertension on the pulmonary circulation, acute increases and decreases in PA pressure produce effects on right ventricular load that are best described in terms of the low-frequency properties of the PA system. Improvement in low-frequency impedance diminishes hydraulic power requirements and thus reflects improved ventricular-vascular coupling, irrespective of distending PA pressure. Efforts to treat or prevent right heart failure in the presence of pulmonary hypertension should take account of the potential benefit of changes in low-frequency impedance characteristics of the pulmonary vascular bed.

Persistent Pulmonary Hypertension in Premature Neonates With Severe Respiratory Distress Syndrome

Cardiac catheterization studies have demonstrated that Doppler-derived flow velocities in the ductal flow jet and the left pulmonary artery accurately predict the aortopulmonary pressure difference and left-to-right shunt size in newborns. To assess the presence of persistent pulmonary hypertension in premature newborns with various degrees of respiratory distress syndrome (RDS) severity, we estimated pulmonary artery pressure from the aortopulmonary pressure difference and pulmonary blood flow from the left pulmonary artery flow velocity with color-flow-directed, pulsed Doppler echocardiography. Seventy-nine premature neonates were divided into three groups--no or mild RDS (n = 27), severe RDS (n = 38), and fatal RDS (n = 14)--and compared with a group of healthy term neonates (n = 34). In premature and term neonates with no/mild RDS the mean +/- SEM aortopulmonary pressure difference increased from 7.3 +/- 0.4 and 6.6 +/- 0.5 mm Hg to 22.8 +/- 1.4 and 21.4 +/- 1.1 mm Hg over the first 24 hours (P < .001). The mean aortopulmonary pressure difference was 0.9 +/- 0.3 mm Hg during the first 72 hours in neonates with fatal RDS, but increased from 1.5 +/- 0.3 mm Hg at 4 hours to 7.4 +/- 0.6 at 24 hours and 21.5 +/- 0.7 mm Hg at 72 hours of age in neonates with severe RDS. Left pulmonary artery velocity time integrals were 18.3 +/- 0.5 cm in premature and 18.8 +/- 0.5 cm in term neonates with no/mild RDS at 12 hours vs 11.2 +/- 0.4 cm in neonates with severe and 9.9 +/- 0.5 cm in neonates with fatal RDS (P < .001).(ABSTRACT TRUNCATED AT 250 WORDS)

Transesophageal echo-doppler evaluation of the hemodynamic effects of positive-pressure ventilation after coronary artery surgery

Transesophageal echocardiography was used to extend knowledge about the impact of positive end-expiratory pressure (PEEP) during mechanical ventilation on right and left ventricular function and right ventricular impedance. At 20 cmH 20 PEEP, a progressive increase of right ventricular end-diastolic area was seen (27%) that coincided with a reduction of early left ventricular filling velocity (25%) across the mitral valve, and a decrease of both pulmonary artery flow velocity (end-expiration 27% and end-inspiration 42%) and time-velocity index (end-inspiration 25%). As these changes were not accompanied by a change of the fractional area of contraction, the increase of the right ventricular diameter might be explained by right ventricular compensation due to an imbalance between augmented right ventricular impedance and reduced venous return.

Echocardiography for evaluating anatomic repair of transposition of the great arteries.

Fifteen survivors of a single-stage anatomic correction of complete transposition of the great arteries performed at a mean age of 1 month were studied by cross-sectional echocardiography, conventional Doppler echocardiography, Doppler color flow mapping, and catheterization at mean of 10 months after surgery. Small aortic regurgitant jets were documented by angiography and Doppler color flow mapping in seven patients. A trivial supravalvular pulmonary gradient was present in seven patients and a mild to moderate gradient in three. Pulmonary artery flow velocities correlated well with those measured at cardiac catheterization (r = 0.96, standard error of the estimate = 2.6 mm Hg). The present study suggests that combined cross-sectional echocardiography, conventional Doppler echocardiography, and Doppler color flow mapping can be used in the follow-up of patients who have had anatomic repair of transposition of the great arteries, reducing the need for repeated postoperative cardiac catheterizations.

Closure of the ductus arteriosus: Determinant factor in the appearance of transient peripheral pulmonary stenosis of the neonate

We speculated that a relationship may exist between transient peripheral pulmonary stenosis and the closure of the ductus arteriosus. Fifty preterm infants had pulmonary artery and ductal color Doppler flow velocity assessments performed before and after closure of the ductus arteriosus. No flow turbulence or increase in velocity was observed immediately after birth, although a significant discrepancy in size was observed between the main pulmonary artery and its two branches. After closure of the ductus, 15 infants had signs of transient peripheral pulmonary stenosis of the left pulmonary artery in association with a significant decrease of diameter at the origin of the same artery. In all 50 infants, no significant gradient was observed in the right pulmonary artery. We conclude that, at least in the preterm infant, transient peripheral pulmonary stenosis is not present at birth but is an acquired phenomenon closely related to closure of the ductus arteriosus.

Quantitative relation between increased intrapericardial pressure and Doppler flow velocities during experimental cardiac tamponade

To establish whether a quantitative relation exists between pericardial pressure and respiratory variation in intracardiac blood flow velocities, a spontaneously breathing closed chest canine model of pericardial tamponade was created. In seven dogs, pericardial pressure was sequentially increased in stages from a mean of -4 +/- 1 to 10 +/- 2 mm Hg while aortic and pulmonary Doppler flow velocities, pleural pressure changes (respiratory effort), blood pressure and cardiac output were measured. The variation in the Doppler-detected peak transaortic velocity (AV) during inspiration (IV) increased linearly from -5 +/- 3% at baseline (pericardial pressure -4 mm Hg) to -32 +/- 9% at a pericardial pressure of 10 mm Hg [IVAV = -2 (pericardial pressure)--13.1; r = 0.78, p less than 10(-6)]. The inspiratory variation in the peak transpulmonary velocity increased from 13 +/- 3% at baseline to 71 +/- 19% at a pericardial pressure of 10 mm Hg. The inspiratory variation in the pulmonary Doppler peak velocity (IVPV) was dependent on both pericardial pressure and degree of respiratory effort [IVPV = 3.8 (pericardial pressure) + 2.6 (respiratory effort) + 10.9; r = 0.88, p less than 10(-8)]. Thus, quantitative relations exist between increases in intrapericardial pressure and increases in inspiratory variation of peak aortic and pulmonary flow velocities. Additionally, pulmonary artery flow velocity is influenced more than aortic velocity by intrathoracic pressure.

The effects of indomethacin and a β-sympathomimetic agent on the fetal ductus arteriosus during treatment of premature labor: A randomized double-blind study

To study the effect of maternal indomethacin or nylidrine hydrochloride treatment on the fetus ductus arteriosus and the pulmonary artery, 27 women with threatened preterm labor between 24 and 34 weeks' gestation were studied by echocardiography. Fourteen women were treated with indomethacin and 13 with nylidrin. Both systolic and diastolic velocities in the ductus increased after administration of indomethacin indicating constriction in nine fetuses, and exceeded the corresponding velocities in the fetuses of the nylidrin group (p = 0.001). However, there were no changes in pulmonary artery flow velocities (p greater than 0.5). In the indomethacin group, there was a significant linear positive relationship between the gestational age and the change in ductal flow velocity. Three of the nine patients with ductal constriction also had tricuspid regurgitation. These findings indicate that indomethacin, not nylidrin, causes transient constriction of the ductus arteriosus and the constrictive response increases with the gestational age. We recommend echocardiographic surveillance of fetal hemodynamics when prostaglandin synthesis inhibitors are used in the treatment of spontaneous preterm labor.

Intraoperative Estimation of Cardiac Output by Transesophageal Pulsed Doppler Echocardiography

To determine whether transesophageal echocardiography could be used to estimate intraoperative cardiac output, the authors studied 35 consecutive patients undergoing cardiovascular surgery (coronary artery disease [n = 22], aortic valve disease [n = 5], mitral valve stenosis [n = 5], peripheral vascular disease [n = 3]). Two-dimensional echocardiographic and pulsed-wave Doppler signals of the pulmonary artery and mitral valve flow velocity were obtained simultaneously with thermodilution measurements of cardiac output. Cardiac output derived from pulsed Doppler imaging of pulmonary artery systolic flow velocity modestly correlated with the thermodilution-derived cardiac output (r = 0.65), but output determined from the mitral valve diastolic flow velocity did not (r = 0.24). Transesophageal echocardiography of pulmonary artery systolic flow satisfactorily detected intraoperative increases in cardiac output greater than 15% (sensitivity, 71%; specificity, 82%) but not decreases (sensitivity, 54%; specificity, 90%). Although this technique identifies increases in cardiac output greater than 15%, it does not detect decreases as accurately as those detected by thermodilution measurements. At this time, therefore, transesophageal Doppler echocardiography has significant limitations as an off-line monitor of cardiac output.

Spectrum of findings in a family with nonsyndromic autosomal dominant supravalvular aortic stenosis: A doppler echocardiographic study

Nonsyndromic familial supravalvular aortic stenosis is an autosomal dominant disorder. However, for many reported families, systematic study of all family members with echocardiographic or hemodynamic techniques has not been performed and degree of penetrance has not been assessed. The supravalvular stenosis in these family members usually is not associated with mental retardation or other characteristics of Williams syndrome. Although some believe that autosomal dominant supravalvular aortic stenosis is part of the spectrum of Williams syndrome, others believe that these are separate entities.Doppler echocardiograms were analyzed on 23 members of a 34 member family with several known to have supravalvular aortic stenosis; 20 studies were performed by the authors and 3 were done elsewhere and made available for review. No family member had mental retardation, characteristic facies or other findings of Williams syndrome. Three of the 34 had supravalvular aortic stenosis requiring surgery. Of 22 members examined echocardiographically who had not had prior surgical repair, 13 had supravalvular aortic stenosis. Echocardiographic findings ranged widely, from calcification of the ascending aorta in a 71 year old man with minimally increased flow velocity (1.7 m/s) to mild narrowing with mildly increased flow velocity in six members to significant narrowing with impressively increased flow velocity (2 to 4 m/s) in seven. In addition, four patients had mild narrowing of pulmonary artery branches and eight had peak pulmonary artery flow velocity above normal.This study demonstrates complete penetrance with extremely variable expression in this family with autosomal dominant supravalvular aortic stenosis and emphasizes the importance of using echocardiographic techniques in studying the family members who are suspected of having an inherited cardiovascular disease.

Doppler flow velocity mapping in an in vitro model of the normal pulmonary artery

Pulsed Doppler pulmonary artery velocity measurements are useful in evaluating a number of cardiac conditions including pulmonary hypertension, pulmonary stenosis and insufficiency, intracardiac shunts and other congenital abnormalities. However, variations in sample location relative to the arterial wall and valve have been thought to affect pulmonary artery velocity and acceleration measurements clinically. Therefore, pulsed Doppler and color flow mapping were performed in a pulsatile flow apparatus connected to a glass or Plexiglas model of the main pulmonary artery and its bifurcation, which contained a Hancock 29 mm pericardial tissue valve (5.35 cm2orifice). Doppler sample volumes were placed at four sites: 1) at the pulmonary valve leaflet tips, centrally; 2) 2 cm distal to the leaflet tips, centrally; 3) 2 cm distal but laterally near the pulmonary artery wall; and 4) at the pulmonary artery bifurcation, centrally.Doppler peak flow velocity and acceleration time were measured. There was no difference between sites 1 and 2 in peak flow velocity or acceleration time. At site 3, peak flow velocity and acceleration time were both less than at site 1 (mean ± SD, 85 ± 44 versus 105 ± 39 cm/s, p < 0.005, and 162 ± 65 versus 188 ± 46 ms, p < 0.03, respectively). Moreover, the pulmonary artery velocity contour at site 3 exhibited increased spectral dispersion and notching and increased variance on the color spectrum. At site 4, peak flow velocity was less than at site 1 (85 ± 31 versus 105 ± 39 cm/s, p < 0.005), whereas pulmonary artery acceleration time was not significantly different.In this model, Doppler pulmonary artery flow velocity was best recorded within 2 cm of the valve and in the center of the vessel. Similar studies should be performed in the human pulmonary artery to standardize the recording technique and sample sites for Doppler measurements of velocity and acceleration.

Effect of Acute Changes in Heart Rate on Doppler Pulmonary Artery Acceleration Time in a Porcine Model

Doppler measurements of pulmonary artery (PA) acceleration time (AT) have been used clinically to estimate PA pressure. However, these studies have been performed primarily in patients without tachycardia. To determine the effect of acute changes in heart rate on PA AT, atrial pacing studies were performed in seven closed-chest pigs. Pulsed Doppler PA flow velocity recordings were obtained from a parasternal position at pacing rates from 100 to 140 beats/min. PA pressure remained constant (mean +/- SD = 14 +/- 5 mm Hg) over the entire range of paced rates. When PA Doppler measurements were compared at heart rates of 100 and 140 beats/min, there were decreases at the higher heart rate in both acceleration time (110 +/- 12 vs 83 +/- 11 ms, p less than 0.01) and ejection time (ET) (315 +/- 23 vs 237 +/- 21 ms, p less than 0.01). In contrast, there was no change in either PA peak flow velocity (69 +/- 15 vs 62 +/- 18 cm/s) or the ratio of AT/ET (0.35 +/- .02 vs. .36 +/- .03). Consequently, when estimating PA pressure in states of tachycardia, the PA AT/ET ratio may be a more useful measurement than PA acceleration time.

Doppler echocardiographic comparison of haemodynamic results of one- and two-stage anatomic correction of complete transposition

Eighteen children who had single-stage and 18 who had two-stage anatomic correction of complete transposition between the ages of 1 week and 3 years (mean 6.5 months) were investigated with pulsed and continuous wave Doppler ultrasound. Peak mitral flow velocities showed no significant difference from normal after single-stage correction, but were significantly higher than normal after two-stage correction ( P < 0.05). Peak tricuspid flow velocities were significantly higher than normal in both groups ( P < 0.02 and P < 0.001). There was no significant difference in pulmonary artery flow velocities between the two groups, which were means (SD) of 214 (84) cm/sec after single-stage and 179 (87) cm/sec after two-stage repair. Peak velocities in the ascending aorta were within normal limits after single-stage correction, but were lower than normal in the two-stage group ( P < 0.02). Mild aortic regurgitation was detected in 22% of single-stage and 55% of two-stage patients ( P = 0.043, 2 P = 0.085). Both types of repair are associated with higher peak tricuspid flow velocities than normal and have a similar incidence of mild supravalvar pulmonary stenosis. Mitral flow velocities are higher than normal only after two-stage correction. Velocities in the ascending aorta are lower than normal and the incidence of mild aortic regurgitation appears to be increased after two-stage repair, probably due to dilatation of the aortic root following banding of the pulmonary trunk.

Evaluation of pulmonary artery pressure and resistance by pulsed Doppler echocardiography

Pulsed Doppler echocardiography was used to examine the relation between pulmonary valve motion and pulmonary artery (PA) flow velocity patterns in 39 adults. In 16 patients with normal PA pressure (mean pressure less than 20 mm Hg), PA flow velocity accelerated slowly to a peak flow velocity at midsystole (time to peak flow velocity, or acceleration time = 134 ± 20 ms [mean ± standard deviation]), followed by a slow deceleration to the end of ejection, producing a “dome-like” appearance. In contrast, in 23 patients with elevated PA pressure (mean pressure 20 mm Hg or more), flow velocity accelerated rapidly to a peak flow velocity in early systole (acceleration time = 88 ± 25 ms, p <0.01), followed by rapid flow velocity deceleration to a nadir In midsystole. In 13 of these patients, a transient increase in flow velocity occurred in late systole, producing a “spike and dome” appearance. In patients with an acceleration time of 120 ms or less, there was a negative linear correlation with mean PA pressure, expressed by the equation: mean PA pressure = 90 − (0.62 × acceleration time). The standard error of the estimate was 8.3 mm Hg. A similar negative linear correlation was found between PA acceleration time and total pulmonary resistance. Using a PA acceleration time of 100 ms or less resulted in a 78% sensitivity and a 100% specificity for detection of elevated PA pressure. Although this Doppler method carrot precisely estimate PA pressure, I can be helpful in separating patients with normal pressure from those with elevated PA pressure.

A pulsed Doppler echocardiographic study of the postnatal changes in pulmonary artery and ascending aortic flow in normal term newborn infants

Postnatal circulatory adaptations were studied with Doppler echocardiographic measures of flow velocity in the main pulmonary artery (PA) and ascending aorta (Ao) in 45 normal full-term neonates at 5 hours and at 27 hours after birth. PA flow velocity integral (FVI) was measured as the area under the systolic flow velocity curve and reflected total systemic flow in the presence of a left-to-right shunt through the ductus arteriosus. This index increased from 5 and 27 hours age, while Ao FVI, reflecting total pulmonary flow, remained unchanged. Evidence of a left-to-right ductal shunt demonstrated as diastolic retrograde flow in the main PA was detected in 42 neonates at 5 hours and in only four subjects after 27 hours of age, indicating a patent ductus arteriosus at 5 hours of age and its subsequent closure. In the PA, acceleration time (AT) increased while pre-ejection period to ejection time ratio ( PEP ET ) decreased from 5 to 27 hours of age, reflecting the physiologic fall in PA pressure. In the Ao, FVI, AT, and PEP ET remained unchanged, suggesting little change in left ventricular function.

Relationship between age, body size, gender, and blood pressure and Doppler flow measurements in the aorta and pulmonary artery

Previous studies have demonstrated a relationship between both age and body surface area (BSA) and M-mode echocardiographic measurements of left ventricular, left atrial, and aortic root dimensions and left ventricular wall thickness. We evaluated the relationships between age, BSA, gender and blood pressure, and Doppler aortic and pulmonary artery (PA) flow velocity measurements in 97 adults, aged 21 to 78 years, without clinical evidence of cardiac disease. No significant relationship was found between gender or blood pressure and aortic or PA flow velocity measurements. Aortic peak flow velocity, flow velocity integral, and average acceleration decressed with increasing age (all p < 0.001), whereas ejection time (corrected for heart rate) increased, and acceleration time did not change. In contrast, there was no relationship between age and Doppler PA flow velocity measurements. Although there was no relationship between BSA and Doppler aortic flow measurements, PA peak flow velocity and average acceleration increased, while acceleration time decreased with increasing BSA (all p < 0.02). Decreases in aortic peak flow velocity and flow velocity integral may be partly related to known increases in aortic root diameter with aging. The relationship between PA flow velocity measurements and BSA is not readily explained.

Effects of propranolol on cardiopulmonary function in the pony during submaximal exercise.

Cardiopulmonary responses of four ponies were monitored during standard exercise tests (SET), before and after beta-adrenergic receptor blockade with propranolol. The SET consisted of four 5 min increments of increasing speed from 1.0 to 2.8 m/sec on a treadmill at a 7 degrees incline. Data were collected at rest, throughout the SET and recovery. Administration of propranolol to ponies at rest had no effect on cardiopulmonary function. During the SET, increases in heart rate, mean pulmonary artery flow velocity (an index of cardiac output) and right ventricular dP/dt (an index of myocardial contractility) were progressively attenuated as running speed increased. Body temperature and mean pulmonary artery and right ventricular pressures were significantly elevated over normal. Propranolol treatment had no effect on the responses of mean arterial pressure, haematocrit, haemoglobin, blood lactate and arterial blood gases and pH to the SET. These results suggest that in the pony there is no sympathetic activity to the heart at rest and that during exercise there is pulmonary vasodilation mediated by beta-adrenergic receptors.

Fetal doppler echocardiography: Methods and characterization of normal and abnormal hemodynamics

Adequate pulse Doppler echocardiographic (echo) studies of the fetus were performed in 15 of 16 subjects in the third trimester of pregnancy (28 to 36 weeks) using a commercially available Duplex system with a fast Fourier transform analyzer. A preliminary real-time 2-dimensional (2-D) echo examination was first performed to identify the fetal cardiac structures and obtain standard planes. The Doppler beam was then positioned along the long axis of the main pulmonary artery (PA), imaged in the standard short-axis or left ventricular-pulmonic plane, to obtain maximal Doppler frequency shifts. In 6 of 15 fetuses (40%) in whom the inner PA width could be measured, right ventricular (RV) stroke volume ranged from 1.01 to 3.76 ml. RV cardiac output ranged from 148 to 451 ml/min (128 to 239 ml/min/kg when normalized for estimated fetal weight). In 1 of 9 fetuses in whom PA width could not be reliably measured, a marked decrease (60%) in the PA flow velocity curve area and, therefore, in the stroke volume was noted during ectopic beats. In keeping with known fetal physiology, greater Doppler frequency shifts were noted in the right atrium than in the left atrium. Also, increased Doppler frequency shifts were noted in the left atrium during the open position of the valve of foramen ovale compared to its closed position. Our study shows the feasibility of studying normal and abnormal fetal hemodynamics noninvasively using Doppler echocardiography.

Noninvasive prediction of transvalvular pressure gradient in patients with pulmonary stenosis by quantitative two-dimensional echocardiographic Doppler studies.

Recent studies suggest that maximal Doppler velocities measured within the jets that form downstream from stenotic valves can be used to predict aortic valve gradients. To test whether the Doppler method would be useful for evaluation and management of pediatric patients with right ventricular outflow obstruction, we evaluated pulmonary artery flow before catheterization in 16 children with pulmonary valve stenosis. We used a 3.5-MHz, quantitative, range-gated, two-dimensional, pulsed, echocardiographic Doppler scanner with fast Fourier transform spectral output and a 2.5-MHz phased array with pulsed or continuous-mode Doppler. Peak systolic pulmonary artery flow velocities in the jet were recorded distal to the domed pulmonary valve leaflets in short-axis parasternal echocardiographic views. The pulsed Doppler scanner, because of its limitations for resolving high velocities, could quantify only the mildest stenoses; but, especially with the continuous Doppler technique, a close correlation was found between maximal velocity recorded in the jet and transpulmonary gradients between 11 and 180 mm Hg. A simplified Bernoulli equation (transvalvular gradient = 4 x [maximal velocity]2) proposed by Hatle and Angelsen could be used to predict the gradients found at catheterization with a high degree of accuracy (r = 0.98, SEE = +/- 7 mm Hg). Our study shows that recording of maximal Doppler jet velocities appears to provide a reliable measure of the severity of valvular pulmonic stenosis.

Role of kinetic energy in pulmonary valvar pressure gradients.

Peak systolic pulmonary valvar pressure gradients are frequently seen in large intracardiac left-to-right shunt lesions. Conventionally, this has been attributed to "relative" pulmonic stenosis. Theoretical considerations suggest that this gradient is due to differences in expression of the total fluid energy. The side pressure, the downstream pressure, the end pressure, and the flow velocity in the pulmonary artery (PA) and the right ventricle (RV) pressure were measured in 11 dogs in the control state, and after increasing the velocity of the pulmonary arterial flow either by administration of isoproterenol or atropine, or by creating an arteriovenous fistula. The RV pressure and the end PA pressure were not significantly different ( P &gt; 0.05), and were higher ( P &lt; 0.01) than the side and downstream PA pressure in the control state, but increased to higher levels ( P &lt; 0.01) after increasing the velocity of flow in the pulmonary artery. The mean pulmonary valve peak systolic gradient (RV-side PA pressure difference) was 8.8 mm Hg in the control state and increased to 19.1 mm Hg after isoproterenol infusion ( P &lt; 0.01). This change in pulmonary valvar gradient is proportional to the increase in the PA flow velocity. The side pressure measures only the potential energy, and the end pressure measures both the potential and kinetic energies. In the right ventricle, only the potential energy is recorded where the kinetic energy is practically nonexistent. The difference between the RV (or end PA) pressure and side PA pressure is proportional to velocity of flow in the pulmonary artery and is due to partial transformation of fluid energy into kinetic energy. Thus, our study helps to explain the pressure gradient across the pulmonary valve in large left-to-right shunt lesions. These studies also raise questions as to the validity of interpretations of the gradients produced in the RV outflow tract after isoproterenol or exercise.

NIH clinical staff conference. Assessment of cardiac function.

In the past, assessment of cardiac function has centered on techniques that examined the heart's action as a pump. Hemodynamic analysis of cardiac function within the framework of the Frank-Starling relation is valuable when directional changes in the performance under stress of the diseased ventricle are compared with the normal. Recently, principles of skeletal muscle physiology have been extended to the myocardium and applied successfully to examination of the function of the intact heart. Angiography in patients revealed that specific alterations in the pattern of contraction occur in patients with left ventricular disease, principally a decrease in extent and velocity of fiber shortening, associated with decrease in the extent of reduction of ventricular wall tension during contraction. Estimates of contractile state based on the tension-velocity-length relation determined angiographically sensitively quantify the myocardial contractile state in patients, even during abnormal ventricular loading. A second useful method for assessment of cardiac function in patients consists of relating the first derivative of the ventricular pressure to the simultaneously occurring isovolumic pressure. A third promising method measures pulmonary arterial and aortic blood flow velocity by a cathetertip velocity probe. This instrument uses the principle of the external electromagnetic flow meter; its potential applicability to assessment of myocardial function has been shown. Use of the cardiac output response to exercise in the assessment of cardiac function is reviewed. Measurement of the cardiac output when exercise has lowered the mixed venous oxygen saturation to 30% is useful, reliably and sensitively distinguishing performance of the patient with mild or moderate impairment of cardiac function from normal.