Accuracy of the inverse Womersley method for the calculation of hemodynamic variables.

We have studied the accuracy of the inverse Womersley method, a linear theory for the calculation of hemodynamic variables from measured volumetric flow rate or centerline velocity, for two canine arteries with different degrees of arterial wall motion and taper. The results from the linear theory are compared with the estimates from the nonlinear theory of Ling and Atabek for a canine thoracic aorta and femoral artery. For the thoracic aorta, the linear theory underestimates the mean wall shear stress by as much as 77%, when compared with the nonlinear theory. For the femoral artery, on the other hand, the mean wall shear stress value is underestimated by as much as 23%. Estimates of other hemodynamic variables show similar discrepancies between the nonlinear and linear theories. Thus, the inverse Womersley method does not give accurate estimates of hemodynamic quantities. This failure results from the neglect of convective accelerations due to arterial wall motion and taper, with the neglect of arterial taper leading to the largest errors.

Altering hydrodynamic variables influences PGI2 production by isolated lungs and endothelial cells.

Because deformation of lung tissue stimulates prostaglandin synthesis, we wanted to investigate whether hydrodynamic forces would affect lung prostacyclin (PGI2) production. To test the hypothesis that lung prostacyclin synthesis was flow dependent, we examined lung prostacyclin production after flow alterations. Using a salt solution that contained either Ficoll or albumin as a perfusate, we changed the flow to half and to double the control flow. When flow was changed, lung prostacyclin production followed changes in flow and pressure drop. When flow was varied in lungs treated with indomethacin, prostacyclin production was too low to be measurable. Variations in pressure pulsatility at constant mean flow had no influence on lung prostacyclin production. Since vascular distension may also stimulate prostacyclin production, we increased venous pressure. An increase in venous pressure (from 2.1 to 4.8 mmHg) had no effect on prostacyclin production; a further increase in venous pressure (to 7.5 mmHg) initiated edema and caused a large increase in prostacyclin production. When we subjected monolayers of endothelial cells cultured in wells to defined shear rates, the prostacyclin concentration in the supernatant quickly increased to a maximum. The absence of further increase with greater shear may have reflected feedback control of prostacyclin synthesis. The results indicated that hydrodynamic disturbances affect endothelial cells and stimulate arachidonate metabolism. Lung prostacyclin production may be related to flow. However, this effect is small compared with the lung prostacyclin production during edema formation.

A model of embolic chronic pulmonary hypertension in the dog.

Despite numerous efforts, a reliable model of chronic embolic pulmonary hypertension has not been established. To develop such a model five conscious mongrel dogs were embolized repeatedly over 16-30 wk with Sephadex microspheres 286 +/- 70 micron in diameter. Hemodynamic and respiratory measurements were obtained just prior to each embolization. Chronic pulmonary hypertension developed in all dogs. Pulmonary hypertension was not accounted for by increased cardiac output, wedge pressure, right atrial pressure, or systemic arterial pressure. Gas exchange was little altered. Lung histological study revealed microspheres clustered within vessels. In three dogs increased pulmonary arterial pressure was sustained despite cessation of embolization for up to 5 mo. Reembolization in one of these caused further pulmonary hypertension. In two dogs acute pulmonary vasodilation by O2 breathing and administration of prostaglandin E1 reduced, but did not abolish, the increased pulmonary vascular resistance, suggesting some vascular tone was present. An embolic model of chronic pulmonary hypertension in awake dogs allows further investigation into the evolution of pulmonary hypertension.

Thermodilution method overestimates low cardiac output in humans.

We compared 57 cardiac output measurements by the thermodilution and Fick methods in 26 patients and found that thermodilution values were higher in all 16 cases in which Fick outputs were less than 3.5 l/min. In 10 cases where Fick values were less than or equal to 2.5 l/min, thermodilution and Fick measurements differed by an average of 35%. When combined with the results of previous studies comparing the thermodilution, dye dilution, and Fick techniques, these findings suggest that the thermodilution method overestimates true cardiac output in the low output range. This overestimation probably is due to heat loss under conditions of low flow. Because the thermodilution method is used widely in patients with low output states, these findings have potentially important clinical implications.

Effects of unequal pressure swings and different waveforms on distribution of ventilation: a non-linear model simulation.

In an attempt to understand the role of unequal pleural pressure swings and of different waveforms of pleural pressure variation in the distribution of ventilation during cyclic breathing, a mathematical model simulation was performed. The computer model which incorporates non-linear resistances and compliances as well as sinusoidal, square, and triangular waveforms of pleural pressure variations indicates that the distribution of ventilation is insensitive to the waveform of the pleural pressure. The distribution is also little changed by the depth of breathing (amplitude), but it is affected significantly by the pattern of different pressures over the regions of the model. For sinusoidal, triangular, and low amplitude square wave pleural pressures with equal amplitudes on both compartments, air was distributed preferentially to the lower compartment under the influence of the static pressure difference. With unequal amplitudes, more air flowed to the compartment experiencing the larger pressure swing. This was virtually independent of the waveform and of the amplitudes of the pleural pressure variation. Comparison of the present results with a constant flow model reveals that the overall distribution of tidal air during cyclic breathing is very different from the results obtained in constant rate inspiration experiments or in bolus distribution experiments. New experiments performed under cyclic breathing conditions are thus indicated.

Unequal pressures in the central pulmonary arterial branches in patients with pulmonary stenosis. The influence of blood velocity and anatomy.

Significantly different pressures in the right (RPA) and left (LPA) pulmonary artery were observed at catheterization in patients with pulmonary valvar stenosis and no branch stenosis. The lower pressures in the RPA showed a "valley" during systole and were similar in contour and amplitude to the main pulmonary arterial (MPA) pressure; the LPA pressure, however, had a normal contour, and the peak systolic and mean pressures were higher than those in the MPA and RPA. Angiocardiograms, phonograms, and a simple analysis of fluid mechanics suggest that this pressure pattern is related to (1) the high-velocity jet in the MPA and (2) the anatomy of the central pulmonary arterial branches (bifurcation), the LPA originating more distally than the RPA. The high-velocity jet bypasses the origin of the RPA and breaks up in the distal MPA near the origin of the LPA. The kinetic energy is then reconverted into pressure, causing the higher LPA pressures. In patients with transposition of the great arteries and subvalvar pulmonary stenosis, the anatomy of the main pulmonary arterial bifurcation is different from normal, the RPA originating more distally than the LPA. The high-velocity jet may bypass the origin of the LPA and break up near the more distal origin of RPA, and the pressures in the RPA can be higher than those in the MPA and LPA.

Echocardiographic assessment of the relation between left ventricular wall and cavity dimensions and peak systolic pressure in children with aortic stenosis.

Echocardiographic measurements of the left ventricular end diastolic minor axis and posterior and septal wall thickness were obtained in 19 children with congenital aortic stenosis with left ventricular peak systolic pressures ranging from 110 to 225 mm Hg at cardiac catheterization. From these measurements were derived (1) the left ventricular peak circumferential wall stress, (2)the end-diastolic h/r ratio (that is, mean of septal and posterior wall thickness (h) to minor semiaxis (r) ratio), and (3) the LVM/LVV ratio (that is, left ventricular mass (LVM) to left ventricular end-diastolic volume (LVV) ratio). The peak stress was found to be within the normal range and independent of the left ventricular peak systolic pressure. The end-diastolic h/r and LVM/LVV ratios had highly significant linear relations to the left ventricular peak systolic pressure. It is concluded that these easily determined echocardiographic measurements provide a useful noninvasive means of assessing left ventricular peak systolic pressure in patients with aortic stenosis without myocardial decompensation.

Asymmetric distribution of the pulmonary blood flow between the right and left lungs in d-transposition of the great arteries.

Pulmonary angiograms, radionuclide lung images and chest roentgenograms were evaluated regarding the incidence, magnitude and natural evolution of maldistribution of the pulmonary blood flow between the lungs in 63 patients with dextrotransposition of the great arteries. Approximately half of these patients had some degree of greater perfusion of the right relative to the left lung. A significant correlation was demonstrated between the incidence of this maldistribution of blood flow and the angulation between the main and the right pulmonary arteries. For any given angulation between these vessels, additional pulmonary stenosis increased the incidence of disparity in perfusion. Our observations suggest the following developmental mechanisms: The maldistribution in flow results from the abnormal rightward inclination of the main pulmonary artery in the transposition malformation which straightens the flow axis from the main to the right pulmonary artery. Under these circumstances the momentum of the blood in the main pulmonary artery carries the blood preferentially into the right pulmonary artery. This momentum is increased when there is stenosis of the left ventricular outflow tract. Consequent differences in the mechanical properties of the two pulmonary vascular beds can increase this maldistribution. The disparity in perfusion between the lungs is not present in newborns with d-transposition, appears to be progressive in severity and in time may result in almost complete cessation of effective perfusion of the left lung. The effect of the Mustard operation on this abnormality of flow is discussed.