Changes In Pulmonary Blood Volume Research Articles

Measurement of pulmonary transit time and estimation of pulmonary blood volume after exercise using contrast echocardiography.

Pulmonary transit time (PTT) and pulmonary blood volume (PBV) derived from non-invasive imaging correlate with pulmonary artery wedge pressure. The response of PBV to exercise may be useful in the evaluation of cardiopulmonary disease but whether PBV can be obtained reliably following exercise is unknown. We therefore aimed to assess the technical feasibility of measuring PTT and PBV after exercise using contrast echocardiography. In healthy volunteers, PTT was calculated from time-intensity curves generated as contrast traversed the cardiac chambers before and immediately after participants performed sub-maximal exercise on the Standard Bruce Protocol. From the product of PTT and heart rate (HR) during contrast passage through the pulmonary circulation, PBV relative to systemic stroke volume (rPBV) was calculated. The cohort consisted of 14 individuals (age: 46 ± 8years; 2 female) without cardiopulmonary disease. Exercise time was 8 ¾ ± 1 ¾ minutes and participants reached 85 ± 9% of age-predicted maximal HR, which corresponded to a near-doubling of resting HR at the time of post-exercise contrast injection. Data sufficient to derive PTT and rPBV were obtained for all participants. With exercise, the change in PBV from baseline ranged from 56 to 138% of systemic stroke volume, consistent with rPBV and absolute PBV values obtained in prior studies. Acquisition of PTT and rPBV using contrast echocardiography after exercise is achievable and the results are physiologically plausible. As the next step towards clinical implementation, validation of this technique against hemodynamic exercise studies appears reasonable.

Synchrotron Imaging Shows Effect of Ventilator Settings on Intrabreath Cyclic Changes in Pulmonary Blood Volume.

Despite the importance of dynamic changes in the regional distributions of gas and blood during the breathing cycle for lung function in the mechanically ventilated patient, no quantitative data on such cyclic changes are currently available. We used a novel gated synchrotron computed tomography imaging to quantitatively image regional lung gas volume (Vg), tissue density, and blood volume (Vb) in six anesthetized, paralyzed, and mechanically ventilated rabbits with normal lungs. Images were repeatedly collected during ventilation and steady-state inhalation of 50% xenon, or iodine infusion. Data were acquired in a dependent and nondependent image level, at zero end-expiratory pressure (ZEEP) and 9 cm H2O (positive end-expiratory pressure), and a tidal volume (Vt) of 6 ml/kg (Vt1) or 9 ml/kg (Vt2) at an Inspiratory:Expiratory ratio of 0.5 or 1.7 by applying an end-inspiratory pause. A video showing dynamic decreases in Vb during inspiration is presented. Vb decreased with positive end-expiratory pressure (P = 0.006; P = 0.036 versus Vt1-ZEEP and Vt2-ZEEP, respectively), and showed larger oscillations at the dependent image level, whereas a 45% increase in Vt did not have a significant effect. End-inspiratory Vb minima were reduced by an end-inspiratory pause (P = 0.042, P = 0.006 at nondependent and dependent levels, respectively). Normalized regional Vg:Vb ratio increased upon inspiration. Our data demonstrate, for the first time, within-tidal cyclic variations in regional pulmonary Vb. The quantitative matching of regional Vg and Vb improved upon inspiration under ZEEP. Further study is underway to determine whether these phenomena affect intratidal gas exchange.

Change in pulmonary blood volume changes pulmonary artery systolic storage

BackgroundA fraction of right ventricular stroke volume (pulmonary artery systolic storage, [PASS]), which is stored in pulmonary arteries during systole and then discharged to the capillaries, determines the diastolic pulmonary capillary blood flow and hence the capillary blood volume participating in gas diffusion. Possibility that increases in pulmonary blood volume (PBV) increase PASS, leading to an improved distribution of ventilation-to-perfusion ratios (V/Q ), was examined. Methods and resultsIncluded were 34 obese patients undergoing bariatric surgery. We used a nitrous oxide-airway-pneumotachographic method to measure PASS. The measurements were repeated before and after increasing PBV. In 20 patients, PBV was increased with infusion of crystalloids, which was guided by pulmonary capillary wedge pressure (PCWP). There was a good correlation between change in PASS and change in PBV (r2 = 0.741, P < 0.0001). However, when the baseline PASS was high, changes in PASS were much less. In patients with a pulmonary artery diastolic-pulmonary capillary wedge pressure gradient ≥6 mmHg, the baseline PASS was correlated with pulmonary venous resistance (r2 = 0.644, P = 0.017). In 14 patients, in whom PBV was increased with both changes in position and infusion of crystalloids, the physiologic dead space-to-tidal volume ratio (VD/VT) was measured as an index of the distribution of V/Q. There was a good negative correlation between PASS and VD/VT (r2 = 0.697, P < 0.0001). However, at a high baseline PASS, increases in PBV decreased PASS (P = 0.0006) and increased VD/VT (P = 0.0018). ConclusionsChanges in PBV change PASS and thereby the distribution of V/Q, depending on pulmonary venous resistance, which determines the baseline PASS.

Application of carbon monoxide diffusing capacity in the mouse lung

In the past decade the mouse has become the primary animal model of a variety of lung diseases. To assess various mechanisms underlying such pathologies, it is essential to make functional measurements that can reflect the developing pathology. In this regard, the diffusing capacity for carbon monoxide is a variable that directly reflects structural changes in the lung. Although measurement of single-breath diffusing capacity of the lung for carbon monoxide (DL(CO)) has also been previously reported in mice by a number of investigators, a number of technical issues have precluded routine and widespread use of this metric in mouse models. In the present report, we describe a means to quickly and simply measure a dimensionless variable closely related to the DL(CO) in mice, termed a diffusion factor for carbon monoxide (DF(CO)). The DF(CO) procedure involves a 9-s lung inflation with tracer gases in an anesthetized mouse, followed by a 1-min gas analysis time. We have tested the approach with two common models of lung pathology, elastase-induced emphysema and bleomycin-induced fibrosis. Results show a significant 15% reduction in DF(CO) in emphysema, and a 41% reduction in the fibrosis model. Repeat measurements within a mouse were found to be highly reproducible. This pulmonary function test can thus be used to detect structural changes with these pathological models. The method can also be used to measure changes in pulmonary blood volume, since the uptake of CO is highly dependent on this variable in addition to the gas exchange surface area.

Measurement of lung density by photon transmission for monitoring intravascular and extravascular fluid volume changes in the lungs.

Left ventricular (LV) heart failure increases pulmonary blood volume (PBV) and interstitial fluid volume. Continuous measurements of lung density may be a simple non-invasive method for monitoring of the LV function as the lung density should reflect the changes in the PBV and extravascular lung water. The purpose of the study was to optimize transmission measurements of the lung with a gamma camera and a planar source. Another aim was to assess the possibility of transmission monitoring in normal subjects at rest and during exercise and to compare the results with simultaneous measurements of PBV changes. Transmission measurements were made in a water-filled phantom containing lungs of different density. A gamma camera and a planar 57Co source were used. The coefficient of variation in density determination owing to counting statistics in a lung area was calculated for different energy windows, acquisition times and collimation. Dynamic measurements in normal subjects were carried out in a sitting and a supine position at rest and during exercise. Pulmonary blood volume was monitored simultaneously using 99mTc-labelled red blood cells and the registered blood pool activity was corrected for attenuation. Highest precision in relative density determination was obtained with large energy window and uncollimated source. A precision of 1.0% was obtained with 1 min measuring time. About 10% change in transmission corresponding to a 15% change in density was observed during exercise. Changes in blood pool and lung density covariated. We conclude that lung density changes can be monitored with a high degree of statistical precision in a few minutes and with a low radiation dose of radiation using a gamma camera and a planar source.

Effects of partial liquid ventilation with perfluorocarbons on pressure-flow relationships, vascular compliance, and filtration coefficients of isolated blood-perfused rabbit lungs.

The density of perfluorocarbons is almost twice that of blood. Therefore, we hypothesized that partial liquid ventilation with these fluids markedly affects pulmonary hemodynamics and filtration coefficients. To test these hypotheses we studied pressure-flow relationships, vascular compliances, capillary pressures, and filtration coefficients in normal and perfluorocarbon-ventilated rabbit lungs. Controlled animal study with an ex-vivo isolated lung preparation. Research laboratory for experimental anesthesiology at the Heinrich-Heine-University of Düsseldorf. Fourteen New Zealand White rabbits. The lungs were perfused under zone 3 flow conditions with autologous blood at various flow rates (50 to 250 mL/min, closed circuit, roller pump, 37 degrees C) and ventilated with 5% CO2 in air (positive end-expiratory pressure: 2 cm H2O, tidal volume: 10 mL/kg, respiratory rate: 30 breaths/min) without (control group, n=7) and with (n=7) perfluorocarbon administered intratracheally (15 mL/kg). Pulmonary arterial, left atrial, and airway pressures, as well as blood reservoir volume (reflecting changes in pulmonary blood volume) and lung weight, were measured continuously. Inconsistent with our hypothesis, we found no significant differences between both groups in the slopes and intercepts of the pressure-flow relationships. There were no significant differences in capillary pressures determined by double occlusion (6.7+/-1.2 vs. 6.3+/-1.3 cm H2O for control group, p=.53), vascular compliances (0.51+/-0.10 vs. 0.47+/-0.09 mL/cm H2O for control group, p=.38), and filtration coefficients (0.33+/-0.06 vs. 0.37+/-0.07 mL/min/mm Hg/100 g wet weight for control group, p=.80, Mann-Whitney). Partial liquid ventilation with perfluorocarbons has no relevant effects on pulmonary filtration coefficients and global hemodynamic variables of isolated zone 3 lungs. These findings suggest that right ventricular afterload is not changed with partial liquid ventilation. It is likely, however, that intrapulmonary blood flow is redistributed toward less-dependent regions, although relevant global hemodynamic changes are absent during partial liquid ventilation.

Tidal variation of pulmonary blood flow and blood volume in piglets during mechanical ventilation during hyper-, normo- and hypovolaemia

Effects of changes in blood volume on changes in pulmonary blood flow and pulmonary blood volume during the ventilatory cycle during mechanical ventilation with a positive end-expiratory pressure of 2 cm H2O were determined in six pentobarbital anaesthetized, curarized pigs weighing about 10 kg. Haemodynamic variables were analysed for each cardiac cycle in eight ventilatory cycles in four consecutive series under hyper-, normo- and hypovolaemic conditions. Cardiac output was highest in hypervolaemia. Compared with normo- and hypovolaemia, it decreased less during inflation, due to a smaller rise in central venous pressure and presumably a larger filling state of the venous system. The smaller decrease in right ventricular output in hypervolaemia coincided with a larger fall in transmural central venous pressure (right ventricular filling pressure), due to right ventricular action at a higher, less steep part of its function curve. The difference between right ventricular-output (electromagnetic flow measurement) and left ventricular-output (pulse contour) indicated changes in pulmonary blood volume. In hypervolaemia less blood shifted from the pulmonary circulation into the systemic system during inflation than in normo- and hypovolaemia. This difference can be explained by two mechanisms namely, the smaller fall in input into the pulmonary vascular beds and a smaller pulmonary vascular volume decrease as a result of transmural pressure fall at a steeper part of the pressure-volume curve.

Canine pulmonary filtration coefficient calculated from optical, radioisotope, and weight measurements.

Three independent methods were used to estimate filtration coefficient (Kf) in isolated dog lungs perfused with low-hematocrit (Hct) blood. Pulmonary vascular pressure was increased by 12-23 cmH2O to induce fluid filtration. Average Kf (ml.min-1 x cmH2O-1 x 100 g dry wt-1) for six lungs was 0.26 +/- 0.05 (SE) with use of equations describing conservation of optically measured protein labeled with indocyanine green. Good agreement was found when a simplified version of the multiequation theory was applied to the data (0.24 +/- 0.05). Both optical estimates were lower than those predicted by constant slope (0.55 +/- 0.07) or extrapolation (1.20 +/- 0.15) techniques, which are based on changes in total lung weight. Subsequent studies in five dog lungs investigated whether the higher Kf from weight analyses could be caused by prolonged pulmonary vascular filling. We found that 51Cr-labeled red blood cells (RBCs), monitored over the lung, continued to accumulate for 30 min after vascular pressure elevations of 9-16 cmH2O.Kf was determined by subtracting computed vascular filling from total weight change (0.28 +/- 0.06) and by perfusate Hct changes determined from radiolabeled RBCs (0.23 +/- 0.04). These values were similar to those obtained from analysis of optical data with the complete model (0.30 +/- 0.06), the simplified version (0.26 +/- 0.05), and from optically determined perfusate Hct (0.16 +/- 0.03). However, constant slope (0.47 +/- 0.04) and extrapolation (0.57 +/- 0.07) computations of Kf were higher than estimates from the other methods. Our studies indicate that prolonged blood volume changes may accompany vascular pressure elevations and produce overestimates of Kf with standard weight measurement techniques. However, Kf computed from optical measurements is independent of pulmonary blood volume changes.

Pulmonary blood volume and haemodynamic changes with legs raised in chronic lung disease patients

The aim was determine the early effect of a posture change from supine (S) to legs raised 30 degrees above the table plane (LR) on haemodynamics in patients with chronic lung disease. Right heart catheterization was performed as part of a routine evaluation. Pulmonary arterial, pulmonary wedge, right atrial, and systemic arterial pressure were monitored at rest supine and during 8 min (steady values) after LR. Pulmonary blood volume was measured by double dye dilution, at rest S and after 1 and 8 minutes LR, in 14 patients; cardiac output was measured by thermodilution in the remaining 15 subjects, during S and 1, 4, and 8 minutes LR. 29 patients with chronic pulmonary disease of various types, mainly chronic bronchitis and emphysema, were studied when in a stable clinical condition, with no signs of heart failure. Raising the legs produced a sharp increase in all the pressures measured, with a subsequent decline towards a steady value slightly higher than during S. Pulmonary blood volume increased in all patients initially, but stayed elevated only in the normocapnic patients; in the patients with hypercapnia it decreased from 1 to 8 min LR. The pulmonary blood volume change showed a significant correlation with PaCO2 (p less than 0.01), and with the VD/VT ratio (p less than 0.01). The relation between the pulmonary blood volume and the distending pressure changes from S to 1 and 8 min LR was linear in the normocapnic group, but not in the hypercapnic group, where it showed a hysteresis. In patients with chronic lung disease who are hypercapnic, the volume/pressure relation following leg raising cannot be expressed by a single distensibility coefficient.

The influence of positive end-expiratory pressure on pulmonary blood volume changes in adult respiratory distress syndrome

Pathophysiologic changes associated with the Adult Respiratory Distress Syndrome (ARDS), such as the presence of pulmonary vascular occlusions, decreased vascular compressibility, or inceased intrapulmonary shunting, could limit the effect of positive end-expiratory pressure (PEEP) upon pulmonary blood volume (PBV). Accordingly, we determined the effect of 5 and 15 cm H 2O PEEP upon the PBV changes of normal volunteers (n = 9) and patients with moderate or severe ARDS associated with acute pulmonary hypertension (n = 10). Changes of PBV were estimated from equilibrium blood pool scans using Technetium-99m-labeled erythrocytes. The change of PBV induced by PEEP was assessed by measuring the count density over a region of the left lung during 0, 5, and 15 cm H 2O continuous positive airway pressure in the volunteers and during mechanic ventilation with 5 and 15 cm H 2O PEEP in the ARDS patients. Biventricular ejection fractions using gated blood pool angiocardiography and central hemodynamics were also measured in the ARDS patients. In volunteers, 5 and 15 cm H 2O continuous positive airway pressure decreased pulmonary activity by 10% ± 4% and 24% ± 9%, respectively (mean ± SD, P = .0001). In ARDS patients, PBV appeared to be unaffected by decreasing PEEP from 15 to 5 cm H 2O, despite an increased stroke volume, biventricular end-diastolic volume, and venous admixture. Pulmonary vascular resistance and right and left ventricular ejection fraction were unchanged. The ability of PEEP to reduce PBV appears to be decreased during acute lung injury.

Value of Radionuclide-Determined Changes in Pulmonary Blood Volume for the Detection of Coronary Artery Disease

We employed gated equilibrium radionuclide angiography to measure the ratio of pulmonary blood volume at exercise to PBV at rest. We compared this ratio to more commonly utilized ejection fraction measurements in the detection of coronary artery disease. Sensitivity was assessed in 28 patients with angiographically-proven coronary artery disease. Specificity was assessed in 25 patients with a low likelihood of coronary artery disease on the basis of Bayes' theorem. Receiver operator characteristic curves demonstrated that the peak exercise ejection was clearly superior to the PBV ratio in the diagnosis of coronary artery disease. The PBV ratio appears to be less useful for the diagnosis of coronary artery disease than the peak exercise ejection fraction.

Exercise-Induced Changes of Pulmonary Blood Volume in Patients with Uncomplicated Myocardial Infarction

A prospective study was performed in 105 consecutive patients 6-8 weeks after uncomplicated myocardial infarction to assess the clinical significance of exercise-induced pulmonary blood volume ratio measured from equilibrium radionuclide ventriculography which has been described as a sensitive index of left ventricular function. Patients underwent exercise equilibrium radionuclide ventriculography, thallium-201 myocardial perfusion scintigraphy and selective coronary arteriography. Pulmonary blood volume ratio was calculated from radionuclide ventriculography by dividing the average counts from a lung region of interest at maximal exercise by the average counts of a similar region of lung at rest. A control group of 62 normal subjects also underwent radionuclide ventriculography. Mean ± SD pulmonary blood volume ratio in the patients was 1.36 ± 0.39, significantly higher than that in normal subjects (1.24 ± 0.25; p < 0.05). There was no difference between pulmonary blood volume ratio in patients with normal or abnormal (< 48 %) resting ejection fraction. Pulmonary blood volume ratio was unable to discriminate between patient subgroups according to the severity of coronary artery disease and those with reversible ischaemia or fixed ‘scar’ on thallium-201 scintigraphy (1.37 ± 0.41 vs. 1.31 ± 0.34, p = NS, respectively). There was a poor correlation between pulmonary blood volume ratio and exercise thallium heart/lung ratio (a sensitive measure of exercise-induced left ventricular dysfunction). In contrast to previously published work, we find pulmonary blood volume ratio, determined by radionuclide ventriculography, to be of limited clinical value in assessing patients with uncomplicated myocardial infarction. The study underlines the importance of validating reported techniques for every laboratory before application to clinical studies.

Right ventricular ejection fraction response to exercise in patients with coronary artery disease: influence of both right coronary artery disease and exercise-induced changes in right ventricular afterload

To determine the influence of proximal right coronary artery disease and right ventricular afterload on right ventricular ejection fraction response to exercise, 64 patients were studied at rest and after supine exercise with gated equilibrium radionuclide angiography and coronary angiography. Right ventricular afterload response to exercise was estimated from determinations of exercise-induced changes in pulmonary blood volume, previously shown to correlate with exercise-induced changes in pulmonary capillary wedge pressure. Values for right ventricular ejection fraction decreased from rest to exercise (48 +/- 5% to 42 +/- 9%, p less than 0.001) in patients with an elevated pulmonary blood volume ratio. Values were unchanged in patients with isolated proximal right coronary artery disease (rest 49 +/- 3%, exercise 47 +/- 7%), decreased in patients with combined right and left coronary disease (rest 48 +/- 6%, exercise 39 +/- 10%, p less than 0.001) and increased (rest 47 +/- 5%, exercise 52 +/- 6%, p less than 0.001) in patients with isolated left coronary artery disease. To determine the coinfluence of coronary anatomy and changes in pulmonary blood volume, patients were classified by pulmonary blood volume ratio. Among patients with a normal pulmonary blood volume ratio, right ventricular ejection fraction did not change significantly in those with proximal right coronary artery disease during exercise, but increased significantly in patients with isolated left coronary disease. Among patients with an elevated pulmonary blood volume ratio, right ventricular ejection fraction during exercise increased significantly in those with proximal right coronary artery disease but was unchanged in patients with isolated left coronary disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Pulmonary blood flow: A potential factor in the pathogenesis of pulmonary edema

The purpose of this study is to examine the hemodynamics of the pulmonary circulation and the potential role of pulmonary blood flow in the pathogenesis of cardiogenic pulmonary edema. To do so, the pulmonary circulation was isolated and controlled such that, within a closed circuit, pulmonary blood flow and left atrial pressure (LAP) could be regulated independently: the first by a constant flow pump, the second by a variable height reservoir. The effect of pulmonary blood flow on pulmonary artery pressure and intravascular blood volume was then determined at different LAPs. Contrary to our expectations, the results indicate that (1) pulmonary vascular resistance does not change appreciably as flow increases, (2) the microcirculation comprises the major capacitance vessels of the lung, and (3) increased pulmonary flow in the normal lung causes little change in intravascular pulmonary blood volume, whereas, by contrast, major changes in pulmonary blood volume occur as LAP rises. Next, the effect of pulmonary blood flow on edema formation in the lungs was examined. Below a critical level of LAP (15 mm Hg in these experiments), pulmonary blood flow up to 5 L/min did not produce pulmonary edema. Above this level, however, such an effect was clear. Thus, at an LAP of 20 mm Hg, edema did not develop if pulmonary flow was low (0.7 L/min) but did if flow was increased to 2 L/min. As well, if the LAP was 17.5 mm Hg and pulmonary flow 3.5 L/min, severe pulmonary edema also resulted.

Pulmonary blood volume: Relationship to changes in left ventricular end-diastolic pressure during atrial pacing

Little data exist about the relationship between changes in cardiac end-diastolic pressure and changes in pulmonary blood volume. To assess this relationship, we studied 11 patients with coronary heart disease during atrial pacing in an attempt to produce multiple pressure-volume points. During catheterization, we obtained Millar pressure recordings of end-diastolic pressure along with equilibrium radionuclide angiograms. Cardiac output, ejection fraction, and pulmonary blood volume were obtained by means of recently validated radionuclide techniques. During pacing, substantial changes in pulmonary blood volume occurred only with marked increase in end-diastolic pressure volume (≥ 15 mm Hg) and rarely exceeded 15% of control pulmonary blood volume. Cardiac output did not change, while ejection fraction declined during pacing. There was a fair correlation between the absolute change in pulmonary activity (or pulmonary blood volume) or the percentage of change in pulmonary activity over the control value with end-diastolic pressure when all the data points were evaluated (n = 74, r > 0.70). However, the scatter in the data precluded making accurate estimates of pressure changes from changes in radionuclide volume changes. We conclude that large changes in cardiac filling pressure must occur during atrial pacing, where cardiac output does not change, before visible pulmonary blood volume changes occur. This may limit the extrapolation of presumed pressure changes from known pulmonary blood volume when changes are small.

Regional distribution of pulmonary blood volume: An index of pulmonary capillary wedge pressure determined from blood pool scintigraphy

Progressive redistribution of pulmonary blood flow to the lung apices occurs with increasing degrees of left ventricular failure, and correlates with increasing pulmonary capillary wedge pressure (PCWP). If similar changes in pulmonary blood volume (PBV) occur, then technetium-99m equilibrium blood pool scintigraphy, by assessing relative distribution of PBV, may allow prediction of PCWP. Therefore 30 patients being monitored with pulmonary artery balloon flotation catheters underwent imaging. PCWP was compared with the average radioactive count density arising from apical (A) and basal (B) regions of interest within the right lung, expressed as an AB ratio. Correlation was strong for patients imaged erect, either posteriorly (r = 0.864, p = 0.001) or in the 45 ° left anterior oblique position (r = 0.842, p = 0.001), and only slightly less impressive for patients imaged supine (r = 0.678, p = 0.001). Especially when imaging was performed with patients erect, an AB ratio greater than unity identified with high sensitivity (100%) and specificity (83 to 88%) an abnormally elevated PCWP (> 12 mm Hg). Moreover, directional changes in the AB ratio reflected concomitant changes in PCWP after intervention. Thus, analysis of lung AB radioactive count ratios obtained by equilibrium blood pool scintigraphy may be used to evaluate PCWP.

Radionuclide-determined changes in pulmonary blood volume and thallium lung uptake in patients with coronary artery disease

Exercise-induced increases in radionuclide-determined pulmonary blood volume (PBV) and thallium lung uptake have been described in patients with coronary artery disease (CAD) and have been shown to correlate with transient exercise-induced left ventricular dysfunction. To compare these 2 techniques in the same patients, 74 patients (59 with and 15 without significant CAD) underwent supine bicycle exercise twice on the same day--first for thallium myocardial and lung imaging and then for technetium-99m gated blood pool imaging for the PBV ratio determination. Thallium activity of lung and myocardium was determined to calculate thallium lung/heart ratio. Relative changes in PBV from rest to exercise were expressed as a ratio of pulmonary counts (exercise/rest). Previously reported normal ranges for thallium lung/heart ratio and PBV ratio were used. The PBV ratio and thallium lung/heart ratio were abnormal in 71 and 36%, respectively, of patients with CAD (p less than 0.01). Both ratios were normal in all patients without CAD. Although the resting ejection fractions did not differ significantly in patients with normal versus those with abnormal PBV ratios or thallium lung/heart ratios, abnormal PBV ratios and thallium lung/heart ratios were associated with an exercise-induced decrease in ejection fraction. Propranolol use was significantly higher in patients with abnormal than in those with normal thallium lung/heart ratios (p less than 0.01). No significant difference in propranolol use was present in patients with abnormal or normal PBV ratios. (1) the prevalence of an abnormal thallium lung/heart ratio is less than that of the PBV ratio in patients with CAD; (2) both tests are normal in normal control subjects; (3) propranolol does not cause abnormal results in normal control subjects; however, propranolol may influence lung thallium uptake in patients with CAD; and (4) when both tests are abnormal, there is a high likelihood of multivessel disease.

Phenylephrine stress in the evaluation of patients with congestive cardiomyopathies.

To analyze the effects of acute elevations in arterial blood pressure on pulmonary blood volume (PBV) and left ventricular function, 21 outpatients with congestive cardiomyopathies and stable condition and eight normal control subjects were studied using equilibrium radionuclide angiography during the infusion of phenylephrine. The myopathy patients were subdivided into seven patients who developed rales during phenylephrine infusion and 14 who did not. All of the myopathy subjects had reduced ejection fractions and enlarged end-diastolic volumes at rest. With phenylephrine, the patients who developed rales (Group 1) and those who did not (Group 2) had similar changes in left ventricular parameters (ie, ejection fraction declined and end-diastolic volume increased). With phenylephrine, however, the patients with rales had marked increases in radionuclide estimates of PBV (48.2 +/- 1.2 to 71.2 +/- 4.1 units, P less than .01, a mean increase of 48%), while in the subjects without rales, PBV increased from 48 +/- 11 to 54.6 +/- 2.2 (P less than .05, a mean increase of only 14%). Normal individuals (Group 3) had a qualitatively similar response to phenylephrine as did the myopathy patients (a decline in ejection fraction and an increase in end-diastolic volume), with no significant change in PBV. Noninvasive phenylephrine radionuclide imaging may help characterize patients with varying forms of congestive cardiomyopathies, direct appropriate therapy, and help explain the pathophysiology of clinical findings.

Radionuclide analysis of pulmonary blood volume: The response to spontaneous angina pectoris and sublingual nitroglycerin in patients with coronary artery disease

By manually assigning pulmonary regions of interest and deriving pulmonary time-activity (volume) curves, we were able to make count estimates of pulmonary blood volume (PBV) from gated cardiac blood pool scans. Five patients with coronary heart disease developed angina spontaneously while under a gamma camera. This produced an increase in cardiac volumes ( p < 0.05), a reduction in left ventricular ejection fraction ( p < 0.01), along with a marked increase in PBV (0.010 ± 0.002 to 0.015 ± 0.003 untils, p < 0.05). Nitroglycerin was then administered and reduced PBV in association with a return to normal in cardiac systolic function and size. In patients with stable chronic ischemic heart disease, sublingual nitroglycerin also reduced PBV ( p < 0.05), although not as much as when administered during an anginal episode. We conclude that gated imaging of the chest can be utilized to follow changes in PBV serially. These changes can be utilized to evaluate clinically important changes in hemodynamic status and the response to pharmacologic interventions.

Canine thoracic electrical impedance with changes in pulmonary gas and blood volumes.

The purpose of this study was to evaluate transthoracic impedance (Z) as an index of total lung liquid content at constant lung gas volume (LGV). To this end we produced rapid changes in pulmonary blood volume (PBV) in anesthetized, paralyzed, closed-chest dogs with the airway occluded at functional residual capacity. Changes in PBV produced by inflation of balloons on catheters positioned in the left atrium (LA) or inferior vena cava (IVC) were estimated from the changes in chest wall recoil pressure, using the chest wall as a plethysmograph after calibration with changes in LGV. Whereas Z increased linearly with decreases in PBV (1-6 ml/kg) produced by the IVC balloon (% delta Z/delta PBV = -0.43 ml/kg, r = -0.81), Z did not change significantly with increases in PBV (1-6 ml/kg) produced by the LA balloon. These observations indicate that changes in PBV are not the primary determinant of changes in Z and raise the possibility that other hemodynamic events are more important. Whereas aortic pressure decreased with both IVC and LA balloon inflations, right atrial pressure (Pra) increased with mitral valve obstruction and decreased with IVC obstruction. Changes in chest wall blood volume in response to changes in Pra could explain the changes in thoracic impedance. Thus, even at constant LGV, events in the systemic circulation appear to invalidate Z as an indicator of lung liquid content.