Pulmonary Blood Volume In Patients Research Articles

Differential diagnosis of acute pulmonary embolism using contrast echocardiography.

Acute pulmonary embolism (aPE) leads to a significant decrease in antegrade pulmonary blood volume (PBV), which can be measured by contrast echocardiography at the bedside. The aim of this work was to evaluate the feasibility and performance of PBV differentiating between patients with and without aPE. A total of 89 patients underwent computed tomography pulmonary angiography (CTPA) for suspected aPE were enrolled in the study. Their clinical and conventional echocardiographic characteristics were collected. Contrast echocardiography with measurements of PBV were performed. There were 57 patients with aPE, with a mean Mastora pulmonary artery obstruction index (PAOI) of 56.14%. Pulmonary transit time (PTT), normalized PTT (nPTT) and PBV in patients with aPE was less than one half of those in patients without PE (p<0.05). There was significant negative correlation between PBV and Mastora PAOI (r=-0.897, p<0.01). None of the conventional echocardiographic parameters had an area under the receiver operating characteristic curve of >0.5, while it was 0.997(0.984~1.010) for PBV in differentiating between patients with aPE or not. The optimal cutoff valueof PBV was 370ml, with a sensitivity of 100%, a specificity of 95.45% and an accuracy of 96.55%. PBV had a powerful performance in differentiating between patients with aPE or not, and a PBV of <370ml indicated aPE. Contrast echocardiography is enormously useful in the recognition and differentiation of PE and can assess the severity of the PE and the patient's response to therapy.

Measurement of Pulmonary Circulation Parameters Using Time-Resolved MR Angiography in Patients After Ross Procedure

The purposes of our study were to retrospectively evaluate the pulmonary circulation parameters of pulmonary transit time and pulmonary blood volume in patients after Ross procedures using time-resolved MR angiography and to investigate associations with right ventricular dysfunction in the same group of patients. Sixteen patients who had undergone a Ross procedure (12 men, four women; mean age, 42.13 +/- 14.24 years; age range, 21-68 years) and 16 age- and sex-matched control patients (12 men, 4 women; mean age, 42.25 +/- 14.62 years; age range, 21-68 years) were evaluated using cardiac MRI and Argus postprocessing software. Right and left ventricular volumetric parameters, including ejection fraction, end-systolic volume, and end-diastolic volume, were measured from cine true fast imaging with steady-state precession images. Pulmonary circulation parameters, including pulmonary transit time, were measured using dynamic time-resolved MR angiography and pulmonary blood volume was calculated. Pulmonary circulation parameters were correlated with volumetric parameters. The results were statistically analyzed using the Mann-Whitney U test, paired-samples Student's t test, Pearson's correlation, and linear regression. Pulmonary circulation parameters were significantly prolonged in patients after the Ross procedure compared with control patients (p < 0.01). Strong correlations exist between pulmonary circulation parameters and right ventricular function, especially pulmonary transit time and right ventricular ejection fraction (R > 0.60, p < 0.001). Patients after undergoing the Ross procedure had prolonged pulmonary transit times compared with normal control patients; this and other pulmonary circulation parameters best correlate with worsened right ventricular ejection fraction and may be predictors of right ventricular dysfunction in this group of patients.

Extravascular lung water and pulmonary blood volume in patients undergoing mitral valve replacement

Extravascular lung water and pulmonary blood volume in patients undergoing mitral valve replacement

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.

Regional pulmonary blood volume in patients with abnormal blood pressure or flow in the pulmonary circulation.

We studied the effects of a chronic increase in flow and of chronic hypertension on regional pulmonary blood volume and extravascular lung density (lung tissue and interstitial water per unit thoracic volume) in one group of patients with intracardiac, left-to-right shunt and in another group with Eisenmenger's syndrome or primary pulmonary hypertension. We used positron computerized tomography to measure regional lung density (transmission scans) and blood volume (labelling with 11CO). The distribution of pulmonary blood volume was more uniform in patients with a chronic increase in pulmonary blood flow than in normal subjects. There were also indications of an absolute increase in intrapulmonary blood volume. In patients with chronic pulmonary arterial hypertension, the regional distribution of blood volume was abnormally uniform, but there were no indications of substantial abnormalities in overall intrapulmonary blood volume.

Regional extravascular lung density and fractional pulmonary blood volume in patients with chronic pulmonary venous hypertension.

Using a technique based on positron transmission and emission tomography, we measured regional extravascular lung density (lung tissue and interstitial water per unit thoracic volume) and fractional pulmonary blood volume (volume of blood per unit thoracic volume) in normal subjects and in patients with cardiomyopathy and chronic pulmonary venous hypertension. We found an increase in extravascular lung density in the patients. Extravascular density was increased in all parts of the lung studied, but higher values were seen in the dorsocaudal portion than in the ventrocaudal portion of the lung (average 151% and 130% of normal, respectively). Fractional blood volume was markedly reduced in the dorsocaudal part of the lung (mean 74% of normal). The increase in extravascular density probably reflects structural changes in the lung as well as accumulation of interstitial fluid. The distribution of extravascular density is consistent with previous radiological and morphological studies, and may reflect a higher tendency to oedema formation in the dependent parts of the lung. The measurements of fractional blood volume suggest that intrapulmonary blood volume is reduced in chronic pulmonary venous hypertension. This may reflect a decrease in the distensibility of the pulmonary vessels due to structural abnormalities, as well as functional changes in the pulmonary vasculature.

Radionuclide-Determined Change in Pulmonary Blood Volume with Exercise

To assess the clinical usefulness of radionuclide-determined changes in pulmonary blood volume in patients with or without substantial coronary-artery disease, we determined the ratio of pulmonary blood volume at rest as compared with that during exercise. We used multigated blood-pool images obtained at rest and during supine exercise to determine the blood-volume ratio in patients subsequently undergoing coronary arteriography for evaluation of chest pain. Exercise tests were performed by use of a submaximal-workload protocol, although all tests were limited according to each patient's symptoms. The mean exercise/rest pulmonary-blood-volume ratios were lower for persons without coronary-artery disease (0.94 +/- 0.06 [S.D.], 10 patients) and for those with disease confined to the right coronary artery (0.99 +/- 0.12, five patients), as compared with all others with coronary-artery disease (1.14 +/- 0.15, 37 patients) (P less than 0.01). A pulmonary-blood-volume ratio equal to or greater than 1.06 had a sensitivity of 79 per cent. Patients with coronary-artery disease not confined to the right coronary artery usually show an increase in pulmonary blood volume during supine exercise. No such change occurs in persons without coronary-artery disease.

Effects of acute digitalization on the pulmonary blood volume in patients with heart disease.

Basic hemodynamic data and the pulmonary blood volume (PBV) were determined in 23 patients before and after intravenous administration of acetyl strophanthidin during right and left heart catheterization. These patients were divided into two groups depending upon whether or not digitalization produced a significant fall in left ventricular end-diastolic pressure (LV D ). Group I consisted of 11 patients who manifested a significant decrease in LV D , while in group II no change was noted after digitalization. In both groups, a significant rise in LV stroke volume, stroke work, and maximal rate of rise of LV systolic pressure (dp/dt) was recorded. In group I, a significant decrease in the pulmonary vascular distending pressure (P d ) was accompanied by a decrease in PBV. In contrast, no change in P d or PBV was noted in the patients in group II. Changes in pulmonary vascular resistance (PVR) were inconsistent. It is concluded that: (1) in patients of group I the concordant decrease in P d and PBV represented a passive effect on the pulmonary vascular bed mediated by improved LV performance and decrease in LV D ; (2) in patients of group II, despite evidence of significant positive inotropic effects on the left ventricle, the failure of LV D to fall prevented a decrease in P d and PBV; (3) no evidence of active vasomotor effects of acetyl strophanthidin in the lung could be demonstrated. Changes in PVR were capricious and not apparently useful in assessment of the presence or absence of pulmonary vasomotor effects induced by digitalis. The results of this study differ from the findings of other investigators in cardiac patients and experimental animals. Some of the differences may be attributed to different experimental methods and to species variation in vascular reactivity. Also, the findings in this report contrast with those previously reported for isoproterenol and aminophylline, agents that produce both positive inotropic effects on the heart and active vasomotion in the pulmonary circulation.

Effects of isoproterenol on the pulmonary blood volume in patients with valvular heart disease and primary myocardial disease.

The effects of intravenous isoproterenol upon the pressure-flow-volume relationships in the pulmonary vascular bed were studied in 34 patients and one normal subject during simultaneous right and transseptal left heart catheterization. In five patients with primary myocardial disease and in one normal subject, active pulmonary vasodilation was demonstrated by a significant increase in pulmonary blood volume (PBV) and a concomitant fall in pulmonary vascular distending pressure (P D ). Infusion of the drug into 18 patients with mitral stenosis resulted in a concordant rise in PBV and PD, strongly suggesting passive distention of the pulmonary vascular bed. In contrast to the responses of these two groups of patients, isoproterenol infusion into 11 patients with aortic valve disease failed to change the PBV, but caused a significant decrease in P D . It is concluded that the response of different groups of patients to isoproterenol cannot be explained by a single mechanism. Multiple actions of the drug must be considered, including active pulmonary vasodilation, a positive inotropic action upon the heart, and bronchomotor effects.

Pulmonary edema in dogs, especially the sequence of fluid accumulation in lungs.

Pulmonary edema in dogs, especially the sequence of fluid accumulation in lungs.

Effect of exercise on the pulmonary blood volume in patients with acquired heart disease.

The effect of supine exercise on the pulmonary blood volume was studied in 14 patients with valvular heart disease and in one patient with cardiomyopathy. Statistically significant increases occurred in the pulmonary blood volume (88.6 ± S.E. 20.9 ml./M. 2 ) and in the central blood volume (121.9 ± S.E. 29.2 ml./M. 2 ), whereas left atrial to brachial arterial volume remained unchanged. These results support the concept that, with exercise, increases in central blood volume reflect increases in pulmonary blood volume in patients with acquired heart disease. The increase in pulmonary blood volume and in pulmonary distending pressure suggests a passive expansion of the pulmonary vascular bed with exercise.

Effects of inhalation of 100 per cent oxygen on the pulmonary blood volume in patients with organic heart disease.

The effect of breathing 100 per cent oxygen on the pulmonary blood volume, pulmonary arterial pressure, left atrial pressure, and pulmonary vascular distending pressure was studied during cardiac catheterization in eight patients with organic heart disease. In half of the patients, a significant decrease in pulmonary blood volume was observed. This decline in pulmonary blood volume in the face of a decrease or no change in the pulmonary distending pressure is interpreted as evidence for a passive mechanism of action for 100 per cent oxygen. The effects of hyperoxia are compared to those of acetylcholine, which works by actively dilating the pulmonary vascular bed.