Intrapulmonary Blood Flow Research Articles

Intrapulmonary distribution of blood flow during exercise in pulmonary hypertension assessed by a new combination technique.

Hyperventilation and inadequate cardiac output (CO) increase are the main causes of exercise limitation in pulmonary hypertension (PH). Intrapulmonary blood flow partitioning between ventilated and unventilated lung zones is unknown. Thoracic impedance cardiography and inert gas rebreathing have been both validated in PH patients for non-invasive measurement of CO and pulmonary blood flow (PBF), respectively. This study sought to evaluate CO behaviour in PH patients during exercise and its partitioning between ventilated and unventilated lung areas, in parallel with ventilation partitioning between ventilated and unventilated lung zones. Eighteen PH patients (group 1 or 4) underwent a cardiopulmonary exercise test (CPET) with a three-step loaded workload protocol. The steps occurred at 0%, 20%, 40%, and 60% of peak workload reached during a preliminary maximum CPET. Ventilatory parameters, arterial blood gases, CO, PBF, and intrapulmonary shunt (calculated as the difference between CO and PBF) were obtained at each step, combining thoracic impedance cardiography and an inert gas rebreathing technique. Dead space ventilation observed throughout the exercise was about 40% of total ventilation. A progressive increase of CO from 4.86 ± 1.24 L/min (rest) to 9.41 ± 2.63 L/min (last step), PBF from 3.81 ± 1.41 L/min to 7.21 ± 2.93 L/min, and intrapulmonary shunt from 1.05 ± 0.96 L/min to 2.21 ± 2.28 L/min was observed. Intrapulmonary shunt was approximately 20% of CO at each exercise step. Although the study population was small, the combined non-invasive CO measurement seems a promising tool for deepening our knowledge of lung exercise haemodynamics in PH patients. This technique could be applied in future studies to evaluate PH treatment influences on CO partitioning, since a secondary increase of intrapulmonary shunt is undesirable.

CT-based Analysis of Vascular Tree Abnormalities in Different Phenotypes of COVID-19 Pneumonia

In this paper, Computed Tomography (CT) images of six confirmed COVID-19 patients were analyzed in order to investigate the physiological abnormalities in the vascular tree in response to the disease-induced hypoxia. The CT images were classified into an L-type and H-type groups based on the cumulative voxel distribution of the CT scan. A 3-Dimentional model of the vascular tree was reconstructed out of each CT image following a computational framework. Then, the Cross-Sectional Area (CSA) of the vessels belonging to each vascular tree was computed. The acquired results were compared against averaged measurements of three healthy subjects that were computed following the same approach. The results showed that as the severity of COVID-19 lean towards H-type phenotype, signs of vasoconstriction in small blood vessels with a CSA less than 10 mm2 tend to decreases, whereas signs of vasodilation in medium to large blood vessels increases. The intensity of dilated blood vessels proximal to consolidated areas of the lung was found to increase significantly as the disease progresses in the lungs. Furthermore, signs of vasoconstriction and vasodilation in the vascular tree were observed in all lobes of the lung in both phenotypes including seemingly healthy lobes. The results in this paper are suggestive of intrapulmonary blood flow shunting towards unaerated areas of the lungs which may lead to a ventilation/perfusion mismatch even at minor cases of COVID-19. The results also suggest that subject-specific regulated use of vasodilating medication may reduce the number of cases that require mechanical ventilation.

Discussion

Discussion

Detection of circulatory disturbance after pulmonary vein division during a living donor lobectomy.

Indocyanine green (ICG) is widely used during thoracic surgery to enhance visualization, allowing assessment of the intersegmental plane based on intrapulmonary blood flow (Travis et al. in Ann Thorac Surg 108(2):363-369, 2019; Seshiru et al. in Gen Thorac Cardiovasc Surg 66(2):81-90, 2018). Using ICG to detect blood flow disruption after lung resection, however, has not been addressed. We therefore report a case in which the left lingular pulmonary vein was incidentally divided during left lower lobectomy in a living-lung donor. Intraoperative ICG-enhanced near-infrared fluoroscopic imaging to assess intrapulmonary blood flow detected the problem. We thus avoided potential postoperative residual lung complications in this patient.

Longitudinal changes in lung size and intrapulmonary-artery Doppler during the second half of pregnancy in fetuses with congenital diaphragmatic hernia.

The objectives of the study are to evaluate longitudinal changes in lung size and intrapulmonary-artery (IPa) Doppler in fetuses with congenital diaphragmatic hernia (CDH) and assess their contribution in predicting neonatal survival. The observed/expected lung-to-head ratio (O/E-LHR) and IPa-pulsatility index (PI) and peak early diastolic reversed flow (PEDRF) were evaluated in a cohort of left-sided CDH fetuses managed expectantly during pregnancy. Longitudinal changes were analyzed by multilevel analysis, and their value to predict survival using the multiple logistic regression and decision-tree analysis was assessed. A total of 232 scans were performed on 69 CDH fetuses. The O/E-LHR values remained unchanged during fetal monitoring, whereas IPa-PI and PEDRF showed a progressive increase throughout follow-up, becoming abnormal on average at 30weeks of gestation. Absent/reversed end-diastolic velocity (EDV) in the IPa was observed in 20.3%. O/E-LHR and IPa Doppler indices were significantly associated with probability of survival (O/E-LHR≥26%, odds ratio [OR] 19.0; IPa-PI <+2.0 z score, OR 3.0; and positive EDV, OR 7.4). All cases with IPa-reversed EDV died after birth. While lung size remains stable during pregnancy, CDH fetuses show progressive deterioration in intrapulmonary blood flow. IPa Doppler evaluation may aid in predicting survival of CDH fetuses managed expectantly during pregnancy.

High adventure shunts old notions of pulmonary vascular control during hypoxic exercise: contrasting views that might just burst your bubble!

High adventure shunts old notions of pulmonary vascular control during hypoxic exercise: contrasting views that might just burst your bubble!

Quantification in Echocardiography

Until recently, more than 2200 Swan Ganz catheters were used annually in the operating rooms (OR) and intensive care unit (ICU) of the Catharina Hospital in Eindhoven, The Netherlands. After cardiologists who were specialists in echocardiography (ECHO) trained anesthesiologists in ECHO, the need for these catheters in cardiac and noncardiac surgery was reduced. Initially intended as a local teaching project, an ECHO teaching compact disk (CD) was produced during the training and distributed later worldwide, thanks to a positive review in a major anesthesiology publication. By reducing the number of Swan Ganz catheters, the hospital could finance and acquire two echocardiography machines for the OR and ICU. The availability of these machines resulted in a further reduction of the number of Swan Ganz catheters. However, the need for quantification (eg, measurements of cardiac output) remained. During the creation of the ECHO teaching CD, the idea was born to apply indicator-dilution principles on injected echo contrast. This study was performed in cooperation with the Signal Processing Department of the Eindhoven University of Technology. Advanced signal processing and modelling were used to develop algorithms to enable quantification of intrapulmonary blood volume, ejection-fraction, and flow from the transesophageal echocardiography approach. These quantitative measurements, which can be performed on an outpatient basis, may become a real asset in cardiology, anesthesiology, and intensive care.

Importance of hypoxic vasoconstriction in maintaining oxygenation during acute lung injury.

To investigate the role of hypoxic pulmonary vasoconstriction in the intrapulmonary blood flow redistribution and gas exchange protection during oleic acid acute lung injury. Prospective, controlled animal study. Research laboratory of an academic institution. Three groups of five mongrel dogs. Induction of acute lung injury by 0.08 mL/kg oleic acid intravenously. Hypoxic pulmonary vasoconstriction inhibition by Escherichia coli endotoxin microdose (15 microg/kg) pretreatment or by metabolic alkalosis (pH 7.60). Pulmonary arterial and venous resistances were determined by flow-pressure curves and by capillary pressure estimation. Regional lung water and pulmonary blood flow were assessed by positron emission tomography. Oleic acid alone increased the arterial and venous resistances, redistributed blood flow away from edematous areas, and decreased the Pao2 from 507 +/- 16 to 373 +/- 60 torr. on Fio2 1.0 and positive end-expiratory pressure 5 cm H2O. Endotoxin pretreatment inhibited the increase in arterial resistance, suppressed the redistribution, and decreased the Pao2 to 105 +/- 22 torr. Alkalosis inhibited the increase in arterial and venous resistances, suppressed the redistribution, and decreased the Pao2 to 63 +/- 12 torr. Reversal of the alkalosis increased the arterial and venous resistances, restored the perfusion redistribution, and improved the Pao2 to 372 +/- 63 torr. Changes in blood gases conformed to predictions of a computer lung model in which hypoxic pulmonary vasoconstriction was suppressed by endotoxin and alkalosis. We conclude that in oleic acid-induced lung injury, a) pulmonary hypertension results from increases in both arterial and venous resistances; b) the increase in arterial resistance is the primary mechanism responsible for the perfusion redistribution and the gas exchange protection; and c) the increase in arterial resistance is most consistent with hypoxic pulmonary vasoconstriction.

Effect of endotoxin on oleic acid lung injury does not depend on priming.

Recent studies have demonstrated significant synergistic physiological and biochemical effects between low-dose endotoxin (Etx) administration and oleic acid (OA)-induced canine lung injury. To evaluate whether this interaction depends on Etx priming of some key cell population, we compared the effects of giving low-dose Etx both after as well as before inducing lung injury with OA. In addition to hemodynamic and blood-gas measurements, positron emission tomographic imaging was used to measure edema accumulation and intrapulmonary blood flow distribution. Biochemical measurements of the stable metabolites of prostacyclin and thromboxane were obtained as well as measurements of isoprostanes and reactive sulfhydryls as evidence for possible concomitant oxidant production. We found that the physiological and biochemical effects of low-dose Etx developed 30-45 min after its administration, regardless of whether Etx was administered before or after OA. No increase in either isoprostane or reactive sulfhydryl production after Etx and/or OA was detected. These data suggest that the synergistic effect of low-dose Etx and OA-induced lung injury is not due to a priming effect of Etx.

Effects of partial liquid ventilation on regional pulmonary blood flow distribution of isolated rabbit lungs.

Partial liquid ventilation with perfluorocarbons may increase alveolar hydrostatic transmural pressure and may result in a redistribution of pulmonary blood flow from dependent to nondependent lung regions. To test this hypothesis under controlled study conditions, we determined intrapulmonary blood flow distributions during gas and perfluorocarbon ventilation in isolated rabbit lungs. Controlled animal study with an ex vivo isolated lung preparation. Research laboratory for Experimental Anesthesiology at the Heinrich-Heine-University of Düsseldorf. New Zealand White rabbits. The lungs were perfused with autologous blood at constant flow (150 mL/min) and ventilated with 5% C(O2) in air (positive end-expiratory pressure, 2 cm H2O; tidal volume, 10 mL/kg body weight; respiratory rate, 30 breaths/ min) without and with perfluorocarbon administered intratracheally (15 mL/kg). Regional lung perfusion was measured with colored microspheres in apical, central, peripheral, and basal samples before and after bronchial instillation of perfluorocarbons. Compared with gas ventilation, intrapulmonary blood flow during perfluorocarbon ventilation was higher in apical samples (49.4+/-8.6 mL/min/g vs. 38.3+/-6.8 mL/min/g dry weight; p = .03) and lower in basal samples (22.2+/-5.1 mL/min/g vs. 39.9+/-8.2 mL/min/g; p = .04). Our findings suggest that during partial liquid ventilation, intrapulmonary blood flow is redistributed toward less-dependent lung regions. (Crit Care Med 2000; 28:1522-1525)

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.

Synergistic hemodynamic effects of low-dose endotoxin and acute lung injury.

We evaluated the effects of low-dose endotoxin (15 microg/kg) on the pulmonary and systemic responses to oleic acid (OA)-induced acute lung injury in dogs. Animals given endotoxin alone (n = 5) showed a modest decrease in arterial blood pressure, but no effects on pulmonary hemodynamics, blood gases, cardiac output, or lung water accumulation. Animals (n = 6) given only OA (0.08 ml/kg) showed the expected development of mild-moderate pulmonary hypertension, a comparable reduction in arterial blood pressure, hypoxemia, increased lung water concentration, and an altered intrapulmonary perfusion pattern, as assessed by positron emission tomography. Animals (n = 7) given the same dose of endotoxin, followed 30 min later by the same dose of OA, developed a similar increase in lung water concentration as the group given OA alone, but failed to develop pulmonary hypertension or to redistribute pulmonary blood flow away from the edematous lung regions. In addition, arterial blood pressure fell significantly more than in the other groups. These responses were associated with a 30-fold increase in circulating prostacyclin (assayed as 6-keto prostaglandin F1 alpha [PGF1alpha]). The effects on systemic blood pressure, intrapulmonary blood flow redistribution, and eicosanoid production were eliminated by pretreating (n = 5) animals with meclofenamate (2 mg/kg). The results are consistent with a "priming" effect of low-dose endotoxin on the pulmonary endothelium, with exaggerated prostacyclin production in response to a subsequent lung injury. This interaction leads to altered intrapulmonary hemodynamics that exacerbate the development of hypoxemia, and to significant decreases in systemic blood pressure. To the extent that the lung is the most likely source of the increased prostacyclin production, the synergistic effects of low-dose endotoxin and lung injury may produce a kind of "lung shock."

Intrapulmonary bronchial blood flow of rats as studied by the microsphere method

The intrapulmonary bronchial blood flow of the left lung (systemic arterial blood flow to the left lung via the bronchial artery) was determined in 45 anesthetized and artificially ventilated male Wistar rats, weighing 263 +/- 5 g (mean +/- SEM). The microsphere method was employed and designed so that recirculating microspheres across the peripheral arteriovenous anastomoses were prevented from lodging in the left lung, and disturbances of the isovolemic state of the animals became minimal. Under normal conditions with a mean arterial pressure of 115 +/- 2 mmHg (n = 40), the bronchial blood flow of the left lung was found to be 0.307 +/- 0.033 ml/min on average, and amounted to 0.52 +/- 0.06% of the cardiac output. The flow (ml/min) normalized per kg body weight, 100 g wet lung, or 100 g dry lung was 1.14 +/- 0.12, 76 +/- 8, or 368 +/- 39, respectively. The total intrapulmonary bronchial blood flow of the left and right lungs could be estimated by multiplying the intrapulmonary bronchial flow of the left lung by the weight ratio (total:left) of 2.9. The variability of the flow data was small, as confirmed in a study with simultaneous injection of two differently radiolabeled microspheres. The reproducibility of duplicate measurements was excellent.

Intrapulmonary bronchial circulation during hemorrhage.

Experiments were conducted on 119 anesthetized and artificially ventilated rats to evaluate effects of a physiological stimulus (hemorrhage) to the sympothoadrenal system on the bronchial circulation. In the presence of a sufficient dose of a vasopressin V1-receptor antagonist, moderate (81 mmHg on average, 33 rats) or severe hypotension (69 mmHg, 28 rats) was produced by controlled hemorrhage (11 or 9 rats, respectively), or by treatment with phenoxybenzamine (0.1 mg/kg, i.v., 12 rats, or 1.0 mg/kg, 10 rats), or the highly selective alpha 1-adrenoceptor antagonist, bunazosin (0.01 mg/kg i.v., 10 rats, or 0.1 mg/kg, 9 rats). During hypotension, the intrapulmonary bronchial blood flow (microsphere method) was decreased in a dose-dependent manner in the two antagonist-treated groups. However, these decreases were only of a moderate degree compared to the severe decrease in the hemorrhage group. Although the bronchovascular resistance was not significantly changed after treatment with either antagonist, this variable was greatly elevated during severe hemorrhagic hypotension, reaching 240 +/- 51% (P less than 0.001 with either antagonist study) of its baseline level. Changes in the pulmonary arterial and left atrial pressures, plasma vasopressin concentration, and renin activity were found to be less influential on these responses in 58 rats. Overall, we concluded that the sympathoadrenal mechanism powerfully increased the resistance and decreased the blood flow of the intrapulmonary bronchial circulation.

Effect of nifedipine on oxygen delivery in canine asymmetric oleic acid lung injury

Increasing the ratio of tissue oxygen delivery (DO2) to oxygen consumption can improve the survival of critically ill patients, including those with acute respiratory failure. However, under conditions of ventilation/perfusion mismatch, the use of inotropic or vasodilator drugs to augment cardiac output could, in turn, worsen venous admixture. In a canine model of asymmetric oleic acid-induced pulmonary edema, we examined this possibility by studying the effect of 20 and 40-micrograms/kg doses of parenteral nifedipine on oxygenation variables, venous admixture, and intrapulmonary blood flow distribution. After oleic acid injury, nifedipine caused significant increases in cardiac index by 70% as systemic vascular resistance decreased proportionately by 61%. Stroke volume index (SI) and mean pulmonary arterial pressure increased, while venous admixture and the distribution of intrapulmonary blood flow did not change with nifedipine. However, nifedipine significantly improved the tissue DO2 index so that the coefficient of DO2 increased. Thus, nifedipine significantly increased SI in a dose-dependent manner, thereby improving the tissue oxygen supply-demand balance.

Hypoxic pulmonary vasoconstrictor response with asymmetric oleic acid injury in the dog.

The hypoxic pulmonary vasoconstrictive (HPV) response is characterized by two components: intrapulmonary blood flow redistribution and pulmonary artery pressure (PAP) augmentation. Whether both remain intact after oleic acid lung injury has not been assessed. In an asymmetric model of right lung oleic acid edema, we examined the relative magnitude of each component on the HPV response to right lung inspired hypoxia. Before oleic acid administration, right lung hypoxia decreased perfusion to the right lung from 1.41 +/- 0.12 to 1.16 +/- 0.15 L/min (p = .07), while PAP increased from 15.8 +/- 0.8 to 18.1 +/- 0.6 mm Hg (p less than .05). Regional hypoxia caused right lung pulmonary vascular resistance (PVR) to increase from 480 +/- 45 to 797 +/- 114 dyne.sec/cm5 (p less than .01). After right lung injury with oleic acid, regional hypoxia decreased perfusion to the right lung from 0.91 +/- 0.11 to 0.71 +/- 0.10 L/min (p less than .05), while PAP increased from 18.8 +/- 0.8 to 21.5 +/- 1.0 mm Hg (p less than .05). With hypoxia, right lung PVR increased from 1232 +/- 260 to 1933 +/- 336 dyne.sec/cm5 (p less than .01). We conclude that the pulmonary vasoconstrictive response to inspired hypoxia persists after oleic acid lung injury, causing significant increases in PVR. Consequently, both the blood flow redistribution and the PAP augmentation components of the HPV response to inspired hypoxia remain unchanged.

Sodium nitroprusside and positive end-expiratory pressure are not detrimental in canine asymmetric pulmonary edema.

The effects of PEEP and subsequent augmentation of cardiac output by sodium nitroprusside (SNP) were examined in a canine model of asymmetric oleic acid injury to the right lung. PEEP (9.2 +/- 0.5 cm H2O) was added to six animals to decrease venous admixture (Qsp/Qt) from 50.6 +/- 4.4% to 16.0 +/- 1.3% (p less than .05). With PEEP, intrapulmonary blood flow distribution (assessed by radioactive microspheres) decreased significantly to nondependent lung regions while increasing to dependent regions. In six other animals, zero end-expiratory pressure (ZEEP) did not alter intrapulmonary blood flow distribution. SNP was then administered to increase cardiac output by 40% (to 2.60 +/- 0.21 L/min in the ZEEP group and to 1.75 +/- 0.27 L/min in the PEEP group). SNP produced no adverse effects on Qsp/Qt or intrapulmonary blood flow distribution. Specifically, SNP did not preferentially dilate pulmonary vessels injured by oleic acid with or without end-expiratory pressure. Thus, administration of a vasodilator drug in asymmetric pulmonary edema appears well tolerated.

The pulmonary vascular effects of dopamine, dobutamine, and isoproterenol in unilobar pulmonary edema in dogs

Although catecholamine inotropic drugs are often used to support the circulation of critically ill patients with hypoxemic respiratory failure, their effect on the pulmonary circulation and on gas exchange is incompletely understood. In order to improve our understanding of the effects of these drugs on the pulmonary circulation, we made measurements of total and regional intrapulmonary shunt ( Q s Q t ), distribution of pulmonary blood flow, and pulmonary hemodynamics before and after infusions of dopamine ( n = 6, 5 μg/kg/min), dobutamine ( n = 6, 10 μg/kg/min), isoproterenol ( n = 6, 0.1 μg/kg/min), or saline in dogs with unilobar oleic acid-induced pulmonary edema. In addition to permitting determination of the overall hemodynamic and gas exchange effects of these drugs, this preparation allowed measurement of changes in distribution of pulmonary blood flow between normal and edematous lung. In 6 dogs given dobutamine, mean cardiac output (CO) increased by 1 liter/min, while pulmonary arterial pressure ( P PA) increased by 2 mm Hg with no change in pulmonary vascular resistance (PVR) or distribution of pulmonary blood flow. There was a 5% increase in mean Q s/ Q t which, because of the lack of evidence of pulmonary vasoactivity, was attributed to time or to increased CO. Isoproterenol produced a similar increase in CO, but reduced P PA and PVR indicating pulmonary vasodilator activity. Pulmonary vasodilation was most prominent in edematous lung, resulting in an increase in relative blood flow to the edema lung lobe and a substantial increase in Q s/ Q t, exceeding the increase in all other groups. Dopamine, similarly increasing CO, did not change overall PVR but reduced fractional blood flow to the edema lobe by 3.4% of CO. Neither Q s/ Q t nor P aO 2 changed significantly in this group. The differing effects of these agents on pulmonary hemodynamics, intrapulmonary blood flow distribution, and gas exchange have potentially significant implications affecting the choice of drug used for circulatory support in hypoxemic respiratory failure.

Echocardiographic tissue characterization and range-gated Doppler ultrasound for the diagnosis of pulmonary embolism.

We evaluated reflection and absorption indexes of ultrasound as well as Doppler estimates of intrapulmonary blood flow for diagnosing pulmonary embolism. The pulmonary reflection coefficient (PRC), coefficient of tissue attenuation (alpha R) and range-gated blood Doppler signals were studied in 25 patients with pulmonary embolism, 19 with pneumonia, nine with atelectasis, 20 with congestive heart failure, 20 with chronic obstructive lung disease and 10 normal subjects. The PRC was significantly diminished in pulmonary embolism, pneumonia and atelectasis, but was not altered by underlying chronic obstructive lung disease or congestive heart failure. The alpha R in pulmonary embolism was 1.03 +/- 0.04 db/MHz cm, significantly lower than that for pneumonia, 1.48 +/- 0.03 db/MHz cm (p less than 0.001), but not significantly different from that for atelectasis, 0.95 +/- 0.05 db/MHz cm. Doppler signals indicating blood flow in the affected area of lung were present in only two of 25 patients with pulmonary embolism, compared with seven of nine with atelectasis and 17 of 19 with pneumonia. The combined use of PRC, alpha R and blood Doppler signals correctly diagnosed pulmonary embolism in 23 of 25 patients. Thus, ultrasound offers a reliable noninvasive method for diagnosis of pulmonary embolism.

Intrapulmonary blood flow redistribution during hypoxia increases gas exchange surface area.

We have previously shown that airway hypoxia causes pulmonary capillary recruitment and raises diffusing capacity for carbon monoxide. This study was designed to determine whether these events were caused by an increase in pulmonary vascular resistance, which redistributed blood flow toward the top of the lung, or by an increase in cardiac output. We measured capillary recruitment at the top of the dog lung by in vivo microscopy, gas exchange surface area of the whole lung by diffusing capacity for carbon monoxide, and blood flow distribution by radioactive microspheres. During airway hypoxia recruitment occurred, diffusing capacity increased, and blood flow was redistributed upward. When a vasodilator was infused while holding hypoxia constant, these effects were reversed; i. e., capillary "derecruitment" occurred, diffusing capacity decreased, and blood flow was redistributed back toward the bottom of the lung. The vasodilator was infused at a rate that left hypoxic cardiac output unchanged. These data show that widespread capillary recruitment during hypoxia is caused by increased vascular resistance and the resulting upward blood flow redistribution.