Distribution Of Pulmonary Perfusion Research Articles

Effects of positive end-expiratory pressure on pulmonary perfusion distribution and intrapulmonary shunt during one-lung ventilation in pigs A randomized crossover study.

During one-lung ventilation (OLV), positive end-expiratory pressure (PEEP) can improve lung aeration, but might over-distend lung units and increase intrapulmonary shunt. We hypothesized that higher PEEP shifts pulmonary perfusion from the ventilated to the non-ventilated lung, resulting in a U-shaped relationship with intrapulmonary shunt during OLV. In nine anesthetized female pigs, a thoracotomy was performed and intravenous lipopolysaccharide infused to mimic the inflammatory response of thoracic surgery. Animals underwent OLV in supine position with PEEP of 0 cmH2O, 5 cmH2O, titrated to best respiratory system compliance, and 15 cmH2O (PEEP0, PEEP5, PEEPtitr, and PEEP15, respectively, 45 min each, Latin square sequence). Respiratory, hemodynamic, and gas exchange variables were measured. The distributions of perfusion and ventilation were determined by i.v. fluorescent microspheres and computed tomography, respectively. Compared to two lung ventilation, the driving pressure increased with OLV, irrespective of the PEEP level. During OLV, cardiac output was lower at PEEP15 (5.5 ± 1.5 l/min) than PEEP0 (7.6 ± 3 l/min) and PEEP5 (7.4 ± 2.9 l/min; P=0.004), while the intrapulmonary shunt was highest at PEEP0 (PEEP0: 48.1 ± 14.4 %; PEEP5: 42.4 ± 14.8 %; PEEPtitr: 37.8 ± 11.0 %; PEEP15: 39.0 ± 10.7 %; P=0.027). The relative perfusion of the ventilated lung did not differ among PEEP levels (PEEP0: 65.0 ± 10.6 %; PEEP5:68.7 ± 8.7 %; PEEPtitr: 68.2 ± 10.5 %; PEEP15: 58.4 ± 12.8%; P=0.096), but the centers of relative perfusion and ventilation in the ventilated lung shifted from ventral to dorsal, and from cranial to caudal zones with increasing PEEP. In this experimental model of thoracic surgery, higher PEEP during OLV did not shift the perfusion from the ventilated to the non-ventilated lung, thus not increasing intrapulmonary shunt. This study was registered and approved by the Landesdirektion Dresden, Germany (25-5131/496/33).

Modulation of pulmonary blood flow in patients with acute respiratory failure

BackgroundImpairment of ventilation and perfusion (V/Q) matching is a common mechanism leading to hypoxemia in patients with acute respiratory failure requiring intensive care unit (ICU) admission. While ventilation has been thoroughly investigated, little progress has been made to monitor pulmonary perfusion at the bedside and treat impaired blood distribution. The study aimed to assess real-time changes in regional pulmonary perfusion in response to a therapeutic intervention. MethodsSingle-center prospective study that enrolled adult patients with ARDS caused by SARS-Cov-2 who were sedated, paralyzed, and mechanically ventilated. The distribution of pulmonary perfusion was assessed through electrical impedance tomography (EIT) after the injection of a 10-ml bolus of hypertonic saline. The therapeutic intervention consisted in the administration of inhaled nitric oxide (iNO), as rescue therapy for refractory hypoxemia. Each patient underwent two 15-min steps at 0 and 20 ppm iNO, respectively. At each step, respiratory, gas exchange, and hemodynamic parameters were recorded, and V/Q distribution was measured, with unchanged ventilatory settings. ResultsTen 65 [56–75] years old patients with moderate (40%) and severe (60%) ARDS were studied 10 [4-20] days after intubation. Gas exchange improved at 20 ppm iNO (PaO2/FiO2 from 86 ± 16 to 110 ± 30 mmHg, p = 0.001; venous admixture from 51 ± 8 to 45 ± 7%, p = 0.0045; dead space from 29 ± 8 to 25 ± 6%, p = 0.008). The respiratory system's elastic properties and ventilation distribution were unaltered by iNO. Hemodynamics did not change after gas initiation (cardiac output 7.6 ± 1.9 vs. 7.7 ± 1.9 L/min, p = 0.66). The EIT pixel perfusion maps showed a variety of patterns of changes in pulmonary blood flow, whose increase positively correlated with PaO2/FiO2 increase (R2 = 0.50, p = 0.049). ConclusionsThe assessment of lung perfusion is feasible at the bedside and blood distribution can be modulated with effects that are visualized in vivo. These findings might lay the foundations for testing new therapies aimed at optimizing the regional perfusion in the lungs.

Effects of pulsed inhaled nitric oxide delivery on the distribution of pulmonary perfusion in spontaneously breathing and mechanically ventilated anesthetized ponies.

To measure changes in pulmonary perfusion during pulsed inhaled nitric oxide (PiNO) delivery in anesthetized, spontaneously breathing and mechanically ventilated ponies positioned in dorsal recumbency. 6 adult ponies. Ponies were anesthetized, positioned in dorsal recumbency in a CT gantry, and allowed to breathe spontaneously. Pulmonary artery, right atrial, and facial artery catheters were placed. Analysis time points were baseline, after 30 minutes of PiNO, and 30 minutes after discontinuation of PiNO. At each time point, iodinated contrast medium was injected, and CT angiography was used to measure pulmonary perfusion. Thermodilution was used to measure cardiac output, and arterial and mixed venous blood samples were collected simultaneously and analyzed. Analyses were repeated while ponies were mechanically ventilated. During PiNO delivery, perfusion to aerated lung regions increased, perfusion to atelectatic lung regions decreased, arterial partial pressure of oxygen increased, and venous admixture and the alveolar-arterial difference in partial pressure of oxygen decreased. Changes in regional perfusion during PiNO delivery were more pronounced when ponies were spontaneously breathing than when they were mechanically ventilated. In anesthetized, dorsally recumbent ponies, PiNO delivery resulted in redistribution of pulmonary perfusion from dependent, atelectatic lung regions to nondependent aerated lung regions, leading to improvements in oxygenation. PiNO may offer a treatment option for impaired oxygenation induced by recumbency.

Effects of Body Position and Hypovolemia on the Regional Distribution of Pulmonary Perfusion During One-Lung Ventilation in Endotoxemic Pigs

Background: The incidence of hypoxemia during one-lung ventilation (OLV) is as high as 10%. It is also partially determined by the distribution of perfusion. During thoracic surgery, different body positions are used, such as the supine, semilateral, lateral, and prone positions, with such positions potentially influencing the distribution of perfusion. Furthermore, hypovolemia can impair hypoxic vasoconstriction. However, the effects of body position and hypovolemia on the distribution of perfusion remain poorly defined. We hypothesized that, during OLV, the relative perfusion of the ventilated lung is higher in the lateral decubitus position and that hypovolemia impairs the redistribution of pulmonary blood flow.Methods: Sixteen juvenile pigs were anesthetized, mechanically ventilated, submitted to a right-sided thoracotomy, and randomly assigned to one of two groups: (1) intravascular normovolemia or (2) intravascular hypovolemia, as achieved by drawing ~25% of the estimated blood volume (n = 8/group). Furthermore, to mimic thoracic surgery inflammatory conditions, Escherichia coli lipopolysaccharide was continuously infused at 0.5 μg kg−1 h−1. Under left-sided OLV conditions, the animals were further randomized to one of the four sequences of supine, left semilateral, left lateral, and prone positioning. Measurements of pulmonary perfusion distribution with fluorescence-marked microspheres, ventilation distribution by electrical impedance tomography, and gas exchange were then performed during two-lung ventilation in a supine position and after 30 min in each position and intravascular volume status during OLV.Results: During one-lung ventilation, the relative perfusion of the ventilated lung was higher in the lateral than the supine position. The relative perfusion of the non-ventilated lung was lower in the lateral than the supine and prone positions and in semilateral compared with the prone position. During OLV, the highest arterial partial pressure of oxygen/inspiratory fraction of oxygen (PaO2/FIO2) was achieved in the lateral position as compared with all the other positions. The distribution of perfusion, ventilation, and oxygenation did not differ significantly between normovolemia and hypovolemia.Conclusions: During one-lung ventilation in endotoxemic pigs, the relative perfusion of the ventilated lung and oxygenation were higher in the lateral than in the supine position and not impaired by hypovolemia.

Abnormal pulmonary perfusion heterogeneity in patients with Fontan circulation and pulmonary arterial hypertension.

The distribution of pulmonary perfusion is affected by gravity, vascular branching structure and active regulatory mechanisms, which may be disrupted by cardiopulmonary disease, but this is not well studied, particularly in rare conditions. We evaluated pulmonary perfusion in patients who had undergone Fontan procedure, patients with pulmonary arterial hypertension (PAH) and two groups of controls using a proton magnetic resonance imaging technique, arterial spin labelling to measure perfusion. Heterogeneity was assessed by the relative dispersion (SD/mean) and gravitational gradients. Gravitational gradients were similar between all groups, but heterogeneity was significantly increased in both patient groups compared to controls and persisted after removing contributions from large blood vessels and gravitational gradients. Patients with Fontan physiology and patients with PAH have increased pulmonary perfusion heterogeneity that is not explainable by differences in mean perfusion, gravitational gradients, or large vessel anatomy. This probably reflects vascular remodelling in PAH and possibly in Fontan physiology. Many factors affect the distribution of pulmonary perfusion, which may be disrupted by cardiopulmonary disease, but this is not well studied, particularly in rare conditions. An example is following the Fontan procedure, where pulmonary perfusion is passive, and heterogeneity may be increased because of the underlying pathophysiology leading to Fontan palliation, remodelling, or increased gravitational gradients from low flow. Another is pulmonary arterial hypertension (PAH), where gravitational gradients may be reduced secondary to high pressures, but remodelling may increase perfusion heterogeneity. We evaluated regional pulmonary perfusion in Fontan patients (n=5), healthy young controls (Fontan control, n=5), patients with PAH (n=6) and healthy older controls (PAH control) using proton magnetic resonance imaging. Regional perfusion was measured using arterial spin labelling. Heterogeneity was assessed by the relative dispersion (SD/mean) and gravitational gradients. Mean perfusion was similar (Fontan=2.50±1.02mlmin-1 ml-1 ; Fontan control=3.09±0.58, PAH=3.63±1.95; PAH control=3.98±0.91, P=0.26), and the slopes of gravitational gradients were not different (Fontan=-0.23±0.09mlmin-1 ml-1 cm-1 ; Fontan control=-0.29±0.23, PAH=-0.27±0.09, PAH control=-0.25±0.18, P=0.91) between groups. Perfusion relative dispersion was greater in both Fontan and PAH than controls (Fontan=1.46±0.18; Fontan control=0.99±0.21, P=0.005; PAH=1.22±0.27, PAH control=0.91±0.12, P=0.02) but similar between patient groups (P=0.13). These findings persisted after removing contributions from large blood vessels and gravitational gradients (all P<0.05). We conclude that patients with Fontan physiology and PAH have increased pulmonary perfusion heterogeneity that is not explained by differences in mean perfusion, gravitational gradients, or large vessel anatomy. This probably reflects the effects of remodelling in PAH and possibly in Fontan physiology.

Regional pulmonary perfusion patterns in humans are not significantly altered by inspiratory hypercapnia.

Pulmonary vascular tone is known to be sensitive to both local alveolar Po2 and Pco2. Although the effects of hypoxia are well studied, the hypercapnic response is relatively less understood. We assessed changes in regional pulmonary blood flow in humans in response to hypercapnia using previously developed MRI techniques. Dynamic measures of blood flow were made in a single slice of the right lung of seven healthy volunteers following a block-stimulus paradigm (baseline, challenge, recovery), with CO2 added to inspired gas during the challenge block to effect a 7-Torr increase in end-tidal CO2. Effects of hypercapnia on blood flow were evaluated based on changes in spatiotemporal variability (fluctuation dispersion, FD) and in regional perfusion patterns in comparison to hypoxic effects previously studied. Hypercapnia increased FD 2.5% from baseline (relative to control), which was not statistically significant (P = 0.07). Regional perfusion patterns were not significantly changed as a result of increased (P = 0.90). Reanalysis of previously collected data using a similar protocol but with the physiological challenge replaced by decreased ( = 0.125) showed marked flow redistribution (P = 0.01) with the suggestion of a gravitational pattern, demonstrating hypoxia has the ability to affect regional change with a global stimulus. Taken together, these data indicate that hypercapnia of this magnitude does not lead to appreciable changes in the distribution of pulmonary perfusion, and that this may represent an interesting distinction between the hypoxic and hypercapnic regulatory response.NEW & NOTEWORTHY Although it is well known that the pulmonary circulation responds to local alveolar hypoxia, and that this mechanism may facilitate ventilation-perfusion matching, the relative role of CO2 is not well appreciated. This study demonstrates that an inspiratory hypercapnic stimulus is significantly less effective at inducing changes in pulmonary perfusion patterns than inspiratory hypoxia, suggesting that in these circumstances hypercapnia is not sufficient to induce substantial integrated feedback control of ventilation-perfusion mismatch across the lung.

The effect of lung deformation on the spatial distribution of pulmonary blood flow.

Pulmonary perfusion measurement using magnetic resonance imaging combined with deformable image registration enabled us to quantify the change in the spatial distribution of pulmonary perfusion at different lung volumes. The current study elucidated the effects of tidal volume lung inflation [functional residual capacity (FRC)+500ml and FRC+1litre] on the change in pulmonary perfusion distribution. Changes in hydrostatic pressure distribution as well as transmural pressure distribution due to the change in lung height with tidal volume inflation are probably bigger contributors to the redistribution of pulmonary perfusion than the changes in pulmonary vasculature resistance caused by lung tissue stretch. Tidal volume lung inflation results in structural changes in the pulmonary circulation, potentially affecting pulmonary perfusion. We hypothesized that perfusion is recruited to regions receiving the greatest deformation from a tidal breath, thus ensuring ventilation-perfusion matching. Density-normalized perfusion (DNP) magnetic resonance imaging data were obtained in healthy subjects (n=7) in the right lung at functional residual capacity (FRC), FRC+500ml, and FRC+1.0l. Using deformable image registration, the displacement of a sagittal lung slice acquired at FRC to the larger volumes was calculated. Registered DNP images were normalized by the mean to estimate perfusion redistribution (nDNP). Data were evaluated across gravitational regions (dependent, middle, non-dependent) and by lobes (upper, RUL; middle, RML; lower, RLL). Lung inflation did not alter mean DNP within the slice (P=0.10). The greatest expansion was seen in the dependent region (P<0.0001: dependent vs non-dependent, P<0.0001: dependent vs middle) and RLL (P=0.0015: RLL vs RUL, P<0.0001: RLL vs RML). Neither nDNP recruitment to RLL [+500ml=-0.047(0.145), +1litre=0.018(0.096)] nor to dependent lung [+500ml=-0.058(0.126), +1litre=-0.023(0.106)] were found. Instead, redistribution was seen in decreased nDNP in the non-dependent [+500ml=-0.075(0.152), +1litre=-0.137(0.167)) and increased nDNP in the gravitational middle lung [+500ml=0.098(0.058), +1litre=0.093(0.081)] (P=0.01). However, there was no significant lobar redistribution (P<0.89). Contrary to our hypothesis, based on the comparison between gravitational and lobar perfusion data, perfusion was not redistributed to the regions of the most inflation. This suggests that either changes in hydrostatic pressure or transmural pressure distribution in the gravitational direction are implicated in the redistribution of perfusion away from the non-dependent lung.

Quantitative and Semiquantitative Measures of Regional Pulmonary Microvascular Perfusion by Magnetic Resonance Imaging and Their Relationships to Global Lung Perfusion and Lung Diffusing Capacity

The aim of this study was to evaluate the quantitative and semiquantitative measures of regional pulmonary parenchymal perfusion in patients with chronic obstructive pulmonary disease (COPD) in relationship to global lung perfusion (GLP) and lung diffusing capacity (DLCO). A total of 143 participants in the Multiethnic Study of Atherosclerosis COPD Study were examined by dynamic contrast-enhanced pulmonary perfusion magnetic resonance imaging (MRI) at 1.5 T. Pulmonary microvascular blood flow (PBF) was calculated on a pixel-by-pixel basis by using a dual-bolus technique and the Fermi function model. Semiquantitative parameters for regional pulmonary microvascular perfusion were calculated from signal intensity-time curves in the lung parenchyma. Intraoberserver and interobserver coefficients of variation (CVs) and correlations between quantitative and semiquantitative MRI parameters and with GLP and DLCO were determined. Quantitative and semiquantitative parameters of pulmonary microvascular perfusion were reproducible, with CVs for all parameters of less than 10%. Furthermore, these MRI parameters were correlated with GLP and DLCO, and there was good agreement between PBF and GLP. Quantitative and semiquantitative MRI parameters were closely correlated (eg, r = 0.86 for maximum signal increase with PBF). In participants without COPD, the physiological distribution of pulmonary perfusion could be determined by regional MRI measurements. Regional pulmonary microvascular perfusion can reliably be quantified from dynamic contrast-enhanced MRI. Magnetic resonance imaging-derived quantitative and semiquantitative perfusion measures correlate with GLP and DLCO.

ARDS: Who Needs to be Pronated?

Acute Distress Respiratory Syndrome (ARDS) is defined as a severe respiratory failure characterized by marked hypoxemia, bilateral infiltrates on the chest X-ray and the absence of signs of cardiogenic pulmonary edema. ARDS treatment remains primarily supportive and the use of mechanical ventilation with positive and expiratory pressure is required to maintain adequate gas exchange. Lung-protective mechanical ventilation strategy decreases mortality and increases ventilator free days. Prone positioning is considered a rescue therapy despite it improves gas exchange through resolution of dorsal atelectases with lung recruitment, better distribution of pulmonary perfusion and reduction of lung stress and strain. Nevertheless, several randomized controlled trials failed to demonstrate a reduction in mortality in pronated ARDS patients. Recent meta-analysis instead demonstrated a significant reduction of mortality in patients with most severe ARDS (PaO2/FiO2 ratio < 200) ventilated in prone position. These data were confirmed by the results of the PROSEVA study, published in June 2013 that reports a 16% reduction of mortality rate. The results of several meta-analysis and this large clinical trial suggest that prone positioning is a useful strategy that saves lives in more severely ill ARDS patients, when applied earlier and for at least 16 hours/day.

Magnetic Resonance Imaging Quantification of Pulmonary Perfusion using Calibrated Arterial Spin Labeling

This demonstrates a MR imaging method to measure the spatial distribution of pulmonary blood flow in healthy subjects during normoxia (inspired O(2), fraction (F(I)O(2)) = 0.21) hypoxia (F(I)O(2) = 0.125), and hyperoxia (F(I)O(2) = 1.00). In addition, the physiological responses of the subject are monitored in the MR scan environment. MR images were obtained on a 1.5 T GE MRI scanner during a breath hold from a sagittal slice in the right lung at functional residual capacity. An arterial spin labeling sequence (ASL-FAIRER) was used to measure the spatial distribution of pulmonary blood flow and a multi-echo fast gradient echo (mGRE) sequence was used to quantify the regional proton (i.e. H(2)O) density, allowing the quantification of density-normalized perfusion for each voxel (milliliters blood per minute per gram lung tissue). With a pneumatic switching valve and facemask equipped with a 2-way non-rebreathing valve, different oxygen concentrations were introduced to the subject in the MR scanner through the inspired gas tubing. A metabolic cart collected expiratory gas via expiratory tubing. Mixed expiratory O(2) and CO(2) concentrations, oxygen consumption, carbon dioxide production, respiratory exchange ratio, respiratory frequency and tidal volume were measured. Heart rate and oxygen saturation were monitored using pulse-oximetry. Data obtained from a normal subject showed that, as expected, heart rate was higher in hypoxia (60 bpm) than during normoxia (51) or hyperoxia (50) and the arterial oxygen saturation (SpO(2)) was reduced during hypoxia to 86%. Mean ventilation was 8.31 L/min BTPS during hypoxia, 7.04 L/min during normoxia, and 6.64 L/min during hyperoxia. Tidal volume was 0.76 L during hypoxia, 0.69 L during normoxia, and 0.67 L during hyperoxia. Representative quantified ASL data showed that the mean density normalized perfusion was 8.86 ml/min/g during hypoxia, 8.26 ml/min/g during normoxia and 8.46 ml/min/g during hyperoxia, respectively. In this subject, the relative dispersion, an index of global heterogeneity, was increased in hypoxia (1.07 during hypoxia, 0.85 during normoxia, and 0.87 during hyperoxia) while the fractal dimension (Ds), another index of heterogeneity reflecting vascular branching structure, was unchanged (1.24 during hypoxia, 1.26 during normoxia, and 1.26 during hyperoxia). Overview. This protocol will demonstrate the acquisition of data to measure the distribution of pulmonary perfusion noninvasively under conditions of normoxia, hypoxia, and hyperoxia using a magnetic resonance imaging technique known as arterial spin labeling (ASL). Measurement of pulmonary blood flow and lung proton density using MR technique offers high spatial resolution images which can be quantified and the ability to perform repeated measurements under several different physiological conditions. In human studies, PET, SPECT, and CT are commonly used as the alternative techniques. However, these techniques involve exposure to ionizing radiation, and thus are not suitable for repeated measurements in human subjects.

Magnetic Resonance Imaging Quantification of Pulmonary Perfusion using Calibrated Arterial Spin Labeling

This demonstrates a MR imaging method to measure the spatial distribution of pulmonary blood flow in healthy subjects during normoxia (inspired O2, fraction (FIO2) = 0.21) hypoxia (FIO2 = 0.125), and hyperoxia (FIO2 = 1.00). In addition, the physiological responses of the subject are monitored in the MR scan environment. MR images were obtained on a 1.5 T GE MRI scanner during a breath hold from a sagittal slice in the right lung at functional residual capacity. An arterial spin labeling sequence (ASL-FAIRER) was used to measure the spatial distribution of pulmonary blood flow 1,2 and a multi-echo fast gradient echo (mGRE) sequence 3 was used to quantify the regional proton (i.e. H2O) density, allowing the quantification of density-normalized perfusion for each voxel (milliliters blood per minute per gram lung tissue). With a pneumatic switching valve and facemask equipped with a 2-way non-rebreathing valve, different oxygen concentrations were introduced to the subject in the MR scanner through the inspired gas tubing. A metabolic cart collected expiratory gas via expiratory tubing. Mixed expiratory O2 and CO2 concentrations, oxygen consumption, carbon dioxide production, respiratory exchange ratio, respiratory frequency and tidal volume were measured. Heart rate and oxygen saturation were monitored using pulse-oximetry. Data obtained from a normal subject showed that, as expected, heart rate was higher in hypoxia (60 bpm) than during normoxia (51) or hyperoxia (50) and the arterial oxygen saturation (SpO2) was reduced during hypoxia to 86%. Mean ventilation was 8.31 L/min BTPS during hypoxia, 7.04 L/min during normoxia, and 6.64 L/min during hyperoxia. Tidal volume was 0.76 L during hypoxia, 0.69 L during normoxia, and 0.67 L during hyperoxia. Representative quantified ASL data showed that the mean density normalized perfusion was 8.86 ml/min/g during hypoxia, 8.26 ml/min/g during normoxia and 8.46 ml/min/g during hyperoxia, respectively. In this subject, the relative dispersion4, an index of global heterogeneity, was increased in hypoxia (1.07 during hypoxia, 0.85 during normoxia, and 0.87 during hyperoxia) while the fractal dimension (Ds), another index of heterogeneity reflecting vascular branching structure, was unchanged (1.24 during hypoxia, 1.26 during normoxia, and 1.26 during hyperoxia). Overview. This protocol will demonstrate the acquisition of data to measure the distribution of pulmonary perfusion noninvasively under conditions of normoxia, hypoxia, and hyperoxia using a magnetic resonance imaging technique known as arterial spin labeling (ASL). Rationale: Measurement of pulmonary blood flow and lung proton density using MR technique offers high spatial resolution images which can be quantified and the ability to perform repeated measurements under several different physiological conditions. In human studies, PET, SPECT, and CT are commonly used as the alternative techniques. However, these techniques involve exposure to ionizing radiation, and thus are not suitable for repeated measurements in human subjects.

Lung volume does not alter the distribution of pulmonary perfusion in dependent lung in supine humans

There is a gravitational influence on pulmonary perfusion, including in the most dependent lung, where perfusion is reduced, termed Zone 4. Studies using xenon-133 show Zone 4 behaviour, present in the dependent 4 cm at total lung capacity (TLC), affects the dependent 11 cm at functional residual capacity (FRC) and almost all the lung at residual volume (RV). These differences were ascribed to increased resistance in extra-alveolar vessels at low lung volumes although other mechanisms have been proposed. To further evaluate the behaviour of perfusion in dependent lung using a technique that directly measures pulmonary perfusion and corrects for tissue distribution by measuring regional proton density, seven healthy subjects (age = 38 ± 6 years, FEV₁ = 104 ± 7% predicted) underwent magnetic resonance imaging in supine posture. Data were acquired in the right lung during breath-holds at RV, FRC and TLC. Arterial spin labelling quantified regional pulmonary perfusion, which was normalized for regional proton density measured using a fast low-angle shot technique. The height of the onset of Zone 4 behaviour was not different between lung volumes (P = 0.23). There were no significant differences in perfusion (expressed as ml min⁻¹ g⁻¹) between lung volumes in the gravitationally intermediate (RV = 8.9 ± 3.1, FRC = 8.1 ± 2.9, TLC = 7.4 ± 3.6; P = 0.26) and dependent lung (RV = 6.6 ± 2.4, FRC = 6.1 ± 2.1, TLC = 6.4 ± 2.6; P = 0.51). However, at TLC perfusion was significantly lower in non-dependent lung than at FRC or RV (3.6 ± 3.3, 7.7 ± 1.5, 7.9 ± 2.0, respectively; P < 0.001). These data suggest that the mechanism of the reduction in perfusion in dependent lung is unlikely to be a result of lung volume related increases in resistance in extra-alveolar vessels. In supine posture, the gravitational influence on perfusion is remarkably similar over most of the lung, irrespective of lung volume.

Dual-Energy CT: Clinical Applications in Various Pulmonary Diseases

The dual-energy computed tomographic (CT) technique allows the differentiation of materials with large atomic numbers such as iodine and xenon. The basic principle of dual-energy CT is material decomposition based on attenuation differences at different energy levels. By using dual-energy CT angiography for the evaluation of perfusion defects in cases of pulmonary embolism, and using xenon CT for the evaluation of ventilation defects, it may be possible to replace perfusion and ventilation scanning. An iodine map from dual-energy CT can demonstrate the distribution of pulmonary perfusion, whereas xenon ventilation CT can be used to generate a ventilation map. Furthermore, the virtual nonenhanced dual-energy CT technique can be used for the evaluation of pulmonary nodule characteristics without acquisition of true nonenhanced CT images. Knowledge of the applications of dual-energy CT and the typical images produced may lead to wider use of dual-energy CT for pulmonary applications and better interpretation of the results.

Study of pathophysiology of pulmonary circulation in polycythemia using scintigraphy

In order to evaluate the pathophysiology of pulmonary circulation in polycythemia, Tl-201 myocardial scintigraphy and perfusion lung scintigraphy with 99m-Tc MAA were performed in 19 cases with polycythemia including polycythemia rubra vera and in 11 cases with secondary polycythemia due to pulmonary diseases. Tl-201 lung uptake, right ventricular visualization and pulmonary perfusion impairment were studied. In the 19 cases, Tl-201 lung uptake was observed in all cases and 54.5% of them showed moderate lung uptake. The grade of right ventricular visualization was moderate in one case and slight in 16 cases; right ventricular hypertrophy was shown in 89.5% of all cases by Tl-201 scintigraphy, only one of which showed right ventricular hypertrophy on electrocardiography. Abnormalities of lung perfusion consisted of scattered small areas of hypoperfusion in 36.8%, peripheral hypoperfusion in 78.9% and uneven distribution of pulmonary perfusion in 94.7%. The degree of hypoperfusion was slightly related to decrease in FEV1.0%, V25 and PaO2 and increase in circulating blood volume and peripheral red blood cell counts. Abnormalities of pulmonary function consisted of increased RV/TLC in 50.0%, increased CV/VC in 35.7% and decreased V25 in 36.8%. Arterial blood gases showed hypoxemia in 57.1%, the degree of which was slightly related to increase in RV/TLC and CV/VC and decrease in V25. Cases of secondary polycythemia due to pulmonary diseases showed more marked right ventricular visualization, pulmonary perfusion impairment and abnormalities of various kinds of pulmonary function than polycythemia rubra vera cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Rapid intravenous infusion of 20 ml/kg saline does not impair resting pulmonary gas exchange in the healthy human lung

Rapid infusion of intravenous saline, a model of pulmonary interstitial edema, alters the distribution of pulmonary perfusion, raises pulmonary capillary blood volume, and increases bronchial wall thickness in humans. We hypothesized that infusion would disrupt pulmonary gas exchange by increasing ventilation/perfusion ((.)VA/(.)Q) inequality as opposed to a diffusive impairment in O2 exchange. Seven males (26 +/- 3 yr; FEV1: 110 +/- 16% predicted.) performed spirometry and had (.)VA/(.)Q mismatch measured using the multiple inert gas elimination technique, before and after 20 ml/kg iv of normal saline delivered in approximately 30 min. Infusion increased thoracic fluid content from transthoracic impedance by 12% (P < 0.0001) and left FVC unchanged but reduced expiratory flows (FEF(25-75) falling from 5.1 +/- 0.4 to 4.2 +/- 0.4 l/s, P < 0.05). However, (.)VA/(.)Q mismatch as measured by the log standard deviation of the ventilation (LogSD(.)V) and perfusion (LogSD(.)Q) distributions remained unchanged; LogSD(.)V: 0.40 +/- 0.03 pre, 0.38 +/- 0.04 post, NS; LogSD(.)Q: 0.38 +/- 0.03 pre, 0.37 +/- 0.03 post, NS. There was no significant change in arterial PO2 (99 +/- 2 pre, 99 +/- 3 mmHg post, NS) but arterial PCO2 was decreased (38.7 +/- 0.6 pre, 36.8 +/- 1.2 mmHg post, P < 0.05). Thus, infusion compressed small airways and caused a mild degree of hyperventilation. There was no evidence for a diffusive limitation to O2 exchange, with the measured-predicted alveolar-arterial oxygen partial pressure difference being unaltered by infusion at FIO2 = 0.125 (4.3 +/- 1.0 pre, 5.2 +/- 1.0 post, NS). After infusion, the fraction of perfusion going to areas with (.)VA/(.)Q < 1 was increased when a subject breathed a hyperoxic gas mixture [0.72 +/- 0.06 (FIO2 = 0.21), 0.80 +/- 0.06 (FIO2 = 0.30), P < 0.05] with similar effects on ventilation in the face of unchanged (.)VA and (.)Q. These results suggest active control of blood flow to regions of decreased ventilation during air breathing, thus minimizing the gas exchange consequences.

Does hypoxic vasoconstriction influence the normal distribution of human pulmonary blood flow?

elevation of regional pulmonary resistance in response to local alveolar hypoxia is a near-universal response of the mammalian lung to optimize arterial oxygenation ([14][1]). Given the heterogeneity of regional ventilation observed in a normal lung ([11][2], [16][3]), it appears plausible that

A quantitative method of ratio of ventilation and perfusion in COPD patients under general anesthesia with mechanical ventilation

Objective We analyzed the pulmonary ventilation and pulmonary perfusion ratio (VA/Q) during spontaneous breathing and mechanical ventilation in surgical patients using a quantitative method of multiple inert gas elimination technique (MIGET) to guide clinical treatment and to assess the effects of mechanical ventilation. Methods Twelve patients, with ASA physical status Ⅱ-Ⅲ and in stable stage of chronic obstructive pulmonary disease (COPD) were enrolled in the study. All the patients were undertaken femoral artery bypass grafting surgery under intravenous propofol and remifentanil anesthesia. MIGET and artery blood gases (ABG) were measured and compared between the awake and 60 rain after mechanical ventilation. Results Artery oxygen partial pressure (PaO2 ) was higher significantly(P < 0.001 )at 60 rain after ventilation than at awaken. There was no statistical difference in the percentage shunt and dead space ventilation in MIGET. The distribution of logSDQ was increased ( P < 0. 005 ) and total pulmonary blood was decreased by 43% ( P = 0.027 ) at 60 rain after mechanical ventilation. Conclusion The distribution of pulmonary perfusion becomes worsen mismatched with mechanical ventilation in COPD patients at stable stage. The IogSDQ distribution increases which may impair gas exchange during geneval anesthesia. MIGET is a non-invasive and bedside approaching monitoring method without needing special cooperation from patients. Key words: MIGET; anesthesia; mechanical ventilation; COPD

Rebuttal from Drs. Hughes and West

POINT-COUNTERPOINTRebuttal from Drs. Hughes and WestPublished Online:01 May 2008https://doi.org/10.1152/japplphysiol.01092.2007bMoreSectionsPDF (59 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat The areas of agreement in this debate are twofold: 1) mean pulmonary blood flow per horizontal slice [per unit volume or, more accurately, per unit density or “alveolus” (1,6)] increases in the gravity direction, independent (for the most part) of postural orientation, 2) there is considerable inhomogeneity of blood flow within a slice of minimal vertical height. Heterogeneity, whether random or ordered, is inevitable as the spatial resolution increases, just as the length of the shoreline increases indefinitely as the sample size gets smaller. Suffice to say that there are two extremes, 1) a well-expanded, vasodilated lung with low PVR and a mean Ppa level below the top of the lung, and 2) a low volume vasoconstricted lung with high PVR and a Ppa level greater than the lung's vertical height. The effects of gravity will be prominent in the former and largely obscured in the latter.The core of the debate is about the mechanisms responsible for pulmonary blood flow heterogeneity. There has been acceptance (for more than 40 yr) that mean pulmonary blood flow per horizontal slice is influenced by the relations between Ppa, Palv, and Pv (zones I, II, and III) (7), provided the lung is well expanded and PVR is normal. But what determines heterogeneity at the same horizontal level? Between acini, or larger domains, the Seattle group maintains that the architecture of the vascular tree (presumably, arterial) determines local vascular resistance and blood flow by, for example, uneven diameters of the two daughter vessels at a bifurcation. Glenny (5) maintains that this is not random, but forms part of the fractal design of the lung (4). Against this hypothesis is 1) the arterial system contributes only 40% to total PVR (2), and 2) the compliance of the arterial tree means diameters are not fixed, but respond to changes of smooth muscle tone or intra- or extravascular pressures (themselves influenced by gravity from distortion of the lung by its own weight and by other intrathoracic structures).Distal to the arterial tree, at the alveolar septal level, recruitment and distension of vessels occurs (3), independent of arteriolar domains (8), as input pressure increases and exceeds critical opening pressure (9); in the lung periphery, input pressures are a function of vertical height and gravity. So, in subtle ways, gravity may interact with compliant vascular structures to influence local PVR within as well as between horizontal lung slices.REFERENCES1 Anthonisen NR, Milic-Emili J. Distribution of pulmonary perfusion in erect man. J Appl Physiol 21: 760–766, 1966.Link | ISI | Google Scholar2 Dawson CA. Dynamics of blood flow and pressure-volume relationship. In: The Lung: Scientific Foundations, edited by Crystal RG, West JB, et al. Philadelphia: Lippincott-Raven, 1997, p. 1503–1522.Google Scholar3 Glazier JB, Hughes JMB, Maloney JE, West JB. Measurements of capillary dimensions and blood volume in rapidly frozen lungs. J Appl Physiol 26: 65–76, 1969.Link | ISI | Google Scholar4 Glenny RW, Robertson HT. Fractal modelling of pulmonary blood flow inhomogeneity. J Appl Physiol 70: 1024–1030, 1991.Link | ISI | Google Scholar5 Glenny RW. Spatial correlation of regional pulmonary perfusion. J Appl Physiol 72: 2378–2386, 1992.Link | ISI | Google Scholar6 Hughes JMB, Glazier JB, Maloney JE, West JB. Effect of lung volume on the distribution of pulmonary blood flow in man. Respir Physiol 4: 58–72, 1968.Crossref | Google Scholar7 West JB, Dollery CT, Naimark A. Distribution of blood flow in isolated lung; relation to vascular and alveolar pressures. J Appl Physiol 19: 713–724, 1964.Link | ISI | Google Scholar8 Warrell DA, Evans JW, Clarke RO, Kingaby JP, West JB. Pattern of filling in the pulmonary vascular bed. J Appl Physiol 32: 346–356, 1972.Link | ISI | Google Scholar9 West JB, Schneider AM, Mitchell MM. Recruitment in networks of pulmonary capillaries. J Appl Physiol 39: 976–984, 1975.Link | ISI | Google Scholar Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation More from this issue > Volume 104Issue 5May 2008Pages 1535-1535 Copyright & PermissionsCopyright © 2008 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.01092.2007bHistory Published online 1 May 2008 Published in print 1 May 2008 Metrics

Pulmonary gas exchange following rapid intravenous saline infusion

Rapid infusion of i.v. saline, a model of pulmonary interstitial edema, alters the distribution of pulmonary perfusion, raises pulmonary capillary blood volume, and increases bronchial wall thickness in humans. We hypothesized infusion would disrupt pulmonary gas exchange by altering VA/Q matching. Seven males (26±3 years, FEV1 110±16% pred.) performed spirometry and had the distribution of VA/Q measured using MIGET, before and after 20ml/kg i.v. of normal saline delivered in ~30 minutes. Infusion increased thoracic fluid content by 12% (P &lt; 0.0001), left FVC unchanged, but reduced expiratory flows (e.g. FEF25–75 fell from 5.1±0.4 to 4.1±0.4 l/sec, P &lt; 0.05). However, infusion left the distribution of VA/Q unchanged; log SDV 0.40±0.03 pre, 0.38±0.04 post, NS; logSDQ, 0.38±0.03 pre, 0.37±0.03 post, NS. There was no significant change in arterial PO2 (99.2±2.5 pre, 99.5±2.9 mmHg post, NS) but arterial PCO2 was decreased (38.7±0.6 pre, 37.1±1.1 mmHg post, P&lt;0.05). Thus, infusion compressed small airways, and caused a mild degree of hyperventilation, but the matching of ventilation to perfusion was maintained, suggesting active control of blood flow to minimize the gas exchange consequences.

Prone positioning improves distribution of pulmonary perfusion: noninvasive magnetic resonance imaging study in healthy humans

The purpose of this study was to evaluate the effects of prone positioning on pulmonary perfusion using flow-sensitive alternating inversion recovery (FAIR), a noninvasive magnetic resonance imaging technique that requires no contrast medium. Seven healthy volunteers were studied in the supine and prone positions under three respiratory conditions: normal breathing of room air, unassisted breathing of 45% O2, and controlled mechanical ventilation (CMV) with positive end-expiratory pressure. Signal intensities (SIs) were obtained from ventral, middle, and dorsal regions on sagittal lung images and dependent/nondependent SI ratios were calculated to evaluate pulmonary perfusion distribution. In the supine position, SIs increased significantly from the ventral to dorsal region under all three respiratory conditions and prone positioning inverted the perfusion distribution under all conditions. Right lung SI ratios were 2.34 +/- 0.29, 2.74 +/- 0.66, and 2.42 +/- 0.73 in the supine position and 1.68 +/- 0.48, 1.78 +/- 0.36, and 1.92 +/- 0.21 in prone for room air, 45% O2, and CMV, respectively. The difference between supine and prone positions was statistically significant. The left lung showed a similar pattern and the difference was significant only under CMV. No difference was observed between the different respiratory conditions in both lungs. This study demonstrated that the distribution of pulmonary perfusion was more uniform in prone than in the supine position.