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Previous studies have suggested that an extended period of ventilation before delayed cord clamping (DCC) augments birth‐related rises in pulmonary arterial (PA) blood flow. However, it is unknown whether this greater rise in PA flow is accompanied by increases in left ventricular (LV) output and systemic arterial perfusion or whether it reflects enhanced left‐to‐right shunting across the ductus arteriosus and/or foramen ovale (FO), with decreased systemic arterial perfusion. Using an established preterm lamb birth transition model, this study compared the effect of a short (∼40 s, n = 11), moderate (∼2 min, n = 11) or extended (∼5 min, n = 12) period of initial mechanical lung ventilation before DCC on flow probe‐derived perinatal changes in PA flow, LV output, total systemic arterial blood flow, ductal shunting and FO shunting. The LV output was relatively stable during initial ventilation but increased after DCC, with similar responses in all groups. Systemic arterial flow patterns displayed only minor differences during brief and moderate periods of initial ventilation and were similar after DCC. However, an increase in PA flow was augmented with an extended initial ventilation (P < 0.001), owing to an earlier onset of left‐to‐right ductal and FO shunting (P < 0.001), and was accompanied by a pronounced reduction in total systemic arterial flow (P = 0.005) that persisted for 4 min after DCC (P ≤ 0.039). These findings suggest that, owing to increased left‐to‐right shunting and a greater reduction in systemic arterial perfusion, an extended period of ventilation before DCC does not result in greater perinatal circulatory benefits than shorter periods of initial ventilation in the birth transition. Key points: Previous studies suggest that an extended period of initial ventilation before delayed cord clamping (DCC) augments birth‐related rises in pulmonary arterial (PA) blood flow.It is unknown whether this greater rise in PA flow is accompanied by an increased left ventricular output and systemic arterial perfusion or whether it reflects enhanced left‐to‐right shunting across the ductus arteriosus and/or foramen ovale, with decreased systemic arterial perfusion.Anaesthetized preterm fetal lambs instrumented with central arterial flow probes underwent a brief (∼40 s), moderate (∼2 min) or extended (∼5 min) period of ventilation before DCC.Perinatal changes in left ventricular output were similar in all groups, but extended initial ventilation augmented both perinatal increases in PA flow, owing to earlier onset and greater left‐to‐right ductal and foramen ovale shunting, and perinatal reductions in total systemic arterial perfusion.Extended ventilation before DCC does not confer a greater perinatal circulatory benefit than shorter periods of initial ventilation. [ABSTRACT FROM AUTHOR]

Simple Summary: Abnormal hemodynamics and cardiac and pulmonary development intertwine to form the most important features of children with congenital heart diseases (CHDs). Here, we review the varieties of hemodynamic abnormalities that exist in children with CHDs and the recently developed neonatal rodent models of CHDs, which have inspired and brought us new ideas and inspirations in cardiomyocyte proliferation and maturation, as well as in alveolar development. Hemodynamics is the eternal theme of the circulatory system. Abnormal hemodynamics and cardiac and pulmonary development intertwine to form the most important features of children with congenital heart diseases (CHDs), thus determining these children's long-term quality of life. Here, we review the varieties of hemodynamic abnormalities that exist in children with CHDs, the recently developed neonatal rodent models of CHDs, and the inspirations these models have brought us in the areas of cardiomyocyte proliferation and maturation, as well as in alveolar development. Furthermore, current limitations, future directions, and clinical decision making based on these inspirations are highlighted. Understanding how CHD-associated hemodynamic scenarios shape postnatal heart and lung development may provide a novel path to improving the long-term quality of life of children with CHDs, transplantation of stem cell-derived cardiomyocytes, and cardiac regeneration. [ABSTRACT FROM AUTHOR]

Pulmonary arterial pressure (PAH) usually increases after cardiopulmonary bypass (CPB), but this normally does not affect weaning off CPB. Here we report a case of severe PAH in a patient with normal left atrial pressure. Prolonging CPB by 45 min did not lead to lower PAH. Given that lung injury can stimulate secretion of vasoconstrictors that trigger PAH, we decided to gradually increase blood flow into the lungs in an effort to restore the balance between pulmonary vasoconstrictors and vasodilators. Pulmonary artery pressure gradually decreased, allowing the patient to be weaned off CPB, after which she recovered uneventfully. Our experience suggests an approach for managing acute, severe PAH after CPB without the need for mechanical circulatory support. [ABSTRACT FROM AUTHOR]

Background: Extracorporeal membrane oxygenation (ECMO) is indicated for patients with severe respiratory and/or circulatory failure. The standard technique to visualize the extent of pulmonary damage during ECMO is computed tomography (CT). Purpose: This single-center, retrospective study investigated whether pulmonary blood flow (PBF) measured with echocardiography can assist in assessing the extent of pulmonary damage and whether echocardiography and CT findings are associated with patient outcomes. Methods: All patients (>15 years) commenced on ECMO between 2011 and 2017 with septic shock of pulmonary origin and a treatment time >28 days were screened. Of 277 eligible patients, 9 were identified where both CT and echocardiography had been consecutively performed. Results: CT failed to indicate any differences in viable lung parenchyma within or between survivors and non-survivors at any time during ECMO treatment. Upon initiation of ECMO, the survivors (n = 5) and non-survivors (n = 4) had similar PBF. During a full course of ECMO support, survivors showed no change in PBF (3.8 ± 2.1 at ECMO start vs. 7.9 ± 4.3 L/min, p = 0.12), whereas non-survivors significantly deteriorated in PBF from 3.5 ± 1.0 to 1.0 ± 1.1 L/min (p = 0.029). Tidal volumes were significantly lower over time among the non-survivors, p = 0.047. Conclusions: In prolonged ECMO for pulmonary septic shock, CT was not found to be effective for the evaluation of pulmonary viability or recovery. This hypothesis-generating investigation supports echocardiography as a tool to predict pulmonary recovery via the assessment of PBF at the early to later stages of ECMO support. [ABSTRACT FROM AUTHOR]

Introduction: Hypoxic pulmonary vasoconstriction optimises oxygenation in the lung by matching the local‐blood perfusion to local‐ventilation ratio upon exposure to alveolar hypoxia. It plays an important role in various pulmonary diseases, but few imaging evaluations of this phenomenon in humans. This study aimed to determine whether chest digital dynamic radiography could detect hypoxic pulmonary vasoconstriction as changes in pulmonary blood flow in healthy individuals. Methods: Five Asian men underwent chest digital dynamic radiography before and after 60 sec breath‐holding at the maximal inspiratory level in upright and supine positions. Alveolar partial pressure of oxygen and atmospheric pressure were calculated using the blood gas test and digital dynamic radiography imaging, respectively. To evaluate the blood flow, the correlation rate of temporal change in each pixel value between the lung fields and left cardiac ventricles was analysed. Results: Sixty seconds of breath‐holding caused a mean reduction of 26.7 ± 6.4 mmHg in alveolar partial pressure of oxygen. The mean correlation rate of blood flow in the whole lung was significantly lower after than before breath‐holding (before, upright 51.5%, supine 52.2%; after, upright 45.5%, supine 46.1%; both P < 0.05). The correlation rate significantly differed before and after breath‐holding in the lower lung fields (upright, 11.8% difference; supine, 10.7% difference; both P < 0.05). The mean radiation exposure of each scan was 0.98 ± 0.09 mGy. No complications occurred. Conclusions: Chest digital dynamic radiography could detect the rapid decrease in pulmonary perfusion in response to alveolar hypoxia. It may suggest hypoxic pulmonary vasoconstriction in healthy individuals. [ABSTRACT FROM AUTHOR]

The article discusses a study on individuals with Fontan circulation, a type of heart condition, and their ability to tolerate high-altitude exposure. The study found that individuals with Fontan circulation were able to tolerate moderate normobaric hypoxia, equivalent to 8,000 feet, for 24 to 30 hours without experiencing significant clinical symptoms. The study also found that key hemodynamic parameters, such as resting pulmonary pressure and flow, remained stable in these individuals. The findings may provide guidance for physicians caring for individuals with Fontan circulation who are considering long-duration airplane travel or shorter stays at high altitude. [Extracted from the article]

Abstract Background Management of mechanically ventilated patients can be improved with monitoring of key pulmonary function parameters that facilitate individualization and optimization. The VQm Pulmonary Health Monitor™ (PHM) (Rostrum Medical Innovations Inc., Vancouver, Canada) is a new monitor that continuously measures pulmonary blood flow (PBF), functional residual capacity (FRC) and a novel parameter: shunt index (Qsi). The goal of this study was to provide an initial assessment of the performance of the VQm PHM™ when compared with reference measures of PBF, FRC and intra-pulmonary shunt. Methods This was a prospective, experimental, large animal (porcine) study. After baseline measurements, three interventions were performed: increased cardiac output (CO) using dobutamine infusion, increased PEEP (from 4 to 12 cmH2O), and experimental shunt induced by an extracorporeal circuit. PBF, FRC and shunt were measured by the VQm Pulmonary Health Monitor™ (PHM) before and after each intervention. The PHM™ uses sequential gas delivery to deliver targeted alveolar concentrations of CO2 or N2O. PBF and FRC were calculated using CO2 bolus delivery and the modified differential Fick equation. Shunt was estimated from the number of breaths required to eliminate N2O after a 25-breath N2O bolus and expressed as Qsi. PHM™-derived PBF and Qsi were compared to thermodilution CO and calculated Berggren shunt, respectively. Results Studies were completed in 19 animals. Measurements of PBF, FRC and Qsi obtained from the PHM™ trended as expected following each intervention. The mean difference between paired values of PBF was − 0.2 ± 0.9 L/min and the 95% limits of agreement were 1.5 and − 1.9 L/min. Concordance was 94.1%. The mean baseline FRC was 1.7 $$\pm$$ 0.4 L and increased to 2.0 $$\pm$$ 0.6 L, following the increase in PEEP (p = 0.0078). For shunt (Qsi), the mean values during low (1 L/min) and high (50% of baseline CO) shunt value were 40 $$\pm$$ 4 and 27 $$\pm$$ 5, respectively, p = 0.002. Conclusions PBF obtained through the modified differential Fick equation and Qsi obtained through N2O uptake and decay dynamics by the VQm PHM™ provide comparable results to reference standards. FRC measurements trended as expected following interventions.

Abstract Introduction Hypoxic pulmonary vasoconstriction optimises oxygenation in the lung by matching the local‐blood perfusion to local‐ventilation ratio upon exposure to alveolar hypoxia. It plays an important role in various pulmonary diseases, but few imaging evaluations of this phenomenon in humans. This study aimed to determine whether chest digital dynamic radiography could detect hypoxic pulmonary vasoconstriction as changes in pulmonary blood flow in healthy individuals. Methods Five Asian men underwent chest digital dynamic radiography before and after 60 sec breath‐holding at the maximal inspiratory level in upright and supine positions. Alveolar partial pressure of oxygen and atmospheric pressure were calculated using the blood gas test and digital dynamic radiography imaging, respectively. To evaluate the blood flow, the correlation rate of temporal change in each pixel value between the lung fields and left cardiac ventricles was analysed. Results Sixty seconds of breath‐holding caused a mean reduction of 26.7 ± 6.4 mmHg in alveolar partial pressure of oxygen. The mean correlation rate of blood flow in the whole lung was significantly lower after than before breath‐holding (before, upright 51.5%, supine 52.2%; after, upright 45.5%, supine 46.1%; both P

Management of acute respiratory distress syndrome (ARDS) is classically guided by protecting the injured lung and mitigating damage from mechanical ventilation. Yet the natural history of ARDS is also dictated by disruption in lung perfusion. Unfortunately, diagnosis and treatment are hampered by the lack of bedside perfusion monitoring. Electrical impedance tomography is a portable imaging technique that can estimate regional lung perfusion in experimental settings from the kinetic analysis of a bolus of an indicator with high conductivity. Hypertonic sodium chloride has been the standard indicator. However, hypertonic sodium chloride is often inaccessible in the hospital, limiting practical adoption. We investigated whether regional lung perfusion measured using electrical impedance tomography is comparable between indicators. Using a swine lung injury model, we determined regional lung perfusion (% of total perfusion) in five pigs, comparing 12% sodium chloride to 8.4% sodium bicarbonate across stages of lung injury and experimental conditions (body position, positive end-expiratory pressure). Regional lung perfusion for four lung regions was determined from maximum slope analysis of the indicator-based impedance signal. Estimates of regional lung perfusion between indicators were compared in the lung overall and within four lung regions. Regional lung perfusion estimated with a sodium bicarbonate indicator agreed with a hypertonic sodium chloride indicator overall (mean bias 0%, limits of agreement -8.43%, 8.43%) and within lung quadrants. The difference in regional lung perfusion between indicators did not change across experimental conditions. Sodium bicarbonate may be a comparable indicator to estimate regional lung perfusion using electrical impedance tomography. [ABSTRACT FROM AUTHOR]

Neonatal resuscitation (NRP) guidelines suggest targeting 85-95% preductal SpO2 by 10 min after birth. Optimal oxygen saturation (SpO2) targets during resuscitation and in the post-resuscitation management of neonatal meconium aspiration syndrome (MAS) with persistent pulmonary hypertension (PPHN) remains uncertain. Our objective was to compare the time to reversal of ductal flow from fetal pattern (right-to-left), to left-to-right, and to evaluate pulmonary (QPA), carotid (QCA)and ductal (QDA) blood flows between standard (85-94%) and high (95-99%) SpO2 targets during and after resuscitation. Twelve lambs asphyxiated by endotracheal meconium instillation and cord occlusion to induce MAS and PPHN were resuscitated per NRP guidelines and were randomized to either standard (85-94%) or high (95-99%) SpO2 targets. Out of twelve lambs with MAS and PPHN, six each were randomized to standard and high SpO2 targets. Median [interquartile range] time to change in direction of blood flow across the ductus arteriosus from right-to-left, to left-to-right was significantly shorter with high SpO2 target (7.4 (4.4-10.8) min) compared to standard SpO2 target (31.5 (21-66.2) min, p = 0.03). QPA was significantly higher during the first 10 min after birth with higher SpO2 target. At 60 min after birth, the QPA, QCA and QDA were not different between the groups. To conclude, targeting SpO2 of 95-99% during and after resuscitation may hasten reversal of ductal flow in lambs with MAS and PPHN and transiently increase QPA but no differences were observed at 60 min. Clinical studies comparing low and high SpO2 targets assessing hemodynamics and neurodevelopmental outcomes are warranted.

The optimal timing of cord clamping in asphyxia is not known. Our aims were to determine the effect of ventilation (sustained inflation-SI vs. positive pressure ventilation-V) with early (ECC) or delayed cord clamping (DCC) in asphyxiated near-term lambs. We hypothesized that SI with DCC improves gas exchange and hemodynamics in near-term lambs with asphyxial bradycardia. A total of 28 lambs were asphyxiated to a mean blood pressure of 22 mmHg. Lambs were randomized based on the timing of cord clamping (ECC-immediate, DCC-60 s) and mode of initial ventilation into five groups: ECC + V, ECC + SI, DCC, DCC + V and DCC + SI. The magnitude of placental transfusion was assessed using biotinylated RBC. Though an asphyxial bradycardia model, 2-3 lambs in each group were arrested. There was no difference in primary outcomes, the time to reach baseline carotid blood flow (CBF), HR ≥ 100 bpm or MBP ≥ 40 mmHg. SI reduced pulmonary (PBF) and umbilical venous (UV) blood flow without affecting CBF or umbilical arterial blood flow. A significant reduction in PBF with SI persisted for a few minutes after birth. In our model of perinatal asphyxia, an initial SI breath increased airway pressure, and reduced PBF and UV return with an intact cord. Further clinical studies evaluating the timing of cord clamping and ventilation strategy in asphyxiated infants are warranted.

Background: Extracorporeal membrane oxygenation (ECMO) is indicated for patients with severe respiratory and/or circulatory failure. The standard technique to visualize the extent of pulmonary damage during ECMO is computed tomography (CT). Purpose: This single-center, retrospective study investigated whether pulmonary blood flow (PBF) measured with echocardiography can assist in assessing the extent of pulmonary damage and whether echocardiography and CT findings are associated with patient outcomes. Methods: All patients (>15 years) commenced on ECMO between 2011 and 2017 with septic shock of pulmonary origin and a treatment time >28 days were screened. Of 277 eligible patients, 9 were identified where both CT and echocardiography had been consecutively performed. Results: CT failed to indicate any differences in viable lung parenchyma within or between survivors and non-survivors at any time during ECMO treatment. Upon initiation of ECMO, the survivors (n = 5) and non-survivors (n = 4) had similar PBF. During a full course of ECMO support, survivors showed no change in PBF (3.8 ± 2.1 at ECMO start vs. 7.9 ± 4.3 L/min, p = 0.12), whereas non-survivors significantly deteriorated in PBF from 3.5 ± 1.0 to 1.0 ± 1.1 L/min (p = 0.029). Tidal volumes were significantly lower over time among the non-survivors, p = 0.047. Conclusions: In prolonged ECMO for pulmonary septic shock, CT was not found to be effective for the evaluation of pulmonary viability or recovery. This hypothesis-generating investigation supports echocardiography as a tool to predict pulmonary recovery via the assessment of PBF at the early to later stages of ECMO support.

In children with congenital heart disease (CHD), pulmonary blood flow (Qp) contributes to alterations of pulmonary mechanics and gas exchange, while cardiopulmonary bypass (CPB) induces lung edema. We aimed to determine the effect of hemodynamics on lung function and lung epithelial lining fluid (ELF) biomarkers in biventricular CHD children undergoing CPB. CHD children were classified as high Qp (n = 43) and low Qp (n = 17), according to preoperative cardiac morphology and arterial oxygen saturation. We measured ELF surfactant protein B (SP-B) and myeloperoxidase activity (MPO) as indexes of lung inflammation and ELF albumin as index of alveolar capillary leak in tracheal aspirate (TA) samples collected before surgery and in 6 hourly intervals within 24 h after surgery. At the same time points, we recorded dynamic compliance and oxygenation index (OI). The same biomarkers were measured in TA samples collected from 16 infants with no cardiorespiratory diseases at the time of endotracheal intubation for elective surgery. Preoperative ELF biomarkers in CHD children were significantly increased than those found in controls. In the high Qp, ELF MPO and SP-B peaked 6 h after surgery and tended to decrease afterward, while they tended to increase within the first 24 h in the low Qp. ELF albumin peaked 6 h after surgery and decreased afterwards in both CHD groups. Dynamic compliance/kg and OI significantly improved after surgery only in the High Qp. Conclusion: In CHD children, lung mechanics, OI, and ELF biomarkers were significantly affected by CPB, according to the preoperative pulmonary hemodynamics. What is Known: • Congenital heart disease children, before cardiopulmonary run, exhibit changes in respiratory mechanics, gas exchange, and lung inflammatory biomarkers that are related to the preoperative pulmonary hemodynamics. • Cardiopulmonary bypass induces alteration of lung function and epithelial lining fluid biomarkers according to preoperative hemodynamics. What is New: • Our findings can help to identify children with congenital heart disease at high risk of postoperative lung injury who may benefit of tailored intensive care strategies, such as non-invasive ventilation techniques, fluid management, and anti-inflammatory drugs that can improve cardiopulmonary interaction in the perioperative period. [ABSTRACT FROM AUTHOR]

Arterial spin labeling (ASL) magnetic resonance imaging (MRI) is an imaging methodology that uses blood as an endogenous contrast agent to quantify flow. One limitation of this method of capillary blood quantification when applied in the lung is the contribution of signals from non-capillary blood. Intensity thresholding is one approach that has been proposed for minimizing the non-capillary blood signal. This method has been tested in previous in silico modeling studies; however, it has only been tested under a restricted set of physiological conditions (supine posture and a cardiac output of 5 L/min). This study presents an in silico approach that extends previous intensity thresholding analysis to estimate the optimal "per-slice" intensity threshold value using the individual components of the simulated ASL signal (signal arising independently from capillary blood as well as pulmonary arterial and pulmonary venous blood). The aim of this study was to assess whether the threshold value should vary with slice location, posture, or cardiac output. We applied an in silico modeling approach to predict the blood flow distribution and the corresponding ASL quantification of pulmonary perfusion in multiple sagittal imaging slices. There was a significant increase in ASL signal and heterogeneity (COV = 0.90 to COV = 1.65) of ASL signals when slice location changed from lateral to medial. Heterogeneity of the ASL signal within a slice was significantly lower (P = 0.03) in prone (COV = 1.08) compared to in the supine posture (COV = 1.17). Increasing stroke volume resulted in an increase in ASL signal and conversely an increase in heart rate resulted in a decrease in ASL signal. However, when cardiac output was increased via an increase in both stroke volume and heart rate, ASL signal remained relatively constant. Despite these differences, we conclude that a threshold value of 35% provides optimal removal of large vessel signal independent of slice location, posture, and cardiac output.

The use of large animal models in the preclinical setting has expanded and become increasingly valuable for evaluating the safety and efficacy of new therapies and devices. Here, we report normal hemodynamic values, including aortic and pulmonary blood flow, in a bovine model at rest and during exercise after a control procedure. We performed a left lateral thoracotomy and implanted fluid-filled pressure lines (aortic pressure, right atrial pressure, left atrial pressure, pulmonary artery pressure) and left (systemic) and right (pulmonary) flow probe lines. Throughout the postoperative period, the calf’s physiologic pressures, vital signs, aortic and pulmonary blood flow, and pulmonary and systemic vascular resistance were recorded hourly at rest and during treadmill exercise evaluations. When pressures and flow rates at baseline and during treadmill trials were compared, we observed a physiologic response to exercise similar to that seen in humans, with a sympathetic discharge that increased systolic blood pressure. However, the rise in mean arterial pressure was much lower due to an overall decrease in vascular resistance, which increased blood flow. This study provides investigators, device engineers, and manufacturers with normal bovine cardiovascular physiology data that can be used for technical consideration during device development for preclinical trials.

Background: Pulmonary arterial hypertension, impaired cardiac function and lung hypoplasia are common in infants with congenital diaphragmatic hernia (CDH) and are associated with increased morbidity and mortality. Robust noninvasive methods to quantify these abnormalities in early infancy are lacking. Objective: To determine the feasibility of MRI to quantify cardiopulmonary hemodynamics and function in infants with CDH and to investigate left–right blood flow and lung volume discrepancies. Materials and methods: We conducted a prospective MRI study of 23 neonates (isolated left CDH: 4 pre-repair, 7 post-repair, 3 pre- and post-repair; and 9 controls) performed on a small-footprint 1.5-tesla (T) scanner. We calculated MRI-based pulmonary arterial blood flow, left ventricular eccentricity index, cardiac function and lung volume. Using the Wilcoxon rank sum test for continuous data and Fisher exact test for categorical data, we made pairwise group comparisons. Results: The right-to-left ratios for pulmonary artery blood flow and lung volume were elevated in pre-repair and post-repair CDH versus controls (flow: P<0.005; volume: P<0.05 pre−/post-repair). Eccentricity index at end-systole significantly differed between pre-repair and post-repair CDH (P<0.01) and between pre-repair CDH and controls (P<0.001). Conclusion: Cardiopulmonary MRI is a viable method to serially evaluate cardiopulmonary hemodynamics and function in critically ill infants and is useful for capturing left–right asymmetries in pulmonary blood flow and lung volume. [ABSTRACT FROM AUTHOR]

This article provides an overview of the key physiological changes that take place as the fetus transitions to neonatal life. It provides and an overview of fetal transition with a focus on respiratory and cardiovascular changes. [ABSTRACT FROM AUTHOR]

Ultrasound (US) generated by catheters used clinically for US-facilitated thrombolysis can release shear-dependent vasodilators from endothelial and red blood cells. We hypothesized that catheter-based US in the pulmonary artery (PA) decreases downstream vascular resistance and increases pulmonary blood flow. In rhesus macaques, a U.S. Food and Drug Administration-approved multi-element US catheter was placed in a pulmonary artery. Comprehensive echocardiography was performed (i) at baseline, (ii) during hypoxemia (12% FIO2) to increase pulmonary vascular resistance (PVR) and (c) 15 min after initiating US during hypoxemia. Reduced FIO2 produced intended reductions in oxygen saturation (69 ± 3%) and PaO2 (34 ± 5 mm Hg), yet on echocardiography, hypoxemia did not create the intended model, with only modest hypoxia-related increases in PA systolic pressure (24 ± 4 to 28 ± 4 mm Hg, p = 0.05) and no significant change in PVR or multiparametric right ventricular (RV) function. Although US did not further change total PVR, on 99mTc-macroalbumin aggregate single-photon-emission computed tomography imaging, lung perfusion was significantly higher in the lung ipsilateral to the US catheter versus the contralateral control lung (133 ± 48 cpm vs. 103 ± 43 × 103 cpm, p = 0.01). We conclude that PA catheter-based US increases regional lung perfusion, most likely from vasodilators that are conducted downstream. [ABSTRACT FROM AUTHOR]

The diving reflex is an oxygen-saving mechanism which is accompanied by apnea, reflex bradycardia development, peripheral vasoconstriction, spleen erythrocyte release, and selective redistribution of blood flow to the organs most vulnerable to lack of oxygen, such as the brain, heart, and lungs. However, this is a poorly studied form of hypoxia, with a knowledge gap on physiological and biochemical adaptation mechanisms. The reflective sympathetic constriction of the resistive vessels is realized via ADRA1A. It has been shown that ADRA1A SNP (p.Arg347Cys; rs1048101) is associated with changes in tonus in vessel walls. Moreover, the Cys347 allele has been shown to regulate systolic blood pressure. The aim of this work was to evaluate whether the ADRA1A polymorphism affected the pulmonary vascular reactions in men and women in response to the diving reflex. Men (n = 52) and women (n = 50) untrained in diving aged 18 to 25 were recruited into the study. The vascular reactions and blood flow were examined by integrated rheography and rheography of the pulmonary artery. Peripheral blood circulation was registered by plethysmography. The ADRA1A gene polymorphism (p.Arg347Cys; rs1048101) was determined by PCR-RFLP. In both men and women, reflective pulmonary vasodilation did occur in response to the diving reflex, but in women this vasodilation was more pronounced and was accompanied by a higher filling of the lungs with blood.. Additionally, ADRA1A SNP (p.Arg347Cys; rs1048101) is associated with sex. Interestingly, women with the Arg347 allele demonstrated the highest vasodilation of the lung vessels. Therefore, our data may help to indicate women with the most prominent adaptive reactions to the diving reflex. Our data also indicate that women and men with the Cys allele of the ADRA1A gene polymorphism have the highest risk of developing lung hypertension in response to the diving reflex. The diving reflex is an oxygen-saving mechanism which is accompanied by apnea, reflex bradycardia development, peripheral vasoconstriction, spleen erythrocyte release, and selective redistribution of blood flow to the organs most vulnerable to lack of oxygen, such as the brain, heart, and lungs. However, this is a poorly studied form of hypoxia, with a knowledge gap on physiological and biochemical adaptation mechanisms. [ABSTRACT FROM AUTHOR]

Background: In the quantitative assessment of pulmonary blood flow, two different processing algorithms [cross-correlation calculation processing (CCC-pro) and reference frame subtraction processing (RFS-pro)] within dynamic imaging systems have been reported to exhibit high correlations with conventional measurement methods. However, reports still need to evaluate these two processing algorithms regarding the different aspects of pulmonary blood flow. This study aimed to analyze the differences in pulmonary circulation., Methods: We conducted a cross-sectional study to evaluate patients with lung cancer who underwent radical surgery, simultaneous dynamic chest radiography (DCR), and pulmonary perfusion scintigraphy (PPS). We assessed the correlation between PPS and two algorithms (CCC-pro and RFS-pro) regarding calculated blood flow ratio (BFR) using Pearson's correlation and linear regression analysis. Additionally, we evaluated consistency using the Bland-Altman analysis. We compared the pulmonary blood flow distributions across six-division lung fields and evaluated each method's blood flow images and histograms of pixel values., Results: From May 2018 to December 2020, we consecutively enrolled 46 patients with lung cancer who met the inclusion criteria (40 male patients, with a mean age of 72.91 years). In these patients, CCC-pro and RFS-pro were correlated (R=0.718, P<0.01); however, CCC-pro was more strongly correlated with PPS than RFS-pro (R=0.859, P<0.01 vs. R=0.549, P<0.01). The Bland-Altman analysis showed high agreement, although systematic errors were observed in relationships other than RFS-pro to PPS. CCC-pro and RFS-pro showed similar blood flow distributions in the upper and lower lung fields, with RFS-pro being dominant in the middle. RFS-pro showed higher pixel values in the hilar region and a histogram shape similar to PPS; however, posture affected the right upper lung field gradient. RFS-pro showed no difference in the BFR when the pulmonary artery region was symmetric; however, potential inaccuracies existed when it overlapped with the cardiovascular shadow., Conclusions: The CCC-pro algorithm was useful for quantifying BFRs, whereas the RFS-pro algorithm accurately evaluated blood flow distribution in lung fields. Further algorithm development is required to enable versatile pulmonary blood flow analysis., Competing Interests: Conflicts of Interest: The author has completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-24-152/coif). J.H. received a research grant from Konica Minolta Inc. The author has no other conflicts of interest to declare., (2024 Quantitative Imaging in Medicine and Surgery. All rights reserved.)

ObjectivesCongenital heart disease with increased pulmonary blood flow results in progressive pulmonary vascular endothelial dysfunction and associated increased perioperative morbidity. Using our ovine model of congenital heart disease with increased pulmonary blood flow, we have previously demonstrated progressive endothelial dysfunction associated with disruption in carnitine homeostasis, mitochondrial dysfunction, decreased nitric oxide signaling, and enhanced reactive oxygen species generation. However, potential alterations in these parameters in patients with congenital heart disease have not been investigated. The objective of this study was to test the hypothesis that children with increased pulmonary blood flow will have evidence of altered carnitine homeostasis, mitochondrial dysfunction, decreased nitric oxide levels, and increased reactive oxygen species generation.DesignA prospective single-center cohort study.SettingA tertiary care cardiac ICU/PICU.PatientsArterial blood samples from 18 patients with congenital heart disease associated with increased pulmonary blood flow (ventricular septal defect), 20 with congenital heart disease without increased pulmonary blood flow (tetralogy of Fallot), and 10 without heart disease (controls) were obtained.InterventionsPlasma levels of total carnitine, free carnitine, acylcarnitine, and lactate-to-pyruvate ratios, an indicator of mitochondrial function, were determined and compared. In addition, levels of superoxide and hydrogen peroxide were determined and compared in patients with ventricular septal defect and controls. Statistical analysis was performed using an unpaired t test and analysis of variance.Measurements and main resultsBaseline acylcarnitine levels (25.7 ± 13 vs 12.7 ± 8.3; p < 0.05), the acylcarnitine-to-free carnitine ratio (0.8 ± 0.1 vs 0.3 ± 0.05; p < 0.05), and the lactate-to-pyruvate ratio were higher in ventricular septal defect (27.5 ± 3.8 vs 11.1 ± 4.1, p < 0.05) than tetralogy of Fallot; there were no differences between tetralogy of Fallot and control. Superoxide and H2O2 levels were also higher in ventricular septal defect compared with controls, and NOx levels were lower in ventricular septal defect patients compared with tetralogy of Fallot and controls (p < 0.05).ConclusionsThese data suggest that increased pulmonary blood flow from ventricular septal defect results in altered carnitine and mitochondrial homeostasis, decreased nitric oxide signaling, and increased reactive oxygen species production. These data are consistent with our animal data demonstrating that altered carnitine homeostasis results in mitochondrial dysfunction, increased reactive oxygen species production, and decreased bioavailable nitric oxide. Since disruption of carnitine metabolism may contribute to endothelial dysfunction, carnitine supplementation may attenuate endothelial dysfunction associated with increased pulmonary blood flow and warrants further investigation.

Persistent pulmonary hypertension of the newborn (PPHN) is a syndrome of failed circulatory adaptation at birth due to delay or impairment in the normal fall in pulmonary vascular resistance (PVR) that occurs following birth. The fetus is in a state of physiological pulmonary hypertension. In utero, the fetus receives oxygenated blood from the placenta through the umbilical vein. At birth, following initiation of respiration, there is a sudden precipitous fall in the PVR and an increase of systemic vascular resistance (SVR) due to the removal of the placenta from circulation. There is dramatic increase in pulmonary blood flow with a decrease in, and later reversal of shunts at the foramen ovale and ductus arteriosus. The failure of this normal physiological pulmonary transition leads to the syndrome of PPHN. PPHN presents with varying degrees of hypoxemic respiratory failure. Survival of infants with PPHN has significantly improved with the use of gentle ventilation, surfactant and inhaled nitric oxide (iNO). PPHN is associated with significant mortality and morbidity among survivors. Newer agents that target different enzymatic pathways in the vascular smooth muscle are in different stages of development and testing. Further research using these agents is likely to further reduce morbidity and mortality associated with PPHN.

The distribution of pulmonary blood flow is uneven and can be described as a three-zone model, the West zones: zone 1 occurs whenever alveolar pressure exceeds arterial pressure; zone 2 when the arterial pressure is greater than alveolar but the alveolar pressure exceeds the venous pressure; and finally zone 3 when both arterial and venous pressures exceed alveolar pressure. Consequently, the blood flow is almost determined by the difference between the arterial and venous pressures in zone 3 and between arterial and alveolar pressures in zone 2 and ceases in zone 1. The understanding of this subject may be difficult to some medical students. Therefore, to improve the learning of this topic in our physiology course, we used a didactic model to demonstrate the core concept of flow down gradients and its application to pulmonary blood flow. We modeled a Starling resistor by placing a collapsible tube inside a hermetic chamber of variable pressure. Transparent turbine flowmeters were connected to the upstream and downstream extremities of the Starling resistor, and we generated a constant airflow with a brushless motor. By maintaining the input (arterial) pressure constant and varying the chamber (alveolar) pressure, we could simulate the three zones and demonstrate the resulting flow through the turbines. In conclusion, our demonstration using a Starling resistor model combined with visible turbine flowmeters can be used to facilitate comprehension of important concepts in physiology involving flow down gradients, such as pulmonary blood flow. NEW & NOTEWORTHY The understanding of respiratory physiology is a challenge to medical students. To improve the learning of pulmonary blood flow distribution through lung vessels in our physiology course, we modeled a Starling resistor model combined with visible turbine flowmeters. Our model can significantly improve the core concept of flow down gradients teaching and its application to West zones.

Restriction of fetal substrate supply has an adverse effect on surfactant maturation in the lung and thus affects the transition from in utero placental oxygenation to pulmonary ventilation ex utero. The effects on surfactant maturation are mediated by alteration in mechanisms regulating surfactant protein and phospholipid synthesis. This study aimed to determine the effects of late gestation maternal undernutrition (LGUN) and LGUN plus fetal glucose infusion (LGUN+G) compared to Control on surfactant maturation and lung development, and the relationship with pulmonary blood flow and oxygen delivery (DO2) measured by magnetic resonance imaging (MRI) with molecules that regulate lung development. LGUN from 115 to 140 days' gestation significantly decreased fetal body weight, which was normalized by glucose infusion. LGUN and LGUN+G resulted in decreased fetal plasma glucose concentration, with no change in fetal arterial PO2 compared to control. There was no effect of LGUN and LGUN+G on the mRNA expression of surfactant proteins (SFTP) and genes regulating surfactant maturation in the fetal lung. However, blood flow in the main pulmonary artery was significantly increased in LGUN, despite no change in blood flow in the left or right pulmonary artery and DO2 to the fetal lung. There was a negative relationship between left pulmonary artery flow and DO2 to the left lung with SFTP‐B and GLUT1 mRNA expression, while their relationship with VEGFR2 was positive. These results suggest that increased pulmonary blood flow measured by MRI may have an adverse effect on surfactant maturation during fetal lung development. Key points: Maternal undernutrition during gestation alters fetal lung development by impacting surfactant maturation. However, the direction of change remains controversial.We examined the effects of maternal late gestation maternal undernutrition (LGUN) on maternal and fetal outcomes, signalling pathways involved in fetal lung development, pulmonary haemodynamics and oxygen delivery in sheep using a combination of molecular and magnetic resonance imaging (MRI) techniques.LGUN decreased fetal plasma glucose concentration without affecting arterial PO2. Surfactant maturation was not affected; however, main pulmonary artery blood flow was significantly increased in the LGUN fetuses.This is the first study to explore the relationship between in utero MRI measures of pulmonary haemodynamics and lung development. Across all treatment groups, left pulmonary artery blood flow and oxygen delivery were negatively correlated with surfactant protein B mRNA and protein expression in late gestation. [ABSTRACT FROM AUTHOR]

The diving reflex is an oxygen-saving mechanism which is accompanied by apnea, reflex bradycardia development, peripheral vasoconstriction, spleen erythrocyte release, and selective redistribution of blood flow to the organs most vulnerable to lack of oxygen, such as the brain, heart, and lungs. However, this is a poorly studied form of hypoxia, with a knowledge gap on physiological and biochemical adaptation mechanisms. The reflective sympathetic constriction of the resistive vessels is realized via ADRA1A. It has been shown that ADRA1A SNP (p.Arg347Cys; rs1048101) is associated with changes in tonus in vessel walls. Moreover, the Cys347 allele has been shown to regulate systolic blood pressure. The aim of this work was to evaluate whether the ADRA1A polymorphism affected the pulmonary vascular reactions in men and women in response to the diving reflex. Men (n = 52) and women (n = 50) untrained in diving aged 18 to 25 were recruited into the study. The vascular reactions and blood flow were examined by integrated rheography and rheography of the pulmonary artery. Peripheral blood circulation was registered by plethysmography. The ADRA1A gene polymorphism (p.Arg347Cys; rs1048101) was determined by PCR-RFLP. In both men and women, reflective pulmonary vasodilation did occur in response to the diving reflex, but in women this vasodilation was more pronounced and was accompanied by a higher filling of the lungs with blood.. Additionally, ADRA1A SNP (p.Arg347Cys; rs1048101) is associated with sex. Interestingly, women with the Arg347 allele demonstrated the highest vasodilation of the lung vessels. Therefore, our data may help to indicate women with the most prominent adaptive reactions to the diving reflex. Our data also indicate that women and men with the Cys allele of the ADRA1A gene polymorphism have the highest risk of developing lung hypertension in response to the diving reflex. The diving reflex is an oxygen-saving mechanism which is accompanied by apnea, reflex bradycardia development, peripheral vasoconstriction, spleen erythrocyte release, and selective redistribution of blood flow to the organs most vulnerable to lack of oxygen, such as the brain, heart, and lungs. However, this is a poorly studied form of hypoxia, with a knowledge gap on physiological and biochemical adaptation mechanisms.

Aim: To study the long‐term outcome after surgery for pulmonary atresia and ventricular septal defect (PA‐VSD), and to determine association between the contribution of major aorto‐pulmonary collateral arteries (MAPCAs) to the pulmonary blood flow, comorbidity and cause of death. Methods: Patients who had undergone surgery for PA‐VSD from January 1st 1994 to December 31st 2017 were studied retrospectively. Survival was cross‐checked against the Swedish National Population Register. Results: Seventy patients were identified, giving an incidence of 5.3 newborns per 100 000 live births. In 41 patients (59%) the pulmonary blood flow originated from a patent ductus arteriosus (PDA), while 29 patients (41%) had contribution of the pulmonary blood flow from MAPCAs. Extracardiac disease was found in 34 patients (49%), 16 of whom had 22q11‐microdeletion syndrome (23%). Survival at follow‐up was similar in patients with and without MAPCAs (72.4% vs. 75.6%, n.s.), with a median follow‐up time of 14.3 years (3.2–41.8 years). No difference was found in mortality in patients with or without any syndrome or extracardiac disease. Conclusion: Long‐term survival did not differ between those with and without MAPCAs and no difference in mortality was seen in patients with and without concomitant extracardiac disease or any kind of syndrome. [ABSTRACT FROM AUTHOR]

The aim of this study was to establish a neonatal rat model of decreased pulmonary blood flow (PBF) for studying pulmonary pathophysiological changes in newborn lung development with reduced PBF. Horizontal thoracotomy surgery with banding of the main pulmonary artery (PA) was performed on 30 rats in the PA banding (PAB) group and without banding on another 30 rats in the sham group within 6 h after birth. The body growth and mortality were recorded. Constriction of PA was checked by echocardiography on postnatal day 7 (P7). Lung morphology was assessed with computed tomography scanning and three-dimensional reconstruction. Histological differences of two groups were evaluated using hematoxylin and eosin (H&E) staining, Masson's trichrome staining, TdT-mediated dUTP nick-end labeling assay, and CD31 labeling with microscopic examination. PA ultrasound confirmed the establishment of constriction on P7. Relative to the sham group, the neonates' physical growth, survival fraction, and lung geometry volume were decreased in the PAB group over time (p < 0.05). Histologic appearance with reduced PBF characterized a markedly simplified alveolarization with noted lower radial alveolar count and alveolar septal thickness in the PAB group (p < 0.0001), pulmonary arteries with thinner/uneven membranous layers and smaller lumina. The deficient alveolar capillary bed, enhanced pulmonary collagen deposition, and increased apoptotic alveolar epithelium were significant in the PAB group compared to the sham group (p < 0.0001). A neonatal rat PAB model demonstrated that PBF reduction during early infancy impairs alveolarization and pulmonary microvasculature. [ABSTRACT FROM AUTHOR]

Objective: Continuous positive airway pressures (CPAP) used to assist preterm infants at birth are limited to 4–8 cmH2O due to concerns that high-CPAP may cause pulmonary overexpansion and adversely affect the cardiovascular system. We investigated the effects of high-CPAP on pulmonary (PBF) and cerebral (CBF) blood flows and jugular vein pressure (JVP) after birth in preterm lambs.Methods: Preterm lambs instrumented with flow probes and catheters were delivered at 133/146 days gestation. Lambs received low-CPAP (LCPAP: 5 cmH2O), high-CPAP (HCPAP: 15 cmH2O) or dynamic HCPAP (15 decreasing to 8 cmH2O at ~2 cmH2O/min) for up to 30 min after birth.Results: Mean PBF was lower in the LCPAP [median (Q1–Q3); 202 (48–277) mL/min, p = 0.002] compared to HCPAP [315 (221–365) mL/min] and dynamic HCPAP [327 (269–376) mL/min] lambs. CBF was similar in LCPAP [65 (37–78) mL/min], HCPAP [73 (41–106) mL/min], and dynamic HCPAP [66 (52–81) mL/min, p = 0.174] lambs. JVP was similar at CPAPs of 5 [8.0 (5.1–12.4) mmHg], 8 [9.4 (5.3–13.4) mmHg], and 15 cmH2O [8.6 (6.9–10.5) mmHg, p = 0.909]. Heart rate was lower in the LCPAP [134 (101–174) bpm; p = 0.028] compared to the HCPAP [173 (139–205)] and dynamic HCPAP [188 (161–207) bpm] groups. Ventilation or additional caffeine was required in 5/6 LCPAP, 1/6 HCPAP, and 5/7 dynamic HCPAP lambs (p = 0.082), whereas 3/6 LCPAP, but no HCPAP lambs required intubation (p = 0.041), and 1/6 LCPAP, but no HCPAP lambs developed a pneumothorax (p = 0.632).Conclusion: High-CPAP did not impede the increase in PBF at birth and supported preterm lambs without affecting CBF and JVP.

We have previously shown that acute increases in pulmonary blood flow (PBF) are limited by a compensatory increase in pulmonary vascular resistance (PVR) via an endothelin-1 (ET-1) dependent decrease in nitric oxide synthase (NOS) activity. The mechanisms underlying the reduction in NO signaling are unresolved. Thus, the purpose of this study was to elucidate mechanisms of this ET-1-NO interaction. Pulmonary arterial endothelial cells were acutely exposed to shear stress in the presence or absence of tezosentan, a combined ET(A) /ET(B) receptor antagonist. Shear increased NO(x) , eNOS phospho-Ser1177, and H(2) O(2) and decreased catalase activity; tezosentan enhanced, while ET-1 attenuated all of these changes. In addition, ET-1 increased eNOS phospho-Thr495 levels. In lambs, 4 h of increased PBF decreased H(2) O(2) , eNOS phospho-Ser1177, and NO(X) levels, and increased eNOS phospho-Thr495, phospho-catalase, and catalase activity. These changes were reversed by tezosentan. PEG-catalase reversed the positive effects of tezosentan on NO signaling. In all groups, opening the shunt resulted in a rapid increase in PBF by 30 min. In vehicle- and tezosentan/PEG-catalase lambs, PBF did not change further over the 4 h study period. PVR fell by 30 min in vehicle- and tezosentan-treated lambs, and by 60 min in tezosentan/PEG-catalase-treated lambs. In vehicle- and tezosentan/PEG-catalase lambs, PVR did not change further over the 4 h study period. In tezosentan-treated lambs, PBF continued to increase and LPVR to decrease over the 4 h study period. We conclude that acute increases in PBF are limited by an ET-1 dependent decrease in NO production via alterations in catalase activity, H(2) O(2) levels, and eNOS phosphorylation.

Introduction: Catheterisation is the gold standard used to evaluate pulmonary blood flow in patients with a Blalock-Thomas-Taussig shunt. It involves risk and cannot be performed frequently. This study aimed to evaluate if echocardiographic measurements obtained in a clinical setting correlate with catheterisation-derived pulmonary blood flow in patients with a Blalock-Thomas-Taussig shunt as the sole source of pulmonary blood flow., Methods: Chart review was performed retrospectively on consecutive patients referred to the catheterisation lab with a Blalock-Thomas-Taussig shunt. Echocardiographic parameters included peak, mean, and diastolic gradients across the Blalock-Thomas-Taussig shunt and forward and reverse velocity time integral across the distal transverse aorta. In addition to direct correlations, we tested a previously published formula for pulmonary blood flow calculated as velocity time integral across the shunt × heart rate × Blalock-Thomas-Taussig shunt area. Catheterisation parameters included pulmonary and systemic blood flow as calculated by the Fick principle., Results: 18 patients were included. The echocardiography parameters and oxygen saturation did not correlate with catheterisation-derived pulmonary blood flow, systemic blood flow, or the ratio of pulmonary to systemic blood flow. As the ratio of reverse to forward velocity time integral across the transverse aorta increased, the probability of shunt stenosis decreased., Conclusion: Echocardiographic measurements obtained outside the catheterisation lab do not correlate with catheterisation-derived pulmonary blood flow. The ratio of reverse to forward velocity time integral across the transverse aortic arch may be predictive of Blalock-Thomas-Taussig shunt narrowing; this finding should be investigated further.

Fetal lungs have fewer and smaller arteries with higher pulmonary vascular resistance (PVR) than a newborn. As gestation advances, the pulmonary circulation becomes more sensitive to changes in pulmonary arterial oxygen tension, which prepares them for the dramatic drop in PVR and increase in pulmonary blood flow (PBF) that occur when the baby takes its first few breaths of air, thus driving the transition from fetal to postnatal circulation. Dynamic and intricate regulatory mechanisms control PBF throughout development and are essential in supporting gas exchange after birth. Understanding these concepts is crucial given the role the pulmonary vasculature plays in the development of complications with transition, such as in the setting of persistent pulmonary hypertension of the newborn and congenital heart disease. An improved understanding of pulmonary vascular regulation may reveal opportunities for better clinical management., Competing Interests: Disclosure The authors have nothing to disclose., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Background: Quantitative assessment of pulmonary blood flow and visualization of its temporal and spatial distribution without contrast media is of clinical significance. Purpose: To assess the potential of electrocardiogram (ECG)‐triggered pseudocontinuous arterial spin labeling (PCASL) imaging with balanced steady‐state free‐precession (bSSFP) readout to measure lung perfusion under free‐breathing (FB) conditions and to study temporal and spatial characteristics of pulmonary blood flow. Study Type: Prospective, observational. Subjects: Fourteen volunteers; three patients with pulmonary embolism. Field Strength/Sequences: 1.5T, PCASL‐bSSFP. Assessment: The pulmonary trunk was labeled during systole. The following examinations were performed: 1) FB and timed breath‐hold (TBH) examinations with a postlabeling delay (PLD) of 1000 msec, and 2) TBH examinations with multiple PLDs (100–1500 msec). Scan–rescan measurements were performed in four volunteers and one patient. Images were registered and the perfusion was evaluated in large vessels, small vessels, and parenchyma. Mean structural similarity indices (MSSIM) was computed and time‐to‐peak (TTP) of parenchymal perfusion in multiple PLDs was evaluated. Image quality reading was performed with three independent blinded readers. Statistical Tests: Wilcoxon test to compare MSSIM, perfusion, and Likert scores. Spearman's correlation to correlate TTP and cardiac cycle duration. The repeatability coefficient (RC) and within‐subject coefficient of variation (wCV) for scan–rescan measurements. Intraclass correlation coefficient (ICC) for interreader agreement. Results: Image registration resulted in a significant (P < 0.05) increase of MSSIM. FB perfusion values were 6% higher than TBH (3.28 ± 1.09 vs. 3.10 ± 0.99 mL/min/mL). TTP was highly correlated with individuals' cardiac cycle duration (Spearman = 0.89, P < 0.001). RC and wCV were better for TBH than FB (0.13–0.19 vs. 0.47–1.54 mL/min/mL; 6–7 vs. 19–60%). Image quality was rated very good, with ICCs 0.71–0.89. Data Conclusion: ECG‐triggered PCASL‐bSSFP imaging of the lung at 1.5T can provide very good image quality and quantitative perfusion maps even under FB. The course of labeled blood through the lung shows a strong dependence on the individuals' cardiac cycle duration. Level of Evidence: 2 Technical Efficacy Stage: 2 J. MAGN. RESON. IMAGING 2020;52:1767–1782. [ABSTRACT FROM AUTHOR]