Total Pulmonary Volume Research Articles

Antenatal Assessment of the Prognosis of Congenital Diaphragmatic Hernia: Ethical Considerations and Impact for the Management.

Congenital diaphragmatic hernia (CDH) is associated with abnormal pulmonary development, which is responsible for pulmonary hypoplasia with structural and functional abnormalities in pulmonary circulation, leading to the failure of the cardiorespiratory adaptation at birth. Despite improvement in treatment options and advances in neonatal care, mortality remains high, at close to 15 to 30%. Several risk factors of mortality and morbidities have been validated in fetuses with CDH. Antenatal assessment of lung volume is a reliable way to predict the severity of CDH. The two most commonly used measurements are the observed/expected lung to head ratio (LHRo/e) and the total pulmonary volume (TPV) on MRI. The estimation of total pulmonary volume (TPVo/e) by means of prenatal MRI remains the gold standard. In addition to LHR and TPV measurements, the position of the liver (up, in the thorax or down, in the abdomen) also plays a role in the prognostic evaluation. This prenatal prognostic evaluation can be used to select fetuses for antenatal surgery, consisting of fetoscopic endoluminal tracheal occlusion (FETO). The antenatal criteria of severe CDH with an ascended liver (LHRo/e or TPVo/e < 25%) are undoubtedly associated with a high risk of death or significant morbidity. However, despite the possibility of estimating the risk in antenatal care, it is difficult to determine what is in the child’s best interest, as there still are many uncertainties: (1) uncertainty about individual short-term prognosis; (2) uncertainty about long-term prognosis; and (3) uncertainty about the subsequent quality of life, especially when it is known that, with a similar degree of disability, a child’s quality of life varies from poor to good depending on multiple factors, including family support. Nevertheless, as the LHR decreases, the foreseeable “burden” becomes increasingly significant, and the expected benefit is increasingly unlikely. The legal and moral principle of the proportionality of medical procedures, as well as the prohibition of “unreasonable obstinacy” in all investigations or treatments undertaken, is necessary in these situations. However, the scientific and rational basis for assessing the long-term individual prognosis is limited to statistical data that do not adequately reflect individual risk. The risk of self-fulfilling prophecies should be kept in mind. The information given to parents must take this uncertainty into account when deciding on the treatment plan after birth.

Computed Tomography in Pulmonary Evaluation of Children with Acyanotic Congenital Heart Defect and Pulmonary Hyperflow

Respiratory dysfunction is common in children with acyanotic congenital heart defects (ACHD) with pulmonary hyperflow; however, little is known about the pulmonary structure of those patients. The objective of this study was to quantify the volumes of air and tissue, as well as the distribution of pulmonary aeration in this population. After approval by the Ethics Committee of the institution and signing of an informed consent, seven children with ACHD with pulmonary hyperflow underwent computed tomographies of the chest. All images included the left and right pulmonary contour, and pulmonary volumes and weight were calculated using volumetric data. Paired Student t test was used to compare left and right, and exponential regression was used for correlations. Patients had a mean age of 20 months and weight of 9.9 kg. Total pulmonary volume (TPV) was 66.7 +/- 23.1 mL.kg-1, tissue volume of 33.5 +/- 15.7 mL.kg-1, and air volume of 33.1 +/- 8.3 mL.kg-1. The right lung represented 57.9% of TPV and the left, 42.1% (p < 0.001). The pulmonary volume of air on the right was 60.5% of the total air volume (p < 0.001), and the volume of pulmonary parenchyma normally aerated was significantly lower on the left (27.6 +/- 6.8 vs . 18.1 +/- 8%, p < 0.001). The volume of lung tissue was greater than expected in children with ACHD with pulmonary hyperflow, possibly due to interstitial edema. Pulmonary aeration is reduced in the left lung due to the compression of the lung by the heart.

Pulmonary red cell and plasma volumes and pulmonary hematocrit in the normal dog.

Cr51-labeled red cells and Evans blue dye were used to measure cardiac output, circulating pulmonary and total red cell volumes, plasma volumes and resultant pulmonary and body hematocrits in nembutalized dogs. The pulmonary blood volumes were measured simultaneously by the mean circulation time-output, slope output and arteriovenous equilibration methods and averaged 210, 136 and 151 cc/10 kg, respectively, representing 28.6, 18.7 and 20.4% of the total blood volume. Pulmonary hematocrits averaged 37.6, 36.8 and 33.5%, respectively, compared to mean large vessel hematocrit of 39.7%. Total blood volume averaged 736 cc/10 kg. The mean of the ratios of body to large vessel hematocrit was .92. Cardiac outputs determined from plasma and red cell indicator dilution curves were in good agreement. The mean circulation time of red cells was consistently shorter and the exponential washout slope consistently steeper than of plasma. These differences resulted in a larger calculated total pulmonary volume by the mean circulation time and slope output methods using a plasma compared with a red cell tag; the resultant pulmonary hematocrits were significantly lower than large vessel hematocrits. The pulmonary hematocrits determined by the arteriovenous equilibration method were still lower than those calculated with the other methods. The explanation of this is uncertain. The demonstration by all three methods of a pulmonary hematocrit significantly lower than large vessel hematocrit indicates that the pulmonary bed participates in the lowering by capillary blood of large vessel hematocrit.