scholarly journals Isolated Major Aortopulmonary Collateral as the Sole Pulmonary Blood Supply to an Entire Lung Segment

2017 ◽  
Vol 2017 ◽  
pp. 1-3
Author(s):  
Hannah S. Kim ◽  
R. Mark Grady ◽  
Shabana Shahanavaz

Congenital systemic-to-pulmonary collateral arteries or major aortopulmonary collaterals are associated with cyanotic congenital heart disease with decreased pulmonary blood flow. Though it is usually associated with congenital heart diseases, there is an increased incidence of isolated acquired aortopulmonary collaterals in premature infants with chronic lung disease. Interestingly, isolated congenital aortopulmonary collaterals can occur without any lung disease, which may cause congestive heart failure and require closure. We present a neonate with an echocardiogram that showed only left-sided heart dilation. Further workup with a CT angiogram demonstrated an anomalous systemic artery from the descending thoracic aorta supplying the left lower lobe. He eventually developed heart failure symptoms and was taken to the catheterization laboratory for closure of the collateral. However, with the collateral being the only source of blood flow to the entire left lower lobe, he required surgical unifocalization. Isolated aortopulmonary collaterals without any other congenital heart disease or lung disease are rare. Our patient is the first reported case to have an isolated aortopulmonary collateral being the sole pulmonary blood supply to an entire lung segment. Due to its rarity, there is still much to learn about the origin and development of these collaterals that possibly developed prenatally.

1999 ◽  
Vol 9 (2) ◽  
pp. 141-149 ◽  
Author(s):  
Henrik Holmström ◽  
Christian Hall ◽  
Oddvar Stokke ◽  
Harald Lindberg ◽  
Erik Thaulow

AbstractWe postulated previously that variables related to pulmonary flow are independent predictors of levels of atrial natriuretic peptide in children with congenital heart disease. The aim of this study was to test this hypothesis in relation to other hemodynamic and clinical variables.During catheterization we measured the levels of plasma N-terminal atrial natriuretic peptide prohormone in the plasma of 68 children with congenital heart disease. All had undergone complete clinical, echocardiographic and invasive hemodynamic investigations. The influence on the prohormone was analyzed for 10 different variables in a multiple linear regression model. The variability could be explained in large parts (adjusted R2 = 77.2%) by variations in atrial pressures or sizes, together with the degree of excessive pulmonary blood flow and signs of heart failure.A value for atrial natriuretic peptide prohormone above 800 pmol/1 predicted hemodynamic imbalance (defined as elevated pressures in left or right atrium or the pulmonary arteries, and/or Qp/Qs > 1.5) with a specificity of 94%, a sensitivity of 73%, a positive likelihood ratio of 12.2, and a negative likelihood ratio of 0.29.In conclusion, variables related to pulmonary blood flow are influential determinants of the levels of atrial natriureic peptide in children with congenital heart disease. Atrial pressures, and symptoms of heart failure are also of major importance.


2009 ◽  
Vol 25 (1) ◽  
pp. 167-172 ◽  
Author(s):  
Lv Guorong ◽  
Li Shaohui ◽  
Jin Peng ◽  
Lin Huitong ◽  
Li Boyi ◽  
...  

2021 ◽  
Vol 12 (2) ◽  
pp. 213-219
Author(s):  
R. Allen Ligon ◽  
Larry A. Latson ◽  
Mark M. Ruzmetov ◽  
Kak-Chen Chan ◽  
Immanuel I. Turner ◽  
...  

Background: Surgical pulmonary artery banding (PAB) has been limited in practice because of later requirement for surgical removal or adjustment. The aim of this study is to describe our experience creating a dilatable PAB via transcatheter balloon dilation (TCBD) in congenital heart disease (CHD) patients. Methods: Retrospective chart review of adjustable PAB—outline anatomical variants palliated and patient outcomes. Results: Sixteen patients underwent dilatable PAB—median age 52 days (range 4-215) and weight 3.12 kg (1.65-5.8). Seven (44%) of the patients were premature, 11 (69%) had ventricular septal defect(s) with pulmonary over-circulation, four (25%) atrioventricular septal defects, and four (25%) single ventricle physiology. Subsequent to the index procedure: five patients have undergone intracardiac complete repair, six patients remain well palliated with no additional intervention, and four single ventricles await their next palliation. One patient died from necrotizing enterocolitis (unrelated to PAB) and one patient required a pericardiocentesis postoperatively. Five patients underwent TCBD of the PAB without complication—Two had one TCBD, two had two TCBD, and another had three TCBD. The median change in saturation was 14% (complete range 6-22) and PAB diameter 1.7 mm (complete range 1.1-5.2). Median time from PAB to most recent outpatient follow-up was 868 days (interquartile range 190-1,079). Conclusions: Our institution has standardized a PAB technique that allows for transcatheter incremental increases in pulmonary blood flow over time. This methodology has proven safe and effective enough to supplant other institutional techniques of limiting pulmonary blood flow in most patients—allowing for interval growth or even serving as the definitive palliation.


2018 ◽  
pp. 1-6

Background: Hypocapnia is suggested in decreasing pulmonary vascular resistance in cyanotic congenital heart disease patients undergoing definitive repair. But its effects on cerebral and renal circulation are unclear. Hence the effect of changes in arterial blood carbon dioxide tensions (PaCo2 ) on cerebral (ScO2 %) and renal (SsO2 %) oxygenation indices using Near Infrared spectroscopy (NIRS) is examined. Methods: We did a prospective observational study in sixty-eight children who underwent elective cardiac surgery for various cyanotic congenital heart diseases. PaCo2 , ScO2 % and SsO2 % were obtained before induction of anesthesia, after anesthesia induction at normocapnic or mild hypercapnic ventilation (EtCo2 =40 mmHg) and again at hypocapnic ventilation (EtCo2 =30 mmHg). Regression analysis was done between PaCo2 and NIRS-C/ScO2 % and PaCo2 and NIRS-R/SsO2 % at both EtCo2 40 and 30 mmHg. Repeated measure analysis performed to evaluate the significance of change in NIRS-C and NIRS-R from pre-anesthesia induction to when EtCo2 was 40 and then 30 mmHg post anesthesia induction. Results: With decrease in EtCo2 , PaCo2 (p=0.0001), NIRS-C (p=0.0001) and NIRS-R (p=0.0001) decreased significantly. At EtCo2 of 40 and 30 mmHg, PaCo2 had significant positive correlation with NIRS-C (R2 =0.77, p=0.0001 and R2 =0.92, p=0.0001 respectively) and had insignificant correlation with NIRS-R (R2 =0.03, p=0.12 and R2 =0.008, p=0.46 respectively). Significant changes in NIRS-C {p=0.0001} and NIRS-R {p=0.0001} occurred from pre-induction to when EtCo2 was 40 and then to 30 mmHg. Conclusion: A decrease in NIRS-C and NIRS-R is probably from decreased cerebral and splanchnic blood flow during hypocapnic ventilation, leading to demand supply mismatch. Hypocapnic ventilation in cyanotic children has potential to cause cerebral hypoxia. Abbreviations: CCHD: Cyanotic Congenital Heart Disease; QP: Pulmonary blood flow; Do2 : Oxygen delivery; SpO2 : peripheral pulse oximetry; NIRS: Near Infrared Spectroscopy; NIRS-C/ScO2 %: Regional Cerebral Oxygen saturation; NIRS-R/SsO2 %: Regional Somatic/renal Oxygen saturation; HCT: Hematocrit; ECG: Electrocardiography; CPB: cardiopulmonary bypass; TOF: Tetralogy of fallot; BDG: Bidirectional Glenn Shunt; BT shunt: Blalock Taussig shunt; DORV: Double outlet right ventricle; FiO2 : Inspired oxygen concentration; ABG: Arterial blood gas; PaO2 : Arterial oxygen partial pressure; PaCo2 : Arterial carbon dioxide partial pressure; HR: Heart rate; MAP: Mean Arterial Pressure; CVP: Central Venous Pressure


PEDIATRICS ◽  
1954 ◽  
Vol 14 (2) ◽  
pp. 117-121
Author(s):  
ROBERT W. WINTERS ◽  
SAUL J. ROBINSON ◽  
GEORGE BATES

A case of multiple hemangiomata of the liver is reported in an infant who presented signs and symptoms strongly suggesting congenital heart disease. The post mortem examination revealed no gross anomalies of the heart or great vessels, but did show a heart with cardiac hypertrophy. A mechanism to explain the cardiac failure in this case is discussed.


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