Neonates who experience respiratory failure despite maximal ventilatory support have only extracorporeal membrane oxygenation as a rescue therapy, but it has very poor outcomes as a bridge to ...transplantation. A pumpless lung-assist device has been used in adults as a bridge to lung transplantation. An alternative membrane oxygenator, the Quadrox iD, is a suitable size for neonatal blood flow. Here we report the use of the Quadrox iD membrane oxygenator with central cannulation as a paracorporeal respiratory support therapy for a neonate with alveolar capillary dysplasia awaiting lung transplantation.
Background The purpose of this study was to identify factors predicting risk of aortic arch recoarctation after the Norwood procedure. Methods Patient records were reviewed retrospectively for ...consecutive patients who underwent the Norwood procedure from 1996 to 2005. Preoperative and intraoperative parameters were identified for analysis. Aortic arch recoarctation was defined by the need for catheter or surgical reintervention. Data were analyzed using survival analysis, with freedom from intervention as the outcome. Factors predicting need for reintervention were analyzed using Cox proportional hazards regression. Results Thirty-five recoarctations were observed in 117 patients (30%). Freedom from aortic arch reintervention at six months, one, three, and five years were 72%, 63%, 56%, and 52%, respectively. The majority of arch reinterventions occurred in the first six months (63%), involving either surgical (43%) or catheter (57%) techniques. The use of bovine pericardium showed the greatest risk for potential recoarctation (hazard ratio = 1.81 0.90–3.64, p = 0.09). Age, gender, weight, ascending aortic diameter, ventricular morphology, primary anatomic diagnosis, and coarctation shelf resection were not found to be predictors of recoarctation. Conclusions Most interventions for aortic arch recoarctation after the Norwood procedure occur within the first six months of life. The type of patch material used for arch reconstruction appears to influence, most strongly, the long-term risk of aortic arch recoarctation.
Dynamic fluid shifts induced by fetal bypass Baker, R. Scott, BS; Lam, Christopher T., BS; Heeb, Emily A ...
The Journal of thoracic and cardiovascular surgery,
03/2009, Letnik:
137, Številka:
3
Journal Article
Recenzirano
Odprti dostop
Objective Fluid shifts have been suggested to occur with fetal bypass. The degree or mechanisms behind these volume changes (or location) have not been defined. We characterized the preceding and ...correlated the findings to plasma vasopressin concentrations, the critical peptide of osmoregulation. Methods Seventeen ovine fetuses (105–111 days' gestation) were started on bypass and followed 2 hours after bypass. Hemodynamics and volume replacements needed to maintain minimum reservoir volume during bypass and normal physiologic parameters after bypass were recorded. Serial blood samples were collected to assess gas exchange and vasopressin levels. Changes in total tissue water content were measured for several organs and the placenta. Plasma volume, fluid shifts, and osmolarity were calculated. Results Hematocrit values decreased by 15 minutes of bypass to 28% from 33% and then increased to 34% by 120 minutes after bypass, corresponding to a decreased fetal plasma volume of 79 to 72 mL/kg by 120 minutes after bypass. The majority of volume shifts (approximately 100 mL/kg) occurred during bypass, but additional volume replacements were required after bypass to maintain normal hemodynamics, resulting in overall losses of 0.8 mL · kg−1 · min−1 . Losses were not accounted for by placental or organ edema. Vasopressin levels increased dramatically with bypass (39–51.5 pg/mL) and were strongly predicted by increased fetal plasma volumes ( R2 = 0.90), whereas osmolarity was not significantly associated with plasma volumes. Conclusion Fetal bypass leads to significant fluid shifts that correlate strongly with increasing vasopressin levels (but not changes in osmolarity). The placenta is not the primary site of volume loss. Rehydration of the fetus is necessary after bypass.
Fetal Stress Response to Fetal Cardiac Surgery Lam, Christopher T., BS; Sharma, Samar, BS; Baker, R. Scott, BS ...
The Annals of thoracic surgery,
05/2008, Letnik:
85, Številka:
5
Journal Article
Recenzirano
Background A deleterious fetal stress response, although not fully elucidated, may account for poor outcomes after experimental fetal cardiac surgery. We set out to characterize this fetal stress ...response and its potential role in placental dysfunction. Methods Fifteen ovine fetuses at gestational day 100 to 114 were placed on extracorporeal support for 30 minutes and were then followed 2 hours after cardiopulmonary bypass. Fetal plasma samples were analyzed for vasopressin, cortisol, and β-endorphin levels, and correlated to fetal hemodynamics and placental gas exchange. Results Unique temporal patterns of response were seen in release of the three stress hormones. Vasopressin demonstrated the most profound and early response followed by cortisol and β-endorphin, the latter continuing to rise in the post-bypass period. A sharp rise in fetal mean arterial pressure and placental vascular resistance strongly correlated with rising vasopressin levels. Post-bypass deterioration of fetal gas exchange and hemodynamics correlated with the ensuing rise in cortisol and β-endorphin. Rising fetal lactate levels correlated with elevations in all three stress hormones. Conclusions Fetal cardiopulmonary bypass leads to a profound, early rise in vasopressin concentrations that strongly correlates with placental dysfunction after fetal bypass. Vasopressin may play an important mechanistic role in pathogenesis of this placental dysfunction.
Background Mechanisms leading to left ventricular hypoplasia and endocardial fibroelastosis in the fetus remain unknown. Prevailing theory is that obstruction to blood flow through the left ventricle ...leads to elevated end-diastolic pressures, compromised myocardial perfusion, and endocardial ischemia. Fetal interventions are now being performed, based on the presumption that they would prevent such pathogenic mechanisms. Methods Forty first-trimester fetal sheep (mean gestational age, 53 days) were studied. Severe fetal left ventricular outflow obstruction was created by banding the ascending aorta in 25 fetuses; 15 control fetuses underwent “sham” surgery with thoracotomy. Serial fetal echocardiography was used to assess left ventricular growth and fetal hemodynamics. Findings were correlated to morphologic and histopathologic changes, and intracardiac pressure measurements obtained from fetal cardiac catheterization. Results Surviving banded fetuses (n = 13) had one of two phenotypes: compensatory left ventricular hypertrophy (n = 7) or noncompensatory left ventricular dilatation (n = 6) with hydrops and severe left ventricular dysfunction. All fetuses had elevated left ventricular end-diastolic pressures (mean, 21 mm Hg; range, 14 to 28 mm Hg), which correlated to the gradient across the ascending aorta (mean, 41 mm Hg; range, 28 to 73 mm Hg). In vivo echocardiography findings were incongruous with those at autopsy, and demonstrated preservation of left ventricular growth indices in all fetuses. Endocardial fibroelastosis and myocardial fibrosis were not observed in any banded fetus. Conclusions While early gestational obstruction to flow can compromise left ventricular function in the fetus, it does not retard normal growth. Similarly, an elevated left ventricular end-diastolic pressure is not sufficient to cause myocardial fibrosis or endocardial fibroelastosis in the fetus.
Objective Natriuretic peptides, especially brain natriuretic peptide (BNP), have demonstrated great usefulness in pediatric and adult cardiology. We studied their usefulness, based on amniotic fluid ...concentrations, in an ovine model of fetal aortic stenosis and in response to fetal cardiac intervention. Study Design After their natural history was established with gestation (n = 18 fetuses), natriuretic peptide levels were measured in a fetal model of aortic stenosis (50-60 days; term, 148 days; n = 9) and were correlated to the severity of fetal heart disease. Response to fetal cardiac intervention in 3 hydropic fetuses was also assessed. Significance was established with 2-sided paired t -tests at a probability value of <.05. Results Amniotic fluid BNP (but not atrial natriuretic peptide) concentrations were elevated significantly with aortic stenosis (181.9 ± 109.9 pg/mL vs 50.0 ± 40.5 pg/mL in control fetuses), especially if complicated with hydrops (283 ± 74.4 pg/mL), and were correlated positively with the severity of stenosis and left ventricle hypertrophy. In the 1 animal surviving fetal intervention, BNP levels normalized. Conclusion Amniotic fluid BNP concentrations correlate with the severity of fetal aortic stenosis.
Background We previously showed cyclic guanosine 3',5'-monophosphate (cGMP) levels increase with fetal cardiac bypass despite derangements in the placental nitric oxide pathway. The natriuretic ...peptides, atrial (ANP), brain (BNP), and c-type (CNP), are common indicators of cardiac distress, and an alternative pathway for cGMP generation. We hypothesized that these natriuretic peptides may account for the paradoxic rise in cGMP seen with fetal bypass. Methods Six ovine fetuses, 106 to 118 days' gestation, underwent cardiac bypass for 30 minutes and were followed for 120 minutes after bypass. Fetal plasma samples were collected before bypass, during bypass, and 30 and 120 minutes after bypass for natriuretic peptide analysis. Results were compared with 6 sham bypass fetuses and cGMP values from another 14 bypass fetuses (to avoid confounding effects of excess blood sampling). Fetal hemodynamics and metabolics were correlated to ANP, BNP, and CNP values. Statistical analysis was by analysis of variance, Student′s t test, and best-fit correlations, with significance set at p = 0.05 or less. Results The ANP, BNP, and CNP increased with fetal bypass (674 ± 133 pg/mL, 151 ± 52 pg/mL, and 295 ± 45 pg/mL, respectively), remaining elevated after bypass, whereas sham concentrations remained stable at pre-bypass levels. Changes in ANP, BNP, and CNP positively correlated with rising cGMP. There was positive correlation between ANP and CNP and rising fetal lactate levels, but not to other physiologic parameters associated with placental dysfunction. Conclusions There is a substantial rise in natriuretic peptides seen with fetal bypass, likely in part a reflection of myocardial dysfunction. Further, the natriuretic peptide pathway may account for the paradoxic rise in cGMP seen with fetal bypass.
Background The etiology of placental dysfunction after fetal cardiopulmonary bypass remains unknown. The placental nitric oxide (NO) pathway has been implicated in this pathophysiology. We set out to ...examine possible perturbations in this pathway in an ovine model of fetal bypass. Methods Ovine fetuses (n = 14) between 100 and 114 days of gestation, instrumented to measure hemodynamics and umbilical blood flow, were placed on bypass for 30 minutes and followed after bypass for 2 hours. Sham controls (n = 6) were instrumented but did not undergo bypass. Real-time, in-vivo NO concentrations were measured in the placental circulation. To examine other components of the NO pathway, fetal plasma samples were analyzed by immunoassays for total NO metabolite and cyclic guanosine 3′,5′–cyclic monophosphate (cGMP) levels. In addition, the expression of phosphodiesterase-5 was examined in placenta by immunohistochemistry. Statistical analysis was performed using analysis of variance with least significant difference post hoc tests ( p ≤ 0.05). Results With the onset of bypass, an immediate increase occurs in umbilical NO concentrations. These return to baseline with cessation of bypass, and decline thereafter. In contrast, there was a linear increase in fetal plasma cGMP levels and a decline in NO metabolite concentrations through the post-bypass period. There was a dramatic increase in placental phosphodiesterase-5 expression with 30 minutes of bypass. The changes occur simultaneously with decreasing umbilical flows, increased placental vascular resistance, and worsening placental gas exchange. Conclusions Fetal bypass leads to significant reductions in placental NO concentrations despite increases in fetal plasma cGMP and placental phosphodiesterase-5 levels, indicative of perturbations in the fetal-placental NO pathway.
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