VACTERL/VATER Association

Congenitally corrected transposition is a rare cardiac malformation characterized by the combination of discordant atrioventricular and ventriculo-arterial connections, usually accompanied by other cardiovascular malformations. Incidence has been reported to be around 1/33,000 live births, accounting for approximately 0.05% of congenital heart malformations. Associated malformations may include interventricular communications, obstructions of the outlet from the morphologically left ventricle, and anomalies of the tricuspid valve. The clinical picture and age of onset depend on the associated malformations, with bradycardia, a single loud second heart sound and a heart murmur being the most common manifestations. In the rare cases where there are no associated malformations, congenitally corrected transposition can lead to progressive atrioventricular valvar regurgitation and failure of the systemic ventricle. The diagnosis can also be made late in life when the patient presents with complete heart block or cardiac failure. The etiology of congenitally corrected transposition is currently unknown, and with an increase in incidence among families with previous cases of congenitally corrected transposition reported. Diagnosis can be made by fetal echocardiography, but is more commonly made postnatally with a combination of clinical signs and echocardiography. The anatomical delineation can be further assessed by magnetic resonance imaging and catheterization. The differential diagnosis is centred on the assessing if the patient is presenting with isolated malformations, or as part of a spectrum. Surgical management consists of repair of the associated malformations, or redirection of the systemic and pulmonary venous return associated with an arterial switch procedure, the so-called double switch approach. Prognosis is defined by the associated malformations, and on the timing and approach to palliative surgical care.     

Hemodynamic effects of postpulmonary administration of prostaglandin D2 in fetal animals

Dose-response relationships in pulmonary vascular resistance (PVR), mean systemic arterial pressure (SAP), and heart rate (HR) to left atrial administration of prostaglandin D2 (PGD2) were determined in five fetal lambs. Fetuses were delivered by cesarean section from chloralose anesthetized ewes with the umbilical circulation maintained intact. Fetuses were prevented from breathing thus maintaining pulmonary vascular tone in the elevated fetal state. Blood was withdrawn from the inferior vena cava and pumped at constant flow into the lower left lobe of the fetal lung. Postpulmonary infusions of PGD2 brought about dose-dependent decreases in pulmonary vascular resistance. Heart rate tended to increase in fetal lambs. Mean systemic arterial pressure increased in the fetal lambs at all doses tested except for the largest dose (44.14 micrograms/kg X min), which produced slight hypotension. These data demonstrate that exposure to the systemic circulation prior to entering the pulmonary vasculature does not alter the preferential dilator action of PGD2 on fetal pulmonary vessels nor does it produce significant systemic hypotension.     

Shifts in the heart left ventricle function in patients with pulmonary tuberculosis during adequate chemotherapy

To investigate the hemodynamics and myocardic contraction of the heart left ventricle, 61 patients with pulmonary tuberculosis (main group) and 26 healthy subjects (control group) were observed. Higher ultimate systolic and diasystolic volumes of the left ventricle and lower levels of the efflux fraction in the patients with active pulmonary tuberculosis were stated. There was shown inverse correlation of the systemic systolic arterial pressure and the left ventricle efflux fraction with ESR, evident of the tuberculosis intoxication. The most pronounced aggravation of the left ventricle function was recorded in the patients with the most severe tuberculosis process. The impairments in the left ventricle in the patients with active pulmonary tuberculosis were of functional nature. Due to intensive therapy of the tuberculosis, the indices of the left ventricle efflux function improved and the systemic arterial pressure came to normal, along with elimination of the tuberculosis intoxication signs.     

Anomalous origin of the left coronary artery from the pulmonary artery treated by palliative Vineberg operation in an infant

Anomalous origin of the left coronary artery from the pulmonary artery was diagnosed in an infant girl who had evidence of transmural myocardial infarction of the free wall of the left ventricle. At age 13 months, she underwent a palliative left Vineberg implant, and remained asymptomatic until she was 8 years of age. At that time, she underwent suturing of the left coronary ostium for obliteration of the left coronary shunt at the pulmonary artery. At age 13, she underwent aortocoronary bypass to the left main coronary artery, with end-to-end anastomosis. The patient remains asymptomatic to date. We believe that this is the first reported case of a Vineberg operation performed in an infant for palliation of an anomalous left coronary artery originating from the pulmonary artery. This method allows time for the development of collateral circulation to the left coronary artery before definitive surgery is performed.     

Pulmonary arterial distension does not cause pulmonary vasoconstriction

Distension of the main pulmonary artery or its major branches with an intraluminal balloon has been reported to cause pulmonary vasoconstriction by an unknown mechanism. This study was an attempt to confirm the pressor response and explore its cause. Several balloon distension methods were tried and discarded because they caused unintentional obstruction. Ultimately, I inflated a balloon placed retrogradely and confined to the left main pulmonary artery of six anesthetized open-chest dogs after ligating left lobar arterial branches. Blood flow and systemic gas composition were controlled by interposing an external pump oxygenator between the left ventricle and aorta. Pressures in the aorta, main pulmonary artery, and left atrium were recorded. Alveolar hypoxia was used as an independent test of pulmonary vasoreactivity. Although hypoxic pressor responses occurred, challenges with arterial distension did not change lung perfusion pressure. Silicone rubber casts were made of the arteries of six dogs used in pilot experiments. These revealed the limited lengths in which distenders can be placed without unintentional encroachment on flow. I could not support the conclusion that arterial distension causes vasoconstriction and am suspicious that the perfusion pressure increases reported by others may have been caused by undetected obstruction of a major arterial branch.     

Comparison of haemodynamic responses to dopamine and salbutamol in severe cardiogenic shock complicating acute myocardial infarction.

Twelve patients with severe persistent cardiogenic shock complicating acute myocardial infarction underwent single crossover treatment with intravenous dopamine and salbutamol to determine the more beneficial therapy. Salbutamol (10 to 40 microgram/min) reduced systemic vascular resistance and progressively increased both cardiac index and stroke index. Heart rate increased from 95 to 104 beats/min. Changes in mean arterial pressure and pulmonary artery end-diastolic pressure were small and insignificant. Dopamine infusion at rates of 200 and 400 micrograms/min also increased cardiac index and stroke index. Systemic vascular resistance fell slightly but mean arterial pressure rose from 57 to 65 mm Hg. Heart rate increased from 95 to 105 beats/min. Changes in pulmonary artery end-diastolic pressure were again small and insignificant. Dopamine infusion at 800 micrograms/min caused an appreciable increase in systemic vascular resistance; a further increment in mean arterial pressure was observed, though cardiac index fell slightly. Heart rate and pulmonary artery end-diastolic pressure rose steeply. Salbutamol, a vasodilator, increased cardiac output in patients with cardiogenic shock complicating acute myocardial infarction but did not influence blood pressure. If correction of hypotension is essential dopamine in low doses may be the preferred agent. Doses of 800 microgram/min, which is within the therapeutic range, worsen other manifestations of left ventricular dysfunction.     

Pulmonary circulation in embolic pulmonary edema

The ultrasonic method was used in acute experiments on cats with open chest under artificial lung ventilation to obtain blood flow in low-lobar pulmonary artery and vein, the blood pressure in pulmonary artery, as well as the left atrial pressure in fat (olive oil) and mechanical (Lycopodium spores) pulmonary embolism. It is shown that pulmonary embolism produces the decrease in the blood flow in pulmonary artery and vein, the increase of the pressure in pulmonary artery and left atria, the increase of lung vessels resistance. The decrease is observed of systemic arterial pressure, bradycardia, and extrasystole. After 5-10 min the restoration of arterial pressure and heart rhythm occur and partial restoration of blood flow in pulmonary artery and vein. In many experiments the blood flow in vein outdoes that in the artery--it allows to suppose the increase of the blood flow in bronchial artery. After 60-90 min there occur sudden decrease of systemic arterial pressure, the decrease of the blood flow in pulmonary artery and vein. The pressure in pulmonary artery and resistance of pulmonary vessels remain high. Pulmonary edema developed in all animals. The death occurs in 60-100 min after the beginning of embolism.     

Acute and chronic cardiovascular effects of intermittent hypoxia in C57BL/6J mice.

We investigated the effects of 1) acute hypoxia and 2) 5 wk of chronic intermittent hypoxia (IH) on the systemic and pulmonary circulations of C57BL/6J mice. Mice were chronically instrumented with either femoral artery or right ventricular catheters. In response to acute hypoxia (4 min of 10% O2; n = 6), systemic arterial blood pressure fell (P < 0.005) from 107.7 +/- 2.5 to 84.7 +/- 6.5 mmHg, whereas right ventricular pressure increased (P < 0.005) from 11.7 +/- 0.8 to 14.9 +/- 1.3 mmHg. Another cohort of mice was then exposed to IH for 5 wk (O2 nadir = 5%, 60-s cycles, 12 h/day) and then implanted with catheters. In response to 5 wk of chronic IH, mice (n = 8) increased systemic blood pressure by 7.5 mmHg, left ventricle + septum weight by 32.2 +/- 7.5 x 10(-2) g/100 g body wt (P < 0.015), and right ventricle weight by 19.3 +/- 3.2 x 10(-2) g/100 g body wt (P < 0.001), resulting in a 14% increase in the right ventricle/left ventricle + septum weight (P < 0.005). We conclude that in C57BL/6J mice 1) acute hypoxia causes opposite effects on the pulmonary and systemic circulations, leading to preferential loading of the right heart; and 2) chronic IH in mice results in mild to moderate systemic and pulmonary hypertension, with resultant left- and right-sided ventricular hypertrophy.     

Multiscale modelling in biofluidynamics: application to reconstructive paediatric cardiac surgery

Multiscale computing is a challenging area even in biomechanics. Application of such a methodology to quantitatively compare postoperative hemodynamics in congenital heart diseases is very promising. In the treatment of hypoplastic left heart syndrome, which is a congenital heart disease where the left ventricle is missing or very small, the necessity to feed the pulmonary and systemic circulations is obtained with an interposition shunt. Two main options are available and differ from the sites of anastomoses: (i) the systemic-to-pulmonary conduit (Blalock-Taussig shunt known as the Norwood Operation (NO)) connecting the innominate artery (NO-BT) or the aorta (NO-CS) to the right pulmonary artery and (ii) the right ventricle to pulmonary artery shunt (known as Sano operation (SO)). The proposition that the SO is superior to the NO remains controversial. 3-D computer models of the NO (NO-BT and NO-CS) and SO were developed and investigated using the finite volume method. Conduits of 3, 3.5 and 4 mm were used in the NO models, whereas conduits of 4, 5 and 6 mm were used in the SO model. The hydraulic nets (lumped resistances, compliances, inertances and elastances) which represent the systemic, coronary and pulmonary circulations and the heart were identical in the two models. A multiscale approach was adopted to couple the 3-D models with the circulation net. Computer simulation results were compared with post-operative catheterization data. Results showed that (i) there is a good correlation between predicted and observed data: higher aortic diastolic pressure, decreased pulmonary arterial pressure, lower pulmonary-to-systemic flow ratio and higher coronary perfusion pressure in SO; (ii) there is a minimal regurgitant flow in the SO conduit. The close correlation between predicted and observed clinical data supports the use of mathematical modelling, with a mandatory multiscale approach, in the design and assessment of surgical procedures.     

Permanent cardiac stimulation in a patient with isolated dextrocardia and ventricular septal defect

A case of pacemaker implantation because of acquired atrioventricular block third degree in woman aged 39 years with rare isolated dextrocardia with inversion of cardiac ventricles, compensatory transposition of both aorta and pulmonary artery, and ventricular septal defect. The end of electrode has wedged in the apex of the arterial ventricle. Following pacemaker implantation, patients clinical course of gynaecological operation was uneventful.     

Anatomical correction of complete transposition of the great arteries and ventricular septal defect in infancy.

Two patients, aged 8 weeks and 5 years, with D transposition of great arteries and large ventricular septal defect were treated by transection of both aorta and pulmonary arteries and reattaching them to the appropriate ventricles. This included the origins of the coronary arteries. The ventricular septal defect was closed through a transverse ventriculotomy using a Dacron patch. The younger child was operated on as an emergency because of cyanosis and severe heart failure resistant to intensive medical treatment. The older child had had previous banding of the pulmonary artery at the age of 1 year. In both patients pulmonary artery pressure dropped to below half systemic pressure immediately after the operation. Postoperative progress was satisfactory with relief of cyanosis and heart failure. Early anatomical correction of transposition of the great arteries and ventricular septal defect is feasible and should play an important part in the management of these patients.     

Hybrid repair of a very late, post-aortic coarctation surgery thoracic aneurysm: a case report

ABSTRACT: INTRODUCTION: Local aneurysms after surgical repair of coarctation of the aorta occur mainly in patients surgically treated by Dacron patch plasty during adulthood. The management of these patients is always problematic, with frequent complications and increased mortality rates. Percutaneous stent-graft implantation avoids the need for surgical reintervention. CASE PRESENTATION: We report a case involving the hybrid treatment by stent-graft implantation and transposition of the left subclavian artery to the left common carotid artery of an aneurysmal dilatation of the thoracic aorta that occurred in a 64-year-old Caucasian man, operated on almost 40 years earlier with a Dacron patch plasty for aortic coarctation. Our patient presented to our facility for evaluation with back pain and shortness of breath after minimal physical effort. A physical examination revealed stony dullness to percussion of the left posterior thorax, with no other abnormalities. The results of chest radiography, followed by contrast-enhanced computed tomography and aortography, led to a diagnosis of giant aortic thoracic aneurysm. Successful treatment of the aneurysm was achieved by percutaneous stent-graft implantation combined with transposition of the left subclavian artery to the left common carotid artery. His post-procedural recovery was uneventful. Three months after the procedure, computed tomography showed complete thrombosis of the excluded aneurysm, without any clinical signs of left lower limb ischemia or new onset neurological abnormalities. CONCLUSIONS: Our patient's case illustrates the clinical outcomes of surgical interventions for aortic coarctation. However, the very late appearance of a local aneurysm is rather unusual. Management of such cases is always difficult. The decision-making should be multidisciplinary. A hybrid approach was considered the best solution for our patient.     

Cardiomyocyte apoptosis with enhanced expression of P53 and Bax in right ventricle after pulmonary arterial banding.

The aim of this study is to investigate whether the cardiomyocyte apoptosis is induced after experimental right-sided pressure overload and whether the expression of proapoptotic factor is altered or not. Ten-week-old male Sprague-Dawley rats were subjected to right ventricular overload by experimental coarctation of the main pulmonary artery. In pulmonary artery-banded rats, TUNEL method revealed that positive nuclei were observed in cardiomyocytes exclusively in the right ventricle, and Northern blot analysis showed that p53 mRNA level in the right ventricle was 6.2-fold higher at the day 1 than that in sham-operated rats and its level decreased gradually. Bax mRNA in the right ventricle was also increased 3.3-fold at the day 1 in pulmonary artery-banded rats and also gradually decreased. The immunohistochemical study revealed that the immunoreactivity of P53 and Bax was observed exclusively in the right ventricle of the pulmonary artery-banded group. These results demonstrated that the occurrence of TUNEL-positive cardiomyocytes in the acute pressure overload was accompanied by the enhanced expression of apoptosis inducers. It is suggested that acute pressure overload is a potent apoptotic stimulus for cardiomyocytes.     

Pulmonary pressure-flow relationships in the fetal lamb during in utero ventilation

Pressure-flow relationships in the ventilated lung have not been previously determined in undelivered fetal sheep. Therefore we studied 11 late-gestation chronically prepared fetal sheep during positive-pressure ventilation with different gas mixtures to determine the roles of mechanical distension and blood gas tensions on pressure-flow relationships in the lung. Ventilation with 3% O2-7% CO2 produced a substantial fall in pulmonary vascular resistance even though arterial blood gases were not changed. Increases in pulmonary arterial PO2 during ventilation were associated with falls in pulmonary vascular resistance beyond that measured during mechanical distension. Decreases in pulmonary arterial PCO2 and associated increases in pH were also associated with falls in pulmonary vascular resistance. Pulmonary blood flow ceased at a pulmonary arterial pressure that exceeded left atrial pressure, indicating that left atrial pressure does not represent the true downstream component of driving pressure through the pulmonary vascular bed. The slope of the driving pressure-flow relationship in the normal mature fetal lamb was therefore different from the ratio of pulmonary arterial pressure to pulmonary arterial flow. We conclude that mechanical ventilation, increased PO2 and decreased PCO2, and/or increased pH has an important influence on the fall in pulmonary vascular resistance elicited by positive pressure in utero ventilation of the fetal lamb and that the downstream driving pressure for pulmonary blood flow exceeds left atrial pressure.     

慢性缺氧对自发性高血压大鼠血液动力学和血管反应性的影响

本研究观察了鼠龄10周的自发性高血压大鼠(SHR)在慢性缺氧条件下(模拟海拔5000m,15d)体动脉压(SBP)、平均肺动脉压(MPAP)、左、右心室收缩指数(LVIC、RVIC)和舒张指数(LVIR、RVIR)以及血管反应性的变化。结果表明,慢性缺氧明显阻抑SHR大鼠SBP升高(P<0.05),但使SHR大鼠MPAP升高(P<0.001)。慢性缺氧还可增大SHR大鼠LVIC和LVIR,增强SHR大鼠胸主动脉对乙酰胆碱(ACh)的舒张反应,减弱其对5-羟色胺(5-HT)的收缩反应。SHR大鼠肺动脉对ACh和5-HT的反应则与主动脉相反。实验结果提示,慢性缺氧阻抑SHR大鼠血压升高与血管反应性的改变有关。     

Pulmonary vasodilation with structurally altered pulmonary vessels and pulmonary hypertension

To evaluate pulmonary vasodilation in a structurally altered pulmonary vascular bed, we gave endothelium-dependent (acetylcholine) and endothelium-independent [sodium nitroprusside, prostaglandin I2 (PGI2)] vasodilators in vivo and to isolated lobar pulmonary arteries from neonatal calves with severe pulmonary hypertension. Acetylcholine, administered by pulmonary artery infusion, decreased pulmonary arterial pressure from 120 +/- 7 to 71 +/- 6 mmHg and total pulmonary resistance from 29.4 +/- 2.6 to 10.4 +/- 0.9 mmHg.l-1.min without changing systemic arterial pressure (90 +/- 5 mmHg). Although both sodium nitroprusside and PGI2 lowered pulmonary arterial pressure to 86 +/- 4 and 96 +/- 4 mmHg, respectively, they also decreased systemic arterial pressure to 65 +/- 4 and 74 +/- 3 mmHg, respectively. Neither sodium nitroprusside nor PGI2 was as effective as acetylcholine at lowering total pulmonary resistance (18.0 +/- 3.6 and 19.1 +/- 2.2 mmHg.l-1.min, respectively). Right-to-left cardiac shunt through the foramen ovale was decreased by acetylcholine from 1.6 +/- 0.4 to 0.1 +/- 0.2 l/min but was not changed by sodium nitroprusside or PGI2. Isolated lobar pulmonary arteries from pulmonary hypertensive calves did not relax in response to acetylcholine, whereas isolated pulmonary arteries from age-matched control calves did relax in response to acetylcholine. Control and pulmonary hypertensive lobar pulmonary arteries relaxed equally well in response to sodium nitroprusside. We concluded that acetylcholine vasodilation was impaired in vitro in isolated lobar pulmonary arteries but was enhanced in vivo in resistance pulmonary arteries in neonatal calves with pulmonary hypertension.     

Systemic arteriovenous fistula leads to pulmonary artery remodeling and abnormal vasoreactivity in the fetal lamb

Several cases of systemic arteriovenous fistula diagnosed in the human fetus have been associated with the postnatal development of persistent pulmonary hypertension. The aim of this study was to determine the effects of a prenatally created systemic arteriovenous fistula on the structure and reactivity of the pulmonary circulation in the fetal lamb. A fistula between the jugular vein and carotid artery was created in fetal lambs at 119-124 days of gestation. At delivery (134-139 days), left pulmonary artery (LPA) pressure was increased in the fistula group (n = 12) compared with controls (n = 11, P < 0.01). The pulmonary vascular resistance was significantly higher in the fistula group (P < 0.05), whereas mean LPA blood flow was not statistically different between the two groups. Morphometric analysis of the pulmonary vascular bed revealed an increase in the number of peripheral muscular arteries, together with an increase in pulmonary arterial medial thickness in the fistula group. There was no difference in the relative number or size of intraacinar arteries. In vitro organ bath studies on pulmonary arterial rings showed impaired endothelium-dependent relaxation in the fistula group compared with controls. However, endothelial nitric oxide synthase protein expression was similar in both groups, whereas endothelium-independent relaxation to sodium nitroprusside was greater in the fistula group compared with controls. A systemic arteriovenous fistula leads to both structural and functional alteration of the pulmonary vasculature, which might lead to the development of persistent pulmonary hypertension after birth.     

Increased plasma levels of adrenomedullin, a vasoactive peptide, in patients with end-stage pulmonary disease

AIM: To study adrenomedullin (AM) plasma levels in patients with severe lung disease and to analyze the relationship between AM and heart changes, hemodynamics and blood gases. METHODS: Case control study of 56 patients (36 men, 20 women) with severe lung disease and 9 control subjects (7 men, 2 women). Patients with end-stage pulmonary disease, including chronic obstructive pulmonary disease (COPD, n=11), cystic fibrosis (CF, 26), idiopatic pulmonary fibrosis (ILD, n=9), and idiopatic pulmonary arterial hypertension (PAH, n=10), who were evaluated for lung trasplantation between January 1997 and September 2000, and nine patients who underwent lung surgery for a solitary benign nodule. AM plasma levels in pulmonary artery (mixed venous blood, vein) and aorta or femoral artery (arterial, art), art and vein blood gases, pulmonary hemodynamics, systemic hemodynamics, two-dimensional transthoracic echocardiography and echo-Doppler study. RESULTS: Plasma AM (art and ven) levels were higher among patients' group compared to the controls (AMart p<0.02 and AMven p<0.04) for CF, ILD, PAH (AMart, pg ml(-1) Controls 13.7+/-3.6, COPD 22.8+/-6.2, CF 28.1+/-11.4, ILD 34.1+/-14.3, PAH 35.1+/-18.9; AMven, pg ml(-1) Controls 14.2+/-4.8, COPD 28.1+/-12.6, CF 31.7+/-14.1, ILD 38.7+/-16.5, PAH 40.1+/-4.4). We found with a trend towards higher concentration in ILD and PAH patients compared to COPD and CF but no statistical significant differences. Mixed-venous AM was higher than arterial AM in all groups resulting in AM uptake (AMPulmUp pg min(-1) Controls 4.8+/-22.6, COPD 21.1+/-44.9, CF 20.6+/-45.1, ILD 23.7+/-38.5, PAH 29.9+/-49.7). The univariate analysis showed a weak but significant correlation between AMart and mean systemic arterial pressure, heart rate, mean pulmonary arterial pressure and systemic vascular resistance. In the multivariate analysis, four variables emerged as independent factors of AMart including mean pulmonary arterial pressure, heart rate, mean systemic arterial pressure and left ventricular diastolic diameter (F=8.6, p<0.00001, r=0.60, r2=0.32). A similar weak correlation was apparent between AMven, systemic vascular resistance, and mean pulmonary arterial pressure. The results of multivariate analysis identify right atrial enlargement, mean right atrial pressure, heart rate and left ventricular dimensions as the only independent variables related to AMven (F=4.3, p<0.0004 r=0.56, r2=0.26). AM pulmonary uptake was significantly correlated with AMven (r=0.65), but not with hemodynamic, blood gas and echocardiographic variables. CONCLUSIONS: AM plasma levels are elevated in patients with severe lung disease in face of a preserved pulmonary uptake. These results suggest that the high AM plasma levels in patients with severe lung disease are not caused by a reduced pulmonary clearance, instead suggesting a systemic production.     

Pulmonary vascular resistance after cessation of positive end-expiratory pressure

This report describes the pulmonary vascular response of infant lamb lung to abrupt cessation of positive end-expiratory pressure (PEEP) during volume-regulated continuous positive-pressure breathing (CPPB). In an intact, endobronchially ventilated preparation, the increase in left lung blood flow (QL) after abrupt cessation of 11 Torr left lung PEEP was found to be gradual, although peak airway pressure (Pmax) fell promptly from 36 to 14 Torr; 49% of the increase in QL occurred greater than 10 s after cessation of PEEP. Recruitment of zone I vasculature that had been created by balloon occlusion of the left pulmonary artery was found to occur promptly after balloon deflation. Isolated neonatal lamb lungs, perfused at constant flow rate, showed similar persistent elevation of pulmonary vascular resistance after cessation of 15 Torr PEEP, although Pmax fell abruptly from 39 to 12 Torr. This hysteresis was eliminated by calcium channel blockade with verapamil, and the magnitude of the change in pulmonary arterial pressure after either application or cessation of PEEP was reduced (25 and 26%, respectively). These observations suggest that, during CPPB, lung stretch alters neonatal pulmonary vascular tone or, by causing calcium channel-dependent lung volume hysteresis, modulates pulmonary vascular resistance. This interaction exaggerates the effect of airway pressure changes on pulmonary vascular resistance during mechanical ventilation.     

应用同种带瓣管道重建右室流出道的危险因素分析

目的：评价采用同种带瓣管道行右室流出道重建术的临床效果,探讨影响手术效果及临床预后的因素。方法：回顾2002年11月至2010年11月期间应用同种带瓣管道行右室流出道重建患者的临床资料,分析患者手术前后的一般信息、血流动力学表现与临床预后的关系。结果：行右室流出道重建术后49例痊愈出院,5例死亡,存活率90．7％,死亡率9-3％。手术前后比较右室流出道内径较术前明显增加,右室一左室收缩压比值、右室-肺动脉压差较术前明显降低,三尖瓣反流、肺动脉瓣反流较术前加重,肺动脉瓣狭窄较术前减轻。统计分析表明患者死亡的危险因素有术后右室平均压、术后肺动脉-主动脉收缩压比值、术后二尖瓣反流。术后心胸比、术后肺动脉收缩压、术后肺动脉一主动脉收缩压比值、术后三尖瓣反流可能和术后患者ICU时间延长有关。McGoon指数、术后心胸比、术后肺动脉收缩压、术后右室平均压、术后肺动脉一主动脉收缩压比值、合并动脉导管未闭、术后三尖瓣反流可能和术后患者呼吸机时间延长有关。结论：复杂先天性心脏病患者采用同种带瓣管道重建右室流出道可以取得较满意的临床效果,术后流出道梗阻矫正满意,可以防止肺动脉返流导致的心脏损害。