Does the use of leucocyte depletion during cardiopulmonary bypass affect exhaled nitric oxide production?

Fifty patients undergoing elective coronary revascularisation were prospectively randomised to receive either a leucocyte-depleting or a control filter inserted into the arterial line of the cardiopulmonary bypass (CPB) circuit. The concentration of exhaled nitric oxide (NO) was measured 15 min before and 30 min after CPB using a real-time chemiluminescence analyser (Logan Research, Northampton, UK). The baseline rate of exhaled NO production was 2.14 +/- 0.83 ppb/s in the control group, and 2.58 +/- 0.53 ppb/s in leucocyte-depleted group (p = 0.17). Following CPB, the mean rate of exhaled NO production in the control group had increased by 1.51 +/- 0.45 ppb/s to 3.65 +/- 0.81 ppb/s and in the leucocyte- depletion group had increased by 1.05 +/- 0.45 ppb/s to 3.64 +/- 0.62 ppb/s. The increase in exhaled NO production was significantly lower in the leucocyte depleted group (p = 0.002), indicating that leucocyte depletion suppressed the increase in exhaled NO production seen following CPB.     

Calpain inhibition decreases endothelin-1 levels and pulmonary hypertension after cardiopulmonary bypass with deep hypothermic circulatory arrest

OBJECTIVE: Cardiopulmonary bypass in infants and children can result in cardiopulmonary dysfunction through ischemia and reperfusion injury. Pulmonary hypertension and injury are particularly common and morbid complications of neonatal cardiac surgery. Inhibition of calpain, a cysteine protease, has been shown to inhibit reperfusion injury in adult organ systems. The hypothesis is that calpain inhibition can alleviate the cardiopulmonary dysfunction seen in immature animals following ischemia and reperfusion with cardiopulmonary bypass. DESIGN: Animal case study. SETTING: Medical laboratory. SUBJECTS: Crossbred piglets (5-7 kg). INTERVENTIONS: Piglets were cooled with cardiopulmonary bypass to 18 degrees C followed by deep hypothermic circulatory arrest for 120 mins. Animals were rewarmed to 38 degrees C on cardiopulmonary bypass and maintained for 120 mins. Six animals were administered calpain inhibitor (Z-Leu-Leu-Tyr-fluoromethyl ketone; 1 mg/kg, intravenously) 60 mins before cardiopulmonary bypass. Nine animals were administered saline as a control. Plasma endothelin-1, pulmonary and hemodynamic function, and markers of leukocyte activity and injury were measured. MEASUREMENTS AND MAIN RESULTS: Calpain inhibition prevented the increased pulmonary vascular resistance seen in control animals (95.7 +/- 39.4 vs. 325.3 +/- 83.6 dyne.sec/cm, respectively, 120 mins after cardiopulmonary bypass and deep hypothermic circulatory arrest, p = .05). The attenuation in pulmonary vascular resistance was associated with a blunted plasma endothelin-1 response (4.91 +/- 1.72 pg/mL with calpain inhibition vs. 10.66 +/- 6.21 pg/mL in controls, p < .05). Pulmonary function after cardiopulmonary bypass was better maintained after calpain inhibition compared with controls: Po2/Fio2 ratio (507.2 +/- 46.5 vs. 344.7 +/- 140.5, respectively, p < .05) and alveolar-arterial gradient (40.0 +/- 17.2 vs. 128.1 +/- 85.2 mm Hg, respectively, p < .05). Systemic oxygen delivery was higher after calpain inhibition compared with controls (759 +/- 171 vs. 277 +/- 46 mL/min, respectively, p < .001). In addition, endothelial nitric oxide synthase activity in lung tissue was maintained with calpain inhibition. CONCLUSIONS: The reduction in plasma endothelin-1 and maintenance of lung endothelial nitric oxide levels after cardiopulmonary bypass and deep hypothermic circulatory arrest with calpain inhibition were associated with reduced pulmonary vascular resistance. Improved gas exchange and higher systemic oxygen delivery suggest that calpain inhibition may be advantageous for reducing postoperative cardiopulmonary dysfunction commonly associated with pediatric heart surgery and cardiopulmonary bypass.     

体外循环期间肺动脉灌注低温肺保护液及低温氧合血对犬的肺保护作用

目的研究体外循环期间肺动脉灌注低温保护液及低温氧合血对犬的肺保护作用。方法将12只杂种犬随机分为氧合血组及保护液组，各6只，左肺为对照组。体外循环（CPB）前及停CPB后不同时间点，监测气道峰压、肺血管阻力和右肺静脉血氧分压，留取血标本做生化分析以及对肺组织进行光、电镜观察。结果肺保护液组CPB后气道峰压、肺血管阻力、肺静脉氧分压、肺泡．动脉氧压力差、支气管肺泡灌洗液、肺组织MDA及组织学及透射电镜结果均明显优于氧合血组，后者又明显优于对照组。结论肺动脉灌注低温氧合血，有一定的肺保护作用，但该作用明显弱于低温肺保护液，肺动脉灌注含抑肽酶和沐舒坦的低温肺保护液，具有良好的肺保护作用。     

Successful weaning from cardiopulmonary bypass with central venous prostaglandin E1 and left atrial norepinephrine infusion in patients with acute pulmonary hypertension.

OBJECTIVE: Postoperative pulmonary hypertension increases the mortality risk in cardiac surgery. We have used central venous prostaglandin E1 (PGE1) and left atrial norepinephrine (NE) infusion to wean from cardiopulmonary bypass (CPB) patients with refractory postoperative pulmonary hypertension. DESIGN: Observational, nonrandomized study. SETTING: Department of Cardiac Surgery in a university hospital. PATIENTS: We studied 10 nonconsecutive American Society of Anesthesiologists III and New York Heart Association class III-IV patients with postoperative pulmonary hypertension and low cardiac output syndrome preventing separation from CPB. INTERVENTIONS: Patients received right atrial PGE1 (31.5 +/- 6.26 ng/kg/min) and left atrial NE (0.11 +/- 0.02 microg/kg/min) infusion. Hemodynamic data were obtained before CPB (T0), after CPB under maximal inotropes and vasodilator infusion (T1), 10 mins (T2) and 12 hrs (T3) after PGE1 and NE infusion, and 48 hrs after withdrawal of PGE1 and NE (T4). MEASUREMENTS AND MAIN RESULTS: All patients were successfully weaned from CPB and survived. The biatrial infusion of PGE1 and NE caused a dramatic reduction in mean pulmonary artery pressure (from 42.8 +/- 5.1 mm Hg at T1 to 28.5 +/- 2.6 mm Hg at T2 and 20.5 +/- 2.0 mm Hg at T4), pulmonary vascular resistance index (from 1158 +/- 269 dyne x sec/cm5 x m2 at T1 to 501 +/- 99 dyne x sec/cm5 x m2 at T2 and 246 +/- 50 dyne x sec/cm5 x m2 at T4), and pulmonary-to-systemic vascular resistance index ratio (from 0.61 +/- 0.17 at T1 to 0.20 +/- 0.04 at T2 and 0.11 +/- 0.03 at T4). Cardiac index increased from 1.7 +/- 0.2 L/min/m2 at T1 to 2.3 +/- 0.2 L/min/m2 at T2 and 2.9 +/- 0.1 L/min/m2 at T4. CONCLUSIONS: In patients with refractory postoperative pulmonary hypertension, the combined administration of low-dose PGE1 in the right atrium and NE in the left atrium is an effective means to wean patients from cardiopulmonary bypass.     

Inhaled nitric oxide improves hemodynamics in patients with acute pulmonary hypertension after high-risk cardiac surgery

Severe pulmonary hypertension and right-sided circulatory failure (RSCF) represent an increasing cause of morbidity and mortality in patients undergoing high-risk cardiac surgery. Increased pulmonary vascular resistance in the setting of cardiopulmonary bypass (CPB) may further lead to decrease blood flow across the pulmonary vascular bed; thereby decreasing left ventricular filling and cardiac output. Current management techniques for RSCF include both nonspecific vasodilator and inotropic agents (often limited by systemic hypotension) and the placement of right ventricular assist devices (associated with increased perioperative morbidity). Inhaled nitric oxide (NOi) represents a novel, specific pulmonary vasodilator that has been proven efficacious in these clinical settings. We evaluated 34 patients in 38 operations who underwent cardiac surgery at Columbia Presbyterian Medical Center, and who received NOi (20 ppm) through a modified ventilatory circuit for hemodynamically significant elevations in pulmonary vascular resistance. Nine patients underwent cardiac transplantation, three patients bilateral lung transplantation, 16 patients left ventricular assist device placement and 10 patients routine cardiac surgery. Patients receiving NOi exhibited substantial reductions in mean pulmonary artery pressure (mPAP) (34.6 +/- 2.0 to 26.0 +/- 1.7 mmHg, p < 0.0001), with improvements in systemic hemodynamics, mean arterial pressure (68 +/- 3.1 to 75.9 +/- 2.0 mmHg, p = 0.006). In five cases, patients could not be weaned from CPB until NOi was administered. Patients were maintained on NOi from 6 to 240 h postoperatively (median duration 36 h). Inhaled NO induces substantial reductions in mPAP and increases in both cardiac index and systemic blood pressure in patients displaying elevated pulmonary hemodynamics after high-risk cardiac surgery. NO is, therefore, a useful adjunct in these patients in whom acute pulmonary hypertension threatens right ventricular function and hemodynamic stability.     

Effects of ventilation and nonventilation on pulmonary venous blood gases and markers of lung hypoxia in humans undergoing total cardiopulmonary bypass

OBJECTIVE: To assess the effects of lung oxygenation and ventilation vs. lung collapse on pulmonary markers of lung hypoxia. DESIGN: A prospective, nonrandomized, nonblinded comparative study. SETTING: University department of anesthesiology and cardiothoracic surgery. SUBJECTS: Twelve adult patients undergoing coronary bypass grafting requiring total cardiopulmonary bypass. INTERVENTIONS: Single lung ventilation during total cardiopulmonary bypass (tidal volume, 150 mL; respiratory rate, 6 breaths/min; inspiratory oxygen fraction, 0.5) while the contralateral lung was allowed to collapse completely without oxygenation. MEASUREMENTS AND MAIN RESULTS: At the beginning and at the end of total cardiopulmonary bypass (duration, 59-65 mins), blood was aspirated from the right and left pulmonary veins and the radial artery for measurement of blood gases and concentrations of endothelin-1, big-endothelin, thromboxane B2, lactate, and lactate dehydrogenase. Nonventilation during total cardiopulmonary bypass compared with ventilation resulted in lower pulmonary venous P(O2) values (57+/-15 torr [7.6+/-2.0 kPa] vs. 103+/-23 torr [13.7+/-3.1 kPa]) and higher thromboxane B2 concentrations (488+/-95 pg/mL vs. 434+/-92 pg/mL). The concentrations of endothelin-1, big-endothelin, lactate, and lactate dehydrogenase in the pulmonary veins did not differ significantly between nonventilated and ventilated lungs. CONCLUSIONS: Development of pulmonary tissue hypoxia during 1 hr of nonventilation and cardiopulmonary bypass with completely inhibited pulmonary arterial blood flow is unlikely, suggesting that enough oxygen is stored in or is provided to the collapsed lung. Thus, nonventilation during total cardiopulmonary bypass does not appear to contribute to postoperative respiratory dysfunction by causing pulmonary tissue hypoxia. These results, however, do not exclude that mechanical factors of ventilation might benefit the lung during cardiopulmonary bypass.     

体外循环后炎性因子变化及对肺功能的影响

目的探讨体外循环（CPB）后血浆内皮素（ETI）、一氧化氮（NO）、细胞黏附因子（CD11b）、白介素-6（IL-6）、白介素-8（IL-8）的变化及对肺功能的影响。方法32例心血管择期手术病人,在全麻中低温CPB下手术。于术前至术后8h共5个点采血,测定血浆ET1、NO、CD11b、IL-6、IL-8的变化,同时测定肺功能并观察CPB前、后肺组织电镜下的变化。结果体外循环后肺顺应性显著下降、吸气阻力和呼气阻力、峰值压力和平台压力显著升高。CPB后ET1、NO、CD11b、IL-6、IL-8均有不同程度的改变,肺组织病理检查见肺内大量中性粒细胞聚集,有的小血管内可见粒细胞微栓形成,术后肺组织损伤明显。结论在心血管CPB手术中,CPB可导致机体急性全身性炎性改变,ET1、NO、CD11b、IL-6、IL-8变化明显;同时,肺功能降低,肺组织损伤,其改变有相关性。     

吸入左旋精氨酸对心内直视术后肺缺血再灌注损伤的保护作用

【目的】本实验旨在评估风湿性心脏病术后雾化吸入左旋精氨酸对肺缺血再灌注的保护作用。【方法】将32例风湿性心脏病行瓣膜置换术的患者随机分成两组,精氨酸组(A组)于术后雾化吸入左旋精氨酸,对照组(B组)雾化吸入同等剂量的生理盐水。观察患者治疗前后氧合指数(OI),肺泡-动脉氧分压差(PA-aO2),肺内分流差(QS/Qt)以及血浆一氧化氮(NO)及丙二醛(MDA)浓度的变化。【结果】处理组与对照组比较,能增加血浆NO含量(P<0.01)并能减少血浆MDA水平(P<0.05)且PA-aO2及QS/Qt低于对照组(P<0.05),OI高于对照组(P<0.01)。【结论】术后雾化吸入左旋精氨酸能有效缓解肺缺血再灌注损伤,改善肺功能。     

The influence of cardiopulmonary bypass on respiratory function in an early postoperative period

AIM: To investigate the influence of cardiopulmonary bypass (CPB) on pulmonary function early after the operation by evaluating Qs/Qt. MATERIAL AND METHODS: Twenty one patients after elective myocardial revascularization surgery have been analysed. Group 1 included 11 patients who have undergone cardiac surgery with CPB. Group 2 included 10 patients who have undergone cardiac surgery without CPB. Blood gas analysis for intrapulmonary shunt calculations was made 20 minutes after the induction of anesthesia and 4 hours after surgery. Qs/Qt was also calculated. RESULTS: Four hours after surgery Qs/Qt increased compared to preoperative data in group 1 (from 8.6 +/- 2.1 to 16.8 +/- 2.6%, p < 0.02). Intrapulmonary shunt was greater in group 1 vs group 2 four hours after the surgery (16.8 +/- 2.6 and 7.8 +/- 2.1%, p < 0.02). In group 1, alterations in a pulmonary function (81.8%) were caused by atelectasis detected by chest x-ray. In group 2 neither increase in intrapulmonary shunt nor atelectasis were determined. CONCLUSION: Arterial hypoxemia and an increase in the intrapulmonary shunt (due to atelectasis) have proven that alterations in the pulmonary function occur more often and are more pronounced in patients after surgery with cardiopulmonary bypass.     

Time-course of impairment of respiratory mechanics after cardiac surgery and cardiopulmonary bypass.

OBJECTIVE: Cardiopulmonary bypass (CPB) is associated with abnormalities of lung function characterized by an increase in static elastance of the respiratory system. We examined the following: a) the effects of CPB on the total inspiratory volume-pressure (V-P) relationship of the respiratory system; b) the relative contribution of the chest wall and lung to the impairment of respiratory system mechanics; and c) the time-course of such impairment. DESIGN: Prospective, interventional study. SETTING: Surgical and medical intensive care units in a teaching hospital. PATIENTS: Eight adult patients scheduled for elective open heart surgery to correct valvular dysfunction. INTERVENTIONS: V-P curves (interrupter technique) of the respiratory system were partitioned between the chest wall and lung by measurements of esophageal pressure. Measurements were obtained before sternotomy (control), immediately after, 4 hrs after, and 7 hrs after separation from CPB. MEASUREMENTS AND MAIN RESULTS: Control V-P relationships of the respiratory system and lung showed lower inflection points (Pflex) at pressure values of 5.9+/-2.3 and 4.3+/-2.5 cm H2O, respectively. Immediately after and 4 hrs after separation from CPB, both curves had sigmoid shapes because of lower Pflex and formation of upper inflection (UIP) points. The pressures corresponding to the Pflex increased significantly (p < .001) by 56%+/-3% and 78%+/-4%, whereas the UIP corresponded to a pressure value of 42.34+/-8.5 and 35.6+/-7.8 cm H2O in the respiratory system and lung, respectively. A linear V-P relationship of the chest wall was observed during the control condition and after separation from CPB. Four hours later, no further increases in the pressure values corresponding to Pflex were observed on the inspiratory V-P curves of the respiratory system and lung, whereas the UIP occurred at a pressure of 35.6+/-9.1 and 29.7+/-8.4 cm H2O, respectively. A UIP was present on the V-P curve of the chest wall at a volume of 0.77+/-0.02 L. Seven hours after separation from CPB, the inspiratory V-P curves of the respiratory system, chest wall, and lung returned to normal. CONCLUSIONS: Sternotomy and CPB produced immediate changes in lung mechanics. Chest wall mechanics were affected only 4 hrs after sternotomy. Seven hours after disconnection from CPB, all mechanics had returned to normal.     

心内直视手术后长时间呼吸机支持的危险因素分析

目的　分析心内直视手术后影响患者呼吸机辅助时间的危险因素 ,提高心内直视手术后呼吸并发症的诊治水平。方法　回顾性分析我院在 1995年 1月— 2 0 0 3年 8月期间长时间呼吸机辅助呼吸的 5 0例成人患者的临床资料 ,并用多因素线性回归分析模型评价各影响因素的作用大小。结果　本组患者年龄 14～6 5岁 ;体质量 2 8～ 80 kg;男性 2 8例 ,女性 2 2例 ;平均转流时间 (15 6 .38± 5 2 .0 2 ) m in;术后呼吸机辅助时间为 (6 2 .86± 2 2 .5 5 ) h;病死率为 18.0 %。与对照组相比 ,长时间呼吸机辅助呼吸组患者术前心功能差(P<0 .0 0 1) ,体外循环时间与阻断时间长 (P<0 .0 0 1) ,术后动脉血氧分压 (Pa O2 )及氧合指数 (Pa O2 /Fi O2 )低(P<0 .0 0 1) ,而术后肺泡动脉血氧分压差 (A a DO2 )高 (P<0 .0 0 1) ,肺内分流 (Qs/Qt)增大 (P<0 .0 0 1) ,术后肺动态顺应性 (PCD)无明显区别 ,术后引流量较多 (P<0 .0 0 1) ,术后心肌酶谱水平高 (P<0 .0 0 1) ,术后并发症的发生率也较高 (P<0 .0 0 1)。经多因素线性回归分析结果显示 ,术后呼吸机辅助呼吸时间与患者术前心功能、术中转流时间、术后 Pa O2 /Fi O2 、术后心肌酶谱水平及术后引流量明显相关。结论　心内直视手术患者术前心功能差、术中转流时间长、术中心肌     

Changes in biochemical and biophysical surfactant properties with cardiopulmonary bypass in children

OBJECTIVE: The aim of the present study was to characterize pulmonary surfactant properties in children undergoing cardiovascular surgery with cardiopulmonary bypass. DESIGN: Prospective clinical trial. SETTING: University hospital pediatric intensive care unit. PATIENTS: Fifty pediatric patients with congenital cardiac defects undergoing cardiovascular surgery with (n = 35) and without (n = 15) cardiopulmonary bypass procedure. INTERVENTIONS: Tracheal aspirates were collected by saline lavage during routine suctioning before (baseline) and after cardiopulmonary bypass, as well as 4, 8, and 24 hrs after admission to the pediatric intensive care unit. MEASUREMENTS AND MAIN RESULTS: Total protein and phospholipid concentrations were assessed in native tracheal aspirates, in large surfactant aggregates, and in small surfactant aggregates. Phospholipid profiles and phosphatidylcholine fatty acids; surfactant apoproteins SP-A, SP-B, and SP-C (enzyme-linked immunosorbent assay); and surface activity (Pulsating Bubble Surfactometer) were all analyzed in large surfactant aggregates. With cardiopulmonary bypass, an initial increase in total protein content was followed by an increase in phospholipid concentration in tracheal aspirates. Large surfactant aggregates decreased 4 hrs after cardiopulmonary bypass (4 hrs, 22.6 +/- 5.6%; mean +/- SEM; p<.01 compared with baseline, 55.4 +/- 9.2%) but recovered within 24 hrs. The phospholipid-protein ratio of large surfactant aggregates 24 hrs after cardiopulmonary bypass (1.2 +/- 0.2; p<.01) was significantly decreased compared with baseline (2.9 +/- 0.6). The relative amount of phosphatidylglycerol content in the large surfactant aggregates-fraction dropped linearly over time but other phospholipids remained mainly unchanged. Phosphatidylcholine fatty acid profiles remained unaffected by cardiopulmonary bypass. The relative content of SP-B and SP-C in large surfactant aggregates increased approximately three-fold compared with baseline. Altogether, our findings with recovered large surfactant aggregate/small surfactant aggregate ratios and increased phospholipid in tracheal aspirates after 24 hrs represent an approximately ten-fold increase in large surfactant aggregate-associated SP-B and SP-C compared with baseline. Only minor changes were detected in biophysical properties of large surfactant aggregates throughout the observation period. CONCLUSIONS: Cardiopulmonary bypass procedure in children induces profound changes in the surfactant system involving both phospholipid and protein components; biophysical function may have been maintained by compensatory increase in SP-B and SP-C.     

血液滤过膜对心肺转流术后呼吸功能的影响

目的　研究在心肺转流术中使用两种不同的膜材料进行血液滤过对术后呼吸功能的保护效果。方法　选择2 0 0 2 - 10～ 2 0 0 3- 0 9接受心内直视手术患者 2 0例 ,随机分成吸附组 (n =10 )和对照组 (n =10 ) ,前者使用AN6 9膜 ,后者使用PS膜进行术中血液滤过。各组均分别于心肺转流前、心肺转流结束时及心肺转流结束后 6 0、12 0、180、2 4 0min测定气道平台压(PPlateau)、气道峰压 (PPeak)、静态胸肺顺应性 (Cst)、动态胸肺顺应性 (Cdyn)和呼吸指数 (RI)的变化。结果　在心肺转流结束至心肺转流结束后 2 4 0min期间 ,吸附组PPlateau、PPeak和RI升高及Cst和Cdyn降低的程度低于对照组 (P <0 0 5 ) ,持续时间短于对照组 (P <0 0 5 )。两组均无死亡 ,无血红蛋白尿。结论　用AN6 9膜较PS膜血液滤过更明显地减轻心肺转流引起的肺损伤 ,改善呼吸功能     

Na /H+ exchange inhibitor cariporide: effects on respiratory dysfunction after cardiopulmonary bypass

The purpose of the present study was to evaluate the potential of the Na+/H+ exchange inhibitor cariporide to protect the lung from injury after cardiopulmonary bypass (CPB). In a randomized placebo-controlled study, 16 pigs were subjected to CPB for 75 min. Administration of vehicle or cariporide (bolus 180 mg, 40 mg/hour) began 30 min pre-CPB and was continued throughout the protocol. The alveolo-arterial O2-gradient (AaDO2), the pulmonary shunt (Qs/Qt), the compliance (Cpl), haemodynamic variables and glycerol and water content in lung tissue were measured 10 min before and up to 180 min post-CPB. All animals in the control versus 75% in the cariporide group survived the experiment. At 5 and 60 min post-CPB, the mean AaDO2 and at 5, 60 and 180 min post-CPB, the mean pulmonary vascular resistance index were higher in the cariporide group (p < 0.05), respectively. More lung water accumulation was found in the cariporide group (p < 0.05). Mean Cpl decreased; the Qs/ Qt and glycerol in lung tissue increased without significant intergroup difference. In this model, the inhibitor of the Na+/H+ antiporter showed no protective effect on lung injury after CPB and might even have harmful effects on pulmonary vascular tone and function.     

The importance of pulmonary artery circulation during cardiopulmonary bypass

This study sought to determine changes in transpulmonary difference in blood cells and alveolar-arterial oxygen (A-aO2) gradient when pulmonary artery circulation was obstructed in patients undergoing coronary artery bypass grafting (CABG) with cardiopulmonary bypass (CPB). Eighteen patients were divided into group A (control group; X-clamp placed on aorta, n = 9) and group B (pulmonary ischaemia group; X-clamp placed on aorta and pulmonary artery, n = 9). Haematological parameters were compared before CPB and up to 90 min after declamping. A-aO2 gradient differences were compared before and 2 h and 6 h after declamping. A transpulmonary increase in leucocyte levels normalized after 60 min in group A but remained higher in group B. A transpulmonary increase in neutrophils normalized after 60 min in group A and 90 min in group B. Increased lymphocyte levels normalized after 30 min in group A and 90 min in group B. A-aO2 gradient was determined as: group A (294.8 +/- 74.3) and group B (321.2 +/- 73.3) before X-clamping; group A (132.7 +/- 22.7) and group B (236.6 +/- 41.5) 2 h after declamping; and group A (72.2 +/- 22.7) and group B (189.4 +/- 88.9) 6 h after declamping. When pulmonary artery circulation was obstructed during the X-clamping period, leucocyte, neutrophil and lymphocyte sequestration within both lungs increased, and an increased A-aO2 gradient was observed because of tissue damage. To prevent post-operative complications, precautions to maintain normal pulmonary artery circulation are recommended.     

体外循环后急性肺损伤诊断与防治的研究进展

急性肺损伤是体外循环后的重要并发症之一 ,一氧化氮呼出水平下降、前降钙素水平的增加可提示急性肺损伤。体外循环后肺损伤的防治方法较多 ,如白细胞滤过术、抑制细胞因子、补体的活性、减轻全身炎症反应、持续肺灌流 ,液体通气 ,一氧化氮吸入治疗。但其疗效有待进一步评价。     

Pulmonary vascular resistance index during coronary artery bypass surgery with aprotinin

Low pulmonary vascular resistance index (PVRI) reflects favorable redundant pulmonary circulation following coronary artery bypass grafting with cardiopulmonary bypass surgery (CPB). This randomized study investigated whether aprotinin given in different modalities impacts PVRI after coronary artery bypass grafting. A total of 40 patients undergoing coronary artery bypass grafting were randomized to four groups according to aprotinin dose: (1) high dose, (2) early low dose, (3) late low dose, and (4) without aprotinin. Oxygenation index, pulmonary shunt, alveolar-arterial oxygen gradient and PVRI were determined. PVRI was calculated as the transpulmonary pressure gradient divided by cardiac index multiplied by 80. The results showed that PVRI remained relative low in all patients provided aprotinin regardless of treatment dosage; PVRI increased at 4?h after restarting ventilation after CPB in patients without aprotinin as compared with aprotinin (266?±?137, 266?±?115, 244?±?86 vs. 386?±?121, dynes-s-cm^?5, respectively, p?=?.047). Elevated postoperative PVRI was predictive for patients without aprotinin (AUC 0.668; SE 0.40; p?相似文献   

Transpulmonary lactate gradient after hypothermic cardiopulmonary bypass

Objective Several studies demonstrated that the lungs could produce lactate in patients with acute lung injury (ALI). Because after cardiopulmonary bypass (CPB) some patients develop ALI, the effect of CPB on pulmonary lactate release was investigated.Design Prospective observational clinical study.Setting Twenty-beds, surgical ICU at a university hospital.Patients Sixteen deeply sedated, ventilated and post-cardiac surgery patients, all equipped with a pulmonary artery catheter.Measurements and results Lactate concentration was measured using a lactate analyser in simultaneously drawn arterial (A) and mixed venous (V) blood samples. Three measurements per patients were taken at 30-min interval, after body temperature reached 37°C. Concomitantly, measurements of cardiac output were also obtained. Pulmonary lactate release was calculated as the product of transpulmonary A-V lactate and cardiac index. The mean cardiopulmonary bypass duration was 100±44 min (SD), and the aortic cross-clamping time was 71±33 min. After CPB, lactate release was 0.136±0.210 mmol/min m^–2. These values were not correlated with cardiopulmonary bypass duration.Conclusion The present study shows that in patients receiving mechanical ventilation after CPB, the lung is a source of lactate production. This pulmonary release was not dependent on cardiopulmonary bypass duration.     

Effects of normothermia versus hypothermia on extravascular lung water and serum cytokines during cardiopulmonary bypass: a randomized, controlled trial

OBJECTIVE: To evaluate the influence of perfusion temperature on the systemic effects of cardiopulmonary bypass (CPB), including extravascular lung water index (EVLWI), and serum cytokines. DESIGN: Prospective, randomized, controlled study. SETTING: Cardiothoracic intensive care unit of a university hospital. PATIENTS: Patients undergoing elective coronary artery bypass grafting. INTERVENTIONS: Twenty-one patients undergoing elective coronary artery bypass grafting were randomly assigned to receive either normothermic bypass (36 degrees C, n = 8) with intermittent antegrade warm blood cardioplegia (IAWBC), or hypothermic (32 degrees C, n = 13) CPB with cold crystalloid cardioplegia. MEASUREMENTS AND MAIN RESULTS: Mean arterial pressure, heart rate, cardiac output, systemic vascular resistance, mean pulmonary arterial pressure, and pulmonary vascular resistance were determined at baseline, i.e., after induction of anesthesia but before sternal opening (T-1), at arrival in the intensive care unit (T0), and 4 hrs (T4), 8 hrs (T8), and 24 hrs (T24) after surgery. EVLWI, intrathoracic blood volume index (ITBVI), and EVLW/ITBV ratio were obtained by using thermal dye dilution utilizing an arterial thermistor-tipped fiberoptic catheter and were recorded at T-1, T0, T4, T8, and T24. Serial blood samples for cytokine measurements were obtained at each hemodynamic measurement time point. Before, during, and after CPB, there were no differences in the conventional hemodynamic measurements between the groups. There were no changes in EVLWI up to T8 in either group. Furthermore, no change in the ratio EVLW/ITBW was observed between the groups at any time, further indicating the absence of a change in pulmonary permeability. Plasma levels of interleukin-6, tumor necrosis factor-alpha, and interleukin-10 increased during and after CPB, independently of the perfusion temperature. CONCLUSION: Normothermic CPB is not associated with additional inflammatory and related systemic adverse effects regarding cytokine production and EVLWI as compared with mild hypothermia. The potential temperature-dependent release of cytokines and subsequent inflammation has not been observed and normothermic CPB may be seen as a safe technique regarding this issue.