Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Activation of complement and serum changes in anaphylatoxin (C3a and C5a) were studied in 8 patients who underwent open-heart surgery using a membrane oxygenator. C1 esterase inhibitor (C1-EI), C3, C5, CH50, C3a and C5a were measured serially at 7 points. C1-EI, C3, and C5 were measured by single radial immunodiffusion, CH50 by Mayer's method, and C3a and C5a by radioimmunoassay. Levels of C1-EI, C3 and C5 decreased significantly from 10 min after initiation to 120 min after the end of CPB compared with base line values. Degree of activation of complement increased in proportion to duration of CPB. Significant decreases of C3 and C5 continued until first postoperative day. Level of C3a increased significantly 10 min after initiation of CPB, and gradually increased till immediately after the end of CPB, when the level was maximum (4625 +/- 560 ng.ml-1) among 7 points. Level of C3a decreased gradually till 120 min after end of CPB. C5a was not detected during whole course. No patient showed respiratory distress of pulmonary edema. In conclusion, membrane oxygenator activated classical pathway of complement at 10 min after initiation of CPB. C3a increased significantly from 10 min after initiation of CPB to 120 min after end of CPB, but C5a was not detected at all during the whole course. The significant activation of complement continued till first postoperative day.
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PMID:[Activation of complement and serial changes of anaphylatoxin (C3a, C5a) in patients for open-heart surgery using a membrane oxygenator]. 155 59

Potential etiologic factors of postcardiopulmonary bypass (post-CPB) lung edema (LE) were investigated (phase 1 study). Further patient treatment was modified according to the results of phase 1 study and the influence that these changes had on the incidence of the complication was assessed (phase 2 study). In phase 1 study, among 100 patients who underwent coronary bypass graft surgery, prolonged assisted ventilation was required for severe LE in 7 cases, and 6 patients had a moderate form of LE. Patients who suffered from severe LE had left and right ventricular dysfunction and normal pulmonary vascular resistance. Three predictors of LE were evidenced by logistic regression analysis: number of bypass grafts completed with internal mammary arteries (p = 0.013), transfusions of blood collected in mobile units (p = 0.014), and the combination of a significant lesion of the left main stem and the right coronary artery at preoperative angiography (p = 0.040). In phase 2 study, a further group of 100 patients was treated differently by improving myocardial protection during surgery, achieving a higher rectal temperature at the end of CPB, and reducing the amount of transfusions. This resulted in only one case of LE (p < 0.001). In conclusion, the cases of post-CPB LE evidenced in our study were related to postoperative ventricular dysfunction and blood transfusions. Any means of improving postoperative hemodynamic stability and reducing the need for transfusions could thus prevent the latter complication.
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PMID:Postcardiopulmonary bypass lung edema. A preventable complication? 841 43

We experienced a successful treatment of acute myocardial infarction which was due to left main trunk obstruction. A 54-year-old man with no history of angina was transported by a rescue squad in cardiogenic shock, and diagnosed by electrocardiography with a wide range of myocardial infarction. Emergent coronary arteriography was performed under IABP support, revealing 99% stenosis in the left main trunk. Percutaneous transluminal coronary recanalization (PTCR) was performed, but suddenly cardiac arrest was happened. He was put on emergency percutaneous cardiopulmonary support (PCPS). A Palmaz-Schatz stent was implanted for reperfusion, but the patient was hemodynamically unstable with frequent ventricular arrhythmia and pulmonary edema. 24 hours later he underwent coronary artery bypass grafting and CPB could be terminated intraoperatively. His cardiac function was very low and LVEF was 20%. All grafts were patent. On the rehabilitation he was discharged on postoperative day 162 and has returned to work in his office one year postoperatively.
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PMID:[Successful treatment of myocardial infarction of left main trunk by emergent CABG under IABP and PCPS support]. 933 May 11

Membrane oxygenators have now gained wide acceptance. A new hollow-fibre membrane oxygenator, the Dideco D903 Avant 1.7, with an optimized membrane surface (1.7 m2) and a wavy blood flow pattern, was tested for gas transfer and blood path resistance in a standardized setting with surviving animals. Three calves (mean body weight 63.29 +/- 2.9 kg) were connected to cardiopulmonary bypass by jugular venous and carotid arterial cannulation, classic roller pump and the Dideco D903 oxygenator with a mean flow rate of 53 +/- 0.1 ml/kg/min for 6 h. After this time, the animals were weaned from the CPB and thereafter from the ventilator. After 7 days, the animals were killed electively. Blood gas analysis was performed before bypass, after mixing (10 min) and then hourly for the 6 h of perfusion. Further samples were taken 30 min (spontaneous breathing) and 60 min after bypass (extubated). Physiological blood gas values could be maintained throughout perfusion in all animals. Mean arterial oxygen saturation varied between 99.3% and 99.7% for the arterial side of the oxygenator compared to 64.6% and 71% for the venous side. The highest mean pressure drop through the oxygenator was 54 mmHg. Postbypass blood gas analysis showed physiological values and no evidence of major lung trauma or pulmonary oedema in relation to the 6 h perfusion. The hollow-fibre membrane oxygenator, Dideco D903, offers excellent gas exchange capabilities and a low pressure drop under experimental conditions, despite reduced membrane surface area. The post mortem examination did not show any deleterious lesion.
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PMID:Experimental evaluation of the Dideco D903 Avant 1.7 hollow-fibre membrane oxygenator. 977 21

Anesthetic care for patients undergoing pulmonary endarterectomy represents one of the most challenging tasks in cardiac anesthesia. Chronic thromboembolic pulmonary hypertension with its concomitant right ventricular failure may cause hemodynamic instability during anesthetic induction and the precardiopulmonary bypass (CPB) period, and the associated comorbidities (pulmonary, hepatic) may affect the actions and metabolism of anesthetic drugs. During the CPB period, proper perfusion patterns, cerebral oxygenation, and adequate hypothermia for deep hypothermic circulatory arrest must be achieved. During the post-CPB period the anesthesiologist must be prepared to treat residual pulmonary hypertension, pulmonary edema, pulmonary bleeding, right ventricular failure, and various metabolic and cardiovascular sequelae of hypothermic circulatory arrest. This review highlights the main issues the anesthesiologist faces during pulmonary endarterectomy, as well as suggests approaches to their management.
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PMID:Anesthesia for pulmonary endarterectomy. 1718 86