血液透析中低血压临床分析

在我国,肾脏疾病的发病率逐年增高,与此同时,终末期肾病的治疗任务也越来越大,血液透析在肾脏替代治疗中扮演着重要的角色,但透析中低血压(intradialytic hypotension,IDH)的发生已成为影响透析患者预后的主要危险因素之一。IDH主要表现为:恶心、呕吐、腹部不适、心绞痛,严重时会危及患者的生命。因此,对于IDH的预防及治疗至关重要。本文系统分析了IDH的发生机制、高危因素、相关预防及治疗措施。通过对IDH进行充分的认识,积极采取干预措施,减少IDH的发生及其危害,提高患者的透析质量及延长生存时间。     

惰性气体再呼吸法评价心排血量

在心力衰竭管理和治疗中,评价心排血量是判断疾病严重程度的重要环节。理想的测定心排血量的方法应该是无创的。惰性气体再呼吸法是对通气浓度进行连续分析以测定有效肺血流量的方法。在无肺血流分流的情况下可以等同于心排血量,具有准确、安全、简易的特点。该方法的优势在于其结果反映的是运动心血量,测量结果不受呼吸、心率及瓣膜反流等因素的影响。在临床上和6 min步行试验结合使用可以更全面准确地评价心排血量及心脏储备能力。     

Effects of carbonic anhydrase inhibition on ventilation-perfusion matching in the dog lung.

Lung carbonic anhydrase (CA) permits rapid pH responses when changes in regional ventilation or perfusion alter airway and alveolar PCO2. These pH changes affect airway and vascular resistances and lung compliance to optimize the balance of regional ventilation (VA) and perfusion (Q) in the lung. To test the hypothesis that these or other CA-dependent mechanisms contribute to VA/Q matching, we administered acetazolamide (25 mg/kg intravenously) to six anesthetized and paralyzed dogs and measured VA/Q relationships before and after CA inhibition by the multiple inert gas elimination technique. Four other groups of dogs were studied to control for possible confounding effects of time under anesthesia and nonselective CA inhibition by acetazolamide: (a) saline placebo as a control for duration of anesthesia, (b) 4% CO2 inhalation to mimic systemic CO2 retention, (c) 1 mg/kg benzolamide (a selective renal CA inhibitor) or 0.5 meq/kg HCl to mimic systemic metabolic acidosis, and (d) 500 mg/kg 4,4'-dinitrostilbene-2,2'-disulfonate (an inhibitor of red cell band 3 protein) to mimic the respiratory acidosis arising from an intracapillary block to rapid mobilization of plasma HCO3- in CO2 exchange. Acetazolamide increased VA/Q mismatch and reduced arterial PO2 measured at equilibrium but these did not occur in the control group. There was no deterioration in VA/Q matching when systemic respiratory acidosis produced either by CO2 inhalation or 4,4'-dinitrostilbene-2,2'-disulfonate or metabolic acidosis (benzolamide or HCl) were imposed to mimic the effects of acetazolamide apart from its inhibition of lung CA. These results support the concept that lung CA subserves VA/Q matching in the normal lung.     

血液透析中发生血压异常的情况分析

目的 观察不同年龄组血液透析中高血压及低血压的发生率，对有关因素及与超滤量(UFV)和每公斤体重超滤量(UFV／W)的关系进行分析。方法 对我院常规透析的加例患者的1575例次的透析进行观察分析。结果 老年组患者高血压发生率小于非老年组，而低血压发生率较非老年组显著提高。糖尿病、冠心病、心包积液、充血性心力衰竭等并发症的发生率也大于非老年组。老年组透析期间发生低血压时较其正常血压时UFV／W明显增高，UFV无显著性差异。非老年组透析期间发生低血压时较其正常血压时UFV明显增高，UFV／W无显著差异。两组血压增高时分别与其正常血压时UFV及IFV／W无明显差异。结论 血液透析中UFV或UFV／W过高是血压降低的关键，尤其是老年患者。     

Hypoxemia during hemodialysis.

Five mechanically ventilated patients were studied during hemodialysis. The aim was to determine if hypoxemia would develop, and to identify the causes. Respiratory variables (dynamic compliance, peak airway pressure, CO2production); oxygen uptake, and transport variables (alveolar and arterial PO2, pulmonary venous admixture, oxygen consumption); respiratory quotient; pulmonary vascular resistances and white blood cells (WBC) were measured. PaO2 decreased during dialysis, as did PaO2. However, the fall in alveolar oxygen tension failed to explain the hypoxemia. Lung volume did not change significantly, because dynamic compliance, peak airway pressure, and pulmonary vascular resistance were not modified. CO2 losses through the dialysis coil were of little clinical significance. WBC count fell significantly. The authors conclude that ventilation/perfusion and diffusion abnormalities related to leuko-agglutination are responsible for hypoxemia during dialysis.     

Activation of monocytes during hemodialysis

The authors conducted a clinical study of the hypothesis of interleukin-1 regarded as one of the most important topics in the problem of biocompatibility of dialytic membranes. Hemodialyses (HD) were performed using different cellulose and synthetic membranes. During HD research was made into the kinetics of monocytes and lymphocytes, monocytic activation expressed by a stimulation index, and the deposition of blood elements on the membranes of parallel membrane dialysers. All types of cellulose membranes were characterized by acute dialytic monocytopenia. Synthetic membranes produced no considerable monocytopenia. No convincing data on the dependence of the monocytic stimulation effect on membrane material were obtained. Possible mechanisms of monocytic activation during HD were discussed.     

Polymicrobial bacteremia during long-term hemodialysis

A review of hospital epidemiologic data disclosed five cases of polymicrobial bacteremia on a nephrology inpatient service over a period of 30 months. All five cases occurred in patients receiving long-term hemodialysis; four of them had indwelling silicone rubber vascular access devices. Although all patients had risk factors other than uremia and dialysis predisposing to an increased likelihood of infection, no patient had either obvious skin infection at the site of the vascular access or documented visceral infection. One patient died, and the other four recovered after removal of the vascular access device and appropriate antibiotic therapy. The increased risk of polymicrobial bacteremia associated with long-term hemodialysis should be taken into account when empiric antibiotic therapy is undertaken.     

Moxalactam pharmacokinetics during hemodialysis.

To establish dosage recommendations, moxalactam elimination kinetics were studied in six anephric patients during hemodialysis and in four anephric patients during the interdialytic period. After a single 1-g intravenous bolus injection, moxalactam elimination half-life was 18.0 plus or minus 0.6 h with a volume of distribution of 20.2 plus or minus 3.6 liters and a plasma clearance of 12.8 plus or minus 2.0 ml/min in four nondialyzed patients. Moxalactam elimination half-life was decreased to 2.7 plus or minus 0.2 h during hemodialysis in six patients. After 4 h, 48.5% of the dose was recovered in the dialysate. The maintenance dose of moxalactam should be decreased to 15% of a normal dose in patients with creatinine clearances less than 10 ml/min, and 50% of a loading dose should be given after hemodialysis.     

Mechanisms producing hypoxemia during hemodialysis

Arterial hypoxemia occurs frequently during hemodialysis. Proposed mechanisms for this phenomenon have included hypoventilation and embolism of granulocyte aggregates. We studied 18 patients with endstage renal failure who required chronic hemodialysis, and measured arterial blood gases, pulmonary gas exchange, and dialyzer gas exchange. During use of acetate as a dialysate buffer, PaO2 decreased to 80 +/- 6.8 torr, whereas during use of the bicarbonate buffer oxygen tension remained at 92 +/- 4.9 torr or greater. Hypoventilation and microembolism were not sufficient to explain the degree of hypoxemia during acetate dialysis. Hypoxemia occurred only after the 1st exposure to acetate; neither an instantaneous change to bicarbonate nor stopping dialysis restored oxygen tension to normal. We conclude that a pharmacologic action of acetate adversely affects lung function, aggravating the decreased alveolar oxygen tension (PAO2) due to hypoventilation. Hypoxemia was not present when bicarbonate was used. Acetate buffer should not be used for dialysis in patients with unstable cardiovascular or respiratory systems.     

Plasma acetate levels during hemodialysis

Before dialysis, acetate levels in hemodialyzed patients (0.27--1.1 mmol/1) were more dispersed than in normal subjects (0.20--0.65 mmol/l) and the mean value of plasma acetate was slightly higher (0.52 mmol/l versus 0.31 mmol/l). Though dialysis conditions were almost identical, the acetate kinetics during hemodialysis were very different: in most subjects, plasma acetate concentrations reached a "plateau" (mean value 5.6 mmol/l) whereas in others a continuous rise was observed, suggesting that with patients having chronic renal failure there were important individual or occasional differences in the ability to metabolize acetate. The acetate loads per minute (or mass transfers) were calculated from the blood compartment with plasma values (plasma flow and concentrations), rather than from the dialysate and using the combined calculations (plasma and whole blood values). The results ranged between 2.4 and 4.1 mmol/min. A very important and rapid fall in arterial acetate concentrations occurs in the first 20 min after the end of the dialysis and proves the rapid turnover of the acetate in man.     

维持性血液透析患者血液灌流凝血的危险因素分析

目的 了解维持性血液透析患者血液灌流凝血的发生情况,分析其危险因素.方法 对我院血液净化中心行血液灌流治疗的72例维持性血液透析患者进行回顾性研究,收集患者临床资料和生化指标,分析维持性血液透析患者血液灌流凝血的发生率及其危险因素.结果 72例维持性血液透析患者共进行血液灌流302例次,7例患者发生血液灌流凝血16例次,其中Ⅱ级凝血6例次,Ⅲ级凝血10例次.发生过血液灌流凝血的患者合并肿瘤、糖尿病、血管通路功能不良比例及血清低密度脂蛋白、脂蛋白a水平明显高于未发生过血液灌流凝血者,两组患者在年龄、性别、透析龄、超滤速度、机器温度、跨膜压、血肌酐、尿素氮、甘油三酯、总胆固醇、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇、脂蛋白a、血红蛋白、血小板及透析前APTT活化部分凝血酶活酶时间等方面相比,差异无统计学意义（P＞0.05）.凝血发生早期透析器呈现静脉压过低报警,凝血常发生在血液灌流1.5～2 h.结论 维持性血液透析患者常规行血液灌流治疗时存在凝血的风险.血液灌流联合血液透析过程中透析器呈现静脉压过低报警时应警惕凝血发生.合并肿瘤、糖尿病、血管功能不良比例及血清低密度脂蛋白、脂蛋白a水平增高的维持性血液透析患者联合血液灌流治疗时易发生凝血.     

血液透析过程中丙型肝炎病毒感染的预防

目前普遍认为,丙型病毒性肝炎(HCV)感染与输血和血制品的使用密切相关.维持性血液透析患者是HCV的易感人群,丙型肝炎病毒可通过血液透析(HD)和输血过程进行交叉感染,同时由于HD患者多数免疫功能低下,更易发生感染.HCV可发展为慢性肝炎、肝硬化,甚至发生肝癌,严重影响HD患者的生活质量和存活率.因此,如何预防HD过程中HCV感染是目前HD领域关注的焦点 [1] .我们于1999年6月至2004年4月采取了一系列预防HD过程中HCV感染的措施,效果满意,总结如下.     

Non-invasive measurements of cardiac output in atrial fibrillation: Inert gas rebreathing and impedance cardiography

Abstract

Background. Atrial fibrillation (AF) is associated with significant morbidity and mortality. To test the effect of interventions, knowledge of cardiac output (CO) is important. However, the irregular heart rate might cause some methods for determination of CO to have inherent weaknesses. Objective. To assess the validity of these methods in AF, a new inert gas rebreathing device and impedance cardiography was tested with echocardiography as reference. Methods. Using a cross-sectional design, 127 patients with AF and 24 in SR were consecutively recruited. Resting CO was measured using inert gas rebreathing (n = 62) or impedance measurement of intrathoracic blood flow (n = 89) in separate studies with echocardiographic measurement as reference. Results. CO determined with impedance cardiography was mean 4.77 L/min ± 2.24(SD) compared to 4.93 L/min ± 1.17 by echocardiography (n = 89, n.s.) in patients with AF. CO by inert gas rebreathing was 4.98 L/min ± 2.49(SD) compared to 5.70 L/min ± 2.49 by echocardiography (n = 62, n.s.) in patients with AF and SR (AF 5.42 ± 2.9 vs. 6.27, n.s. and SR 4.09 ± 1.08 vs. 4.35 ± 0.86, n.s.). Mean bias between impedance cardiography and echocardiography was 0.14 ± 0.95 L/min and ?0.13 ± 0.98 L/min between inert gas rebreathing and echocardiography. Inert gas rebreathing showed larger intra-patient variation than impedance cardiography (0.11 vs. 0.054). Correlation between inert gas rebreathing and echocardiography was r = ?0.060 and between impedance cardiography and echocardiography was r = 0.128. Impedance cardiography and inert gas rebreathing both underestimated CO compared to echocardiography. Conclusion. Variation between the inert gas rebreathing and the reference method for AF patients was less than desired. Impedance cardiography was superior to inert gas rebreathing and showed acceptable agreement with echocardiography and variability similar to echocardiography.