三尖瓣返流压力差在肺心病肺动脉高压诊断和治疗中应用价值的研究
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摘要
肺动脉高压是临床常见的—种病理生理过程,常继发于胸、肺和心脏疾病,其中以慢性阻塞性肺疾病(COPD)居多。慢性阻塞性肺疾病(COPD)的发病率和死亡率极高,其致死率1997年位居全美第四位,预计在2020年将成为全球第三大致死病因。在我国,近年来COPD所致的肺心病已由原来占器质性心脏病的第二位上升到了首位。COPD是一种具有气流受限特征的疾病,气流受限不完全可逆、呈进行性发展,与肺部对有害气体或有害颗粒的炎症异常反应有关。它的自然病程以进行性呼出气流减少、呼气末肺容量增大、低氧血症、高碳酸血症和进行性肺动脉高压为特征。肺心病的预后较差,其治疗应该是综合治疗,主要包括控制感染、通畅呼吸道、纠正酸碱平衡紊乱及对症治疗等。而肺动脉高压是肺心病发生发展过程中重要的病理生理基础,且肺动脉压的高低是影响肺心病患者预后的重要因素之一,因此防治肺动脉高压对延缓肺心病的发生发展和降低病死率具有重要意义。
    肺循环是一个高流量、低压力的系统。正常肺动脉收缩压约为20mHg(2.67kpa),舒张压约为10mmHg(1.33kpa),肺动脉平均压约为14mmHg(1.53kpa)。肺动脉高压的概念,根据WHO的诊断标准是指肺动脉收缩压(SPAP)大于4.0kPa(30mmHg),舒张压(DPAP)大于2.4kPa(18mmHg),肺动脉平均压(MPAP)大于3.33kPa(25mmHg)时的病理状态。但目前国内外多主张以安静时肺动脉平均压大于或等于2.67kPa(20mmHg),运动时大于或等于4.0kPa(30mmHg)时即诊断为肺动脉高压。对于COPD及其所致的
    
    
    肺心病,有效地防治肺动脉高压可改善患者的预后并降低病死率。
    目前诊断肺动脉高压的方法有很多种,按其对人体有无损伤可分为有创方法和无创方法。有创方法包括右心导管检查术、Swan-Ganz漂浮导管插入肺动脉测量和肺活检。肺动脉压力经典的测量方法是通过右心导管检查术,肺动脉高压其诊断的金标准也是有创性右心导管检查法。但心导管检查由于仪器昂贵,操作复杂,存在并发症等因素不易普及。在多普勒超声心动图问世以后,无创法测压才得以实现。
    多普勒超声心动图对肺心病的诊断、治疗或科研都可以提供重要的信息。它不仅可以提供心脏形态学改变,如测量右心大小,肺动脉宽度,室壁厚度及室间隔的运动变化等,而且提供了肺动脉高压的定量诊断,这是诊断上的一大飞跃。超声心动图对肺动脉高压的检查具有无创性、敏感性高、易重复等特点,可以清楚地显示心脏结构、瓣膜运动、心脏舒缩的时相以及心腔和大血管内的血流频谱,因此不仅对肺动脉高压的病因诊断、定性和定量化诊断都有重要价值,而且可用于疗效观察及随访。由于肺动脉高压患者的右心室增大及肺动脉增粗,可以产生相对性三尖瓣关闭不全及肺动脉瓣关闭不全。尤以多普勒超声心动图应用于临床后,关闭不全检出率更高。而且绝大多数患者因肺动脉压力很高而三尖瓣返流较重,测量相当容易。因为三尖瓣返流速度决定于瓣口两端压差,因此应用连续超声多普勒可记录完整的三尖瓣返流频谱并测量最大返流速度(PVTR)。然后根据简化柏努利方程(ΔP=4×PVTR 2)可计算出跨瓣压差,ΔP即右室与右房间的压差,该压差加上右房压就等于右室收缩压。假设右室流出道与肺动脉
    
    
    之间无压差存在,则右室收缩压就等于肺动脉收缩压。右房压可根据三尖瓣返流程度估测,一般按10mmHg计算,则肺动脉收缩压(mmHg)=PVTR2×4+10,研究表明应用这一方法估测的肺动脉收缩压与心导管测值的相关系数达0.89-0.97,标准误为5-9mmHg。与有创方法相比较,多普勒超声心动检查测定的指标与直接测定结果具有良好的相关性,有重要的临床应用价值。
    同时,超声心动图在肺动脉高压临床治疗效果的评价上也有一定的价值。多普勒超声心动图测压法为临床药物治疗提供了宝贵的血流动力学资料,并可对患者病情进行分析,对判断病情转归及疗效也提供了有力的依据。我们通过对20例肺心病患者在治疗前后三尖瓣返流跨瓣压差的分析,对在肺心病所致肺动脉高压的诊断和观察疗效中测量三尖瓣跨瓣压差的价值加以综合分析。结果可以看到, 本文所观察的病例经过正规合理的治疗后,治疗前后的三尖瓣返流压差以及由此得出的肺动脉压力有19例出现比较明显的降低。一般看来,肺动脉压越高,三尖瓣的返流就越严重。随着△p的下降,绝大多数患者的三尖瓣返流压力降低,三尖瓣返流也减轻了。而且,在治疗前后患者的临床症状也有了很大的改善。
    由此我们可以得出通过超声心动图测量三尖瓣跨瓣返流压力差不仅能反映患者肺动脉压力的水平,而且还可以通过三尖瓣跨瓣返流压力差反映的肺动脉压力来观察疗效的结论。这个结论不仅说明三尖瓣跨瓣返流压力差可以用于临床上对肺心病的诊断及观察治疗效果,而且还是一个比较可靠的指标。
Pulmonary artery hypertension(PAH) is a common pathophysiological state in many diseases of lung,chest and heart,especially chronic obstructive pulmonary diseases(COPD).The morbidity and mortality of COPD are both very high, whose fatality rate was the fourth in USA in 1997, and will be the third in 2020. In China, the incidence rate of pulmonary heart disease (PHD) caused by COPD has ascended to the frist place in all organic heart diseases in recent years. COPD is characteristic of airflow being limited in airway. This procedure is incompletely reversible and progressing development, which is concerned with the inflammatory reaction caused by gases and granules that are harmful to lung.The pathophysiological processes of COPD are processing decreasing expiratory gas, increasing residual volume, hypoxemia, hypercapnia and pulmonary hypertension.The prognosis of PHD is bad, so we should apply combined therapy, including anti-infection, relieving
    
    
    airway obstruction, redressing acid-base imbalance and symptomatic reatment, etc. Because pulmonary hypertension play important roles in the development and prognosis of PHD, it is very significant to diagnose and treat pulmonary hypertension early for postponing the progression of PHD and depressing the fatality ratio.
    The pulmonary circulation is a system with high flow and low pressure. In normal condition, the systolic pressure of pulmonary artery (SPAP) is about 20mmHg(2.67kpa), the diastolic pressure (DPAP) is about 10mmHg(1.33kpa),and the mean pulmonary artery pressure (MPAP) is about 14mmHg(1.53kpa)。According to the diagnostic standard of WHO, the conception of pulmonary hypertension is the pathologic status that the SPAP is more than 4.0kPa(30mmHg) ,the DPAP is more than 2.4kPa(18mmHg) and the MPAP is more than 3.33kPa(25mmHg). But the diagnostic standard of PAH that is more accepted in internal and overseas at present is that
    
    
    the MPAP≥2.67kPa(20mmHg) at resting state or MPAP≥4.0kPa(30mmHg) at activity state.
    At present, there are many kinds of diadynamic methods about PAH, which can be divided into traumatic check and uninjurious one. The former contains the catheterization of right heart and lung biopsy. The classic measurement of the pressure of pulmonary artery is by cardiac catheter of right heart, and the gold standard of PAH is also this method. But because of the expensive equipment,the complex operation and more complication,the cardiac catheterization couldn’t be popularized easily. Since the appearance of Doppler echocardiography, the uninjurous measurements of the pressure of pulmonary artery has been realized.
    Doppler echocardiography can provide many important information for the diagnosis, therapy and research of PHD. It can not only provide the morphological change of heart by measuring cardiac volume, the width of the pulmonary artery, the ventricular thickness and the movement of
    
    
    interventricular septum, but also give the quantitative diagnosis of PAH. Doppler echocardiography is superior to other methods for its features of uninjury, high-sensitivity and easy reduplication in the measurement of PAH. It can show the structure of heart, the movement of interventricular septum and the phase of the systole and diastole of heart. So Doppler echocardiography not only is very valuable to the etiological diagnosis, the qualitative and quantitative diagnosis of PAH, but also can be used in evaluation of prognosis and therapeutic effect. Because of the augmentation of right ventricle and thickening of pulmonary artery, the relative tricuspid insufficiency and pulmonary artery valve insufficiency can be seen in patients with PAH. And it has been very easy to detect the relative tricuspid insufficiency since Doppler echocardiography is applied in clinic. Because we can record the PVTR by measuring regurgitant spectra with Doppler echocardiography and the regurgitant rate of tricuspid valve (PVTR) is decided by
    
    
    the pressure difference of two sides of which, we can calculateΔP, according
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