跨肺压监测在急性主动脉夹层Stanford A型手术后患者中的应用研究

目的探讨跨肺压监测在急性主动脉夹层Stanford A型手术后患者中的应用。方法选择2015年1-10月收治我院重症医学科经CT确诊"急性主动脉夹层Stanford A型"在急诊全麻深低温体外循环下行"Cabrol加升主动脉及全弓替换加降主动脉支架象鼻手术患者19例,随机分为两组,观察组9例,对照组10例。两组患者入室后,每日均给予肺复张治疗,观察组患者通过食道压监测设定呼气末正压(PEEP)值,维持跨肺压为正值;对照组患者则通过PEEP递增法设定PEEP值,观察两组患者0 h、24 h、48 h、72 h肺顺应性、氧合指数、PEEP值及总机械通气时间、住ICU时间、住院时间。结果两组患者0 h及入室时肺顺应性、氧合指数、PEEP值比较差异无统计学意义(P0.05),入室后观察组患者通过食道压监测维持呼气末跨肺压为正值后24 h、48 h、72 h监测肺顺应性、氧合指数、PEEP值高于对照组,两组比较差异有统计学意义(P0.05),观察组总机械通气时间少于对照组(P0.05),两组患者住ICU时间、住院时间比较差异无统计学意义(P0.05)。结论通过食道压监测设定PEEP值在急性主动脉夹层Stanford A型手术后患者跨肺压维持方面具有指导意义,且在维持跨肺压的过程中更需要护士精心护理,规范护理操作,连续监测、自动调整气囊压力,保持呼吸机管路的密闭性。     

跨肺压滴定PEEP在急性主动脉夹层术后低氧血症患者中的临床应用研究

目的探讨跨肺压指导呼气末正压通气(PEEP)选择对急性主动脉夹层术后低氧血症患者氧合、血流动力学及预后的影响。方法采用前瞻性随机对照研究,入选2014年1月—2015年8月急性Stanford A型主动脉夹层术后低氧血症患者28例,随机分为2组:个体化治疗组(n=19),肺复张后通过食道压监测结果调整PEEP;传统机械通气治疗组(n=9),肺复张后按照ARDSnet建议调整PEEP。比较2组患者呼吸、血流动力学参数、机械通气时间、住ICU时间及住院病死率。结果第72 h,个体化治疗组的PEEP、吸气末跨肺压均较传统机械通气治疗组高(P0.05);第72 h,个体化治疗组动脉血氧分压(PO2)、氧合指数高于传统机械通气治疗组(P0.05)。整个实验过程中,2组患者的心率和心排量无明显差异(P0.05)。个体化治疗组患者机械通气时间和住ICU时间均比传统机械通气组时间短(P0.05),2组患者的住院病死率无统计学差异(P0.05)。结论肺复张后应用跨肺压指导PEEP的机械通气策略可改善急性主动脉夹层术后低氧血症患者氧合,缩短机械通气时间、住ICU时间,且不会引起循环波动。     

机械通气患者呼气末正压对膀胱压的影响

目的：探讨机械通气患者呼气末正压（PEEP）对膀胱压的影响。方法选取我院重症医学科机械通气且监测膀胱压的患者40例,将膀胱压正常＜1．47 kPa（15 cmH2 O）的患者23例作为A组,膀胱压增高≥1．47 kPa （15 cm H2 O ）的患者17例作为 B 组,采用自身对照法,观察患者在断开呼吸机及使用呼气末正压0 kPa （0 cmH2O）、0．294 kPa （3 cmH2O）、0．490 kPa（5 cmH2O）、0．981 kPa（10 cmH2O）和1．47 kPa（15 cmH2O）时的膀胱压变化。结果A组患者在不同呼气末正压时膀胱压的变化差异无统计学意义（P＞0．05）。B组患者在呼气末正压＞0．294 kPa（3 cmH2 O）时随着呼气末正压的增高膀胱压也会随之增高,差异有统计学意义（P＜0．05）,呼气末正压为≤0．294 kPa（3 cmH2 O）时与断开呼吸机时测得的膀胱压比较,差异无统计学意义（P＞0．05）。结论膀胱压＜1．47 kPa（15 cm H2 O ）时,可保持呼吸机的呼气末正压正常调整,以保证患者的氧合,保障患者的安全。膀胱压≥1．47 kPa（15 cmH2 O）时,应保持呼吸机的呼气末正压≤0．294 kPa（3 cmH2 O）的水平,以保证患者的氧合,保障患者的安全。     

触发灵敏度对压力支持通气患者肺通气均一性的影响

目的观察呼吸机触发灵敏度对压力支持通气患者肺通气均一性的影响。 方法前瞻性纳入20例使用压力支持模式通气时存在肺不均一性通气的患者,即应用肺电阻抗断层成像监测时重力依赖区通气分布比低于45%。随机使用低和高两种流速触发灵敏度水平通气20 min（采用Servo-i呼吸机流速触发灵敏度的最低和最高限值2 L/min和0.2 L/min）。通过肺电阻抗断层成像评估重力依赖区通气分布和呼气末肺体积,采用食道压监测评估吸气努力和做功。 结果与高触发灵敏度相比,低触发灵敏度增加了患者吸气时重力依赖区通气分布百分比[（33 ± 9）% vs.（36 ± 9）%,t = 3.735,P = 0.001]、食道压变化值[0.8（0.4,1.8）cmH₂O vs. 1.6（1.0,2.1）cmH₂O,Z = 2.722,P = 0.021]、压力时间乘积[29（15,54）cmH₂O·s^-1·min^-1 vs. 48（23,74）cmH₂O·s^-1·min^-1,Z = 3.298,P = 0.044],但跨肺压变化值没有明显变化[（12.6 ± 4.3）cmH₂O vs.（12.8 ± 4.2）cmH₂O,t = 0.906,P = 0.376]。此外,低触发灵敏度的整体呼气末肺容积变化值为78（29,170）mL,且其变化值主要分布于重力依赖区[75（-6,131）mL]。 结论压力支持通气时,降低触发灵敏度可通过增加吸气努力使更多的气体进入肺重力依赖区并改善通气均一性,同时吸气努力和跨肺压仍在可接受范围内。     

呼气末正压水平对脑出血患者颅内压及脑灌注压的影响

脑出血常常合并急性肺损伤／急性呼吸窘迫综合征或者肺部感染,为纠正低氧血症需进行呼吸机正压通气。但呼气末正压（positive end—expiratory pressure,PEEP）的使用可诱导胸腔内高压、减少静脉回流量,有可能影响颅内压及脑灌注压。本研究中探讨不同呼气末正压水平与颅内压、平均动脉压及脑灌注压的变化关系,为临床实际运用提供依据。     

急性Stanford A型主动脉夹层患者术后短期病死率的影响因素

目的探讨急性Stanford A型主动脉夹层患者术后短期病死率的影响因素。 方法回顾性收集新疆医科大学第一附属医院ICU于2017年1月至2021年1月收治的成功完成手术治疗的253例急性Stanford A型主动脉夹层患者的临床资料,其中男性213例（84.19%）;年龄（47.07±9.27）岁。根据患者术后30 d是否死亡分为存活组（216例,85.38%）和死亡组（37例,14.62%）,对患者一般基线特征及围术期临床资料进行分析。通过单因素和多因素logistic回归分析探讨急性Stanford A型主动脉夹层患者术后短期病死率的相关影响因素。 结果单因素分析结果显示,2组患者在年龄,术前伴器官灌注不良综合征,体外循环时间,术后48 h引流量＞1 L、需肾替代治疗的急性肾损伤（RRT-AKI）、低心排之间差异均有统计学意义（P＜0.05）。多因素logistic回归分析结果显示,年龄（OR=1.174,95%CI：1.083~1.272,P＜0.001）、术前伴器官灌注不良综合征（OR=7.339,95%CI：2.221~24.247,P=0.001）、体外循环时间（OR=1.031,95%CI：1.015~1.048,P＜0.001）、术后RRT-AKI（OR=12.490,95%CI：3.477~44.866,P＜0.001）、术后低心排（OR=14.325,95%CI：2.740~74.897,P=0.002）是急性Stanford A型主动脉夹层患者术后短期病死率的独立影响因素。 结论急性Stanford A型主动脉夹层患者术后病死率较高,年龄、术前伴器官灌注不良综合征、体外循环时间、术后发生RRT-AKI和低心排为急性Stanford A型主动脉夹层患者术后短期病死率的独立影响因素。     

驱动压和跨肺压优化肺保护性通气的研究进展

急性呼吸窘迫综合征(acute respiratory distress syndrome, ARDS)是一种难治低氧性呼吸衰竭。机械通气作为其常规治疗手段，虽能改善氧合，但也可引起通气相关肺损伤(ventilatory-associated lung injury, VALI)。随着认识发展，对VALI发生机制的认知逐步发生压力伤、容积伤、剪切伤以及生物伤的转变，最终以应力、应变以及耦合的机械能作为通气相关肺损伤的决定因素。传统的保护性通气策略包含小潮气量、低平台压以及呼气末正压(positive end-expiratory pressure, PEEP)的滴定。为了进一步实现个体化保护，驱动压及跨肺压的临床应用不断被强调。驱动压能在一定程度上反映肺顺应性，当以低水平驱动压为目标进行通气参数调整时能有效降低机械通气下肺的非生理性应变，并降低通气的机械能。而跨肺压作为直接扩张肺的压力，不仅避免了因患者胸壁顺应性差异及腹内压升高带来的对实际肺泡压的误判，同时能更加精准地预测肺的过度膨胀，避免VALI的发生。然而跨肺压的监测需要通过测量食管压，这种操作难度在一定程度上抵消了跨肺压的优势。...     

外科重症加强治疗病房252例次机械通气患者肺复张术分析

目的总结肺复张术对机械通气患者血压、血氧饱和度（SO2）的影响及其临床效果。方法选择2005年7月-2007年2月46例实施肺复张术患者的临床资料,分析其复张效果、肺复张术的不良反应等。肺复张采取固定驱动压、逐渐升高呼气末正压（PEEP）的方法,所有肺复张患者均进行有创动脉血压监测。结果46例患者进行了252次肺复张术,其中1例军团菌肺炎患者发生纵隔气肿;1例患者因存在卵圆孔未闭,复张无效;肺复张总有效率为91%。肺复张中有效PEEP变化较大,最低8cmH2O（1cmH2O=0.098kPa）,最高30cmH2O;SO2维持最短0.4h,最长368h,平均每例患者接受5.48次,其中有1例患者最多接受16次肺复张术。23例患者在肺复张中曾经发生过低氧血症（占50%）,252次肺复张术中发生101次低氧血症（占40%）;开始诱发低氧血症的最低PEEP为8cmH2O,最高为22cmH2O,平均12.7cmH2O。25例患者肺复张中曾发生过血压短暂降低（占54%）,252次肺复张中有93次血压短暂降低（占37%）;开始出现血压下降的最低PEEP为6cmH2O,最高为23cmH2O,平均13.9cmH2O。结论肺复张术可以有效改善SO2,PEEP的设定应遵循个体化的原则。     

Stanford A型主动脉夹层患者术后拔除气管插管预防性给予高流量氧疗的效果评价

目的 探讨高流量氧疗方法在 Stanford A 型主动脉夹层术后拔除气管插管患者中的应用效果。 方法 选取心脏外科因Stanford A型主动脉夹层入院、术后拔除气管插管的患者,2017年1月—4月的45例为对照组,采用普通面罩式雾化器吸氧方式。2017年5月—10月的45例为试验组,采用呼吸机高流量氧疗方式。高流量氧疗组参数设置：氧 浓度（FiO2）40%～60%,氧流速35～60L/min,72 h后更换为普通面罩氧疗。结果 试验组的氧合指数、氧分压在测量时段较对照组均有提高,呼吸频率、二氧化碳分压在测量时段较对照组均有降低,差异有统计学意义（ P＜0.05 ）;试验组在 24 h 、 48 h 、 72 h 后口腔鼻腔干燥症状评分和咽喉疼痛症状评分均低于对照组,差异有统计学意义（P＜0.05）;试验组低氧血症发生率和二次插管发生率低于对照组 （ P＜0.05 ）。 结论 Stanford A 型主动脉夹层术后预防性应用高流量氧疗能够提高PaO2/FiO2、PaO2,降低PaCO2、呼吸频率,减轻呼吸道不适症状,降低低氧血症、二次插管发生率。     

Stanford A型主动脉夹层围术期低氧的原因分析及治疗策略

目的 分析Stanford A型主动脉夹层围术期低氧的原因,总结其治疗策略.方法 回顾性分析我院2005年12月至2011年7月64例Stanford A型主动脉夹层手术患者临床资料,其中慢性夹层9例,55例急性夹层.术前氧合指数＜ 200 mm Hg有51例.所有病例深低温停循环下完成手术.结果 3例死亡.术后呼吸机辅助持续72 h氧合指数＜200 mm Hg有33例,1例气管切开呼吸机辅助9d后撤机,余病例均在呼吸机辅助通气72～120 h后顺利撤机.统计分析发现术后低氧与术前氧合指数＜200mm Hg(P =0.002)、急性夹层(P=0.048)、BMI(P=0.046)、停循环时间(P=0.03)、术中输血量≥3000ml(P =0.001)有关.结论 重视Stanford A型主动脉夹层围术期低氧的相关因素,有助于此型患者度过术后严重低氧阶段,改善预后.     

Mortality and pulmonary mechanics in relation to respiratory system and transpulmonary driving pressures in ARDS

Purpose

The driving pressure of the respiratory system has been shown to strongly correlate with mortality in a recent large retrospective ARDSnet study. Respiratory system driving pressure [plateau pressure?positive end-expiratory pressure (PEEP)] does not account for variable chest wall compliance. Esophageal manometry can be utilized to determine transpulmonary driving pressure. We have examined the relationships between respiratory system and transpulmonary driving pressure, pulmonary mechanics and 28-day mortality.

Methods

Fifty-six patients from a previous study were analyzed to compare PEEP titration to maintain positive transpulmonary end-expiratory pressure to a control protocol. Respiratory system and transpulmonary driving pressures and pulmonary mechanics were examined at baseline, 5 min and 24 h. Analysis of variance and linear regression were used to compare 28 day survivors versus non-survivors and the intervention group versus the control group, respectively.

Results

At baseline and 5 min there was no difference in respiratory system or transpulmonary driving pressure. By 24 h, survivors had lower respiratory system and transpulmonary driving pressures. Similarly, by 24 h the intervention group had lower transpulmonary driving pressure. This decrease was explained by improved elastance and increased PEEP.

Conclusions

The results suggest that utilizing PEEP titration to target positive transpulmonary pressure via esophageal manometry causes both improved elastance and driving pressures. Treatment strategies leading to decreased respiratory system and transpulmonary driving pressure at 24 h may be associated with improved 28 day mortality. Studies to clarify the role of respiratory system and transpulmonary driving pressures as a prognosticator and bedside ventilator target are warranted.

     

无创正压机械通气治疗急性心源性肺水肿的临床研究

目的：研究和探讨应用无创机械通气（NIPPV）治疗急性心源性肺水肿（ACPE）的临床价值。方法：将2005年2月-2006年10月我院急诊科救治的54例ACPE患者随机分为常规治疗组和NIPPV组。NIPPV组在给予常规药物治疗基础上,给予压力支持通气（PSV）加呼气末正压（PEEP）通气模式,PSV8～15cmH2O,PEEP5～8cmH2O,常规治疗组给予Venturi面罩吸氧。在治疗第1、2、24h分别测量血气、血压、心率、呼吸频率及无创心功能等临床指标。将2组数据进行对比。结果：与对照组比较,NIPPV组治疗1、2、24h后,患者临床症状与体征改善明显、迅速,其PaO2、氧合指数显著升高,HR、RR及MAP显著下降（组间及组内治疗前后比较P〈0．05或P〈0．01）,心功能明显改善,气管插管率及住院时间显著降低。NIPPV组28例患者有2例改行气管插管（7．14％）,对照组有6例改行气管插管（23．07％）（P〈0．05）。结论：与常规治疗相比,应用NIPPV治疗ACPE能快速改善氧合、动脉血二氧化碳分压及呼吸困难,减少气管插管,值得在临床推广使用。     

Stanford A型主动脉夹层术后早期的急性肺损伤

目的 探讨Stanford A型主动脉夹层术后早期的急性肺损伤.方法 回顾性分析2006年1月至2013年3月对30例StanfordA型主动脉夹层患者行手术治疗,其中21例患者行全弓置换＋象鼻支架置入手术治疗,9例患者行三分支覆膜支架重建主动脉弓部手术治疗.记录手术前、手术结束时、入ICU时动脉血氧分压（PaO2）、二氧化碳分压（PaCO2）及吸入氧浓度（FiO2）,计算肺泡-动脉血氧分压差（A-aDO2）、氧合指数（OI）,分析术后早期肺通气及氧合功能的变化.结果 A-aDO2、OI两指标手术前、手术结束、入ICU时比较,差异均有统计学意义[（112.47 ±41.06）、（136.13 ±29.51）、（141.37±25.94）mmHg,（535.23±70.15）、（491.50±73.12）、（387.33 ±91.32） mmHg;F值分别为35.926、323.742;P值均为0.000];A-aDO2、OI两指标入ICU时与术前比较,差异均有统计学意义（P均＜0.05）,与手术结束时比较,差异均有统计学意义（P＜0.01,P＜0.05）.结论 Stanford A型主动脉夹层患者术后早期肺氧合及交换功能均受到一定损害,A-aDO2、OI可作为敏感指标为该类患者术后早期的急性肺损伤提供诊治依据.     

Stantord B型主动脉夹层术前肝功能影响因素的相关分析

目的探讨Stanford B型主动脉夹层术前肝功能状态并分析影响因素。方法2004年1月至2013月9月新疆维吾尔自治区人民医院心外科连续收治Stanford B型主动脉夹层患者151例,其中急性期患者89例,亚急性期患者40例,慢性期患者22例。选取年龄和性别匹配的健康体检者95例为对照组。采集各组清晨空腹静脉血测定其肝功能生化指标,采用主动脉CTA测定夹层原发破口及剥离范围,心脏彩超检查评估主动脉瓣反流情况。结果StanfordB型主动脉夹层组术前大部分肝功能指标[胆碱酯酶（CHE）、总胆红素（TBIL）、间接胆红素（IBIL）、总蛋白、白蛋白（ALB）、谷氨酸转氨酶、谷氨酰转肽酶、碱性磷酸酶（ALP）]均显著高于对照组（P均〈0．05）,急性期患者CHE、TBIL、IBIL、ALB、ALP升高更明显（P均〈0．05）。相关分析显示,多个肝功能指标与主动脉夹层分期相关,TBIL、IBIL、ALB分别呈负相关（r=-0．286、P〈0．001,r=-0．261、P=0．002,r=-0．267、P=0．001）,与ALP呈正相关（r=0．272、P=0．001）。 结论主动脉夹层急性期肝功能受损更严重,肝功能损伤程度可能与主动脉夹层的分期相关。     

The esophagus ... not just for food anymore?

Citation

Talmor D, Sarge T, Malhotra A, O''Donnell CR, Ritz R, Lisbon A, Novack V, Loring SH: Mechanical ventilation guided by esophageal pressure in acute lung injury. N Engl J Med 2008, 359:2095-2104 [1].

Background

Survival of patients with acute lung injury or the acute respiratory distress syndrome (ARDS) has been improved by ventilation with small tidal volumes and the use of positive end-expiratory pressure (PEEP); the optimal level of PEEP has been difficult to determine. In this pilot study, we estimated transpulmonary pressure with the use of esophageal balloon catheters. We reasoned that the use of pleural-pressure measurements, despite the technical limitations to the accuracy of such measurements, would enable us to find a PEEP value that could maintain oxygenation while preventing lung injury due to repeated alveolar collapse or overdistention.

Methods

Objective

To evaluate the effectiveness of using an esophageal balloon catheter to measure pleural pressure and guide PEEP titration to achieve normal physiologic parameters in individual patients.

Design

Single center, randomized-controlled pilot trial. Setting: Medical and surgical ICUs at Beth Israel Deaconess Medical Center.

Subjects

61 patients with acute lung injury or ARDS as defined by the American-European Consensus Conference definition.

Intervention

Patients with acute lung injury or ARDS were randomly assigned to undergo mechanical ventilation with PEEP adjusted according to measurements of esophageal pressure (the esophageal-pressure-guided group) or according to the Acute Respiratory Distress Syndrome Network standard-of-care recommendations (the control group).

Outcomes

The primary end point was improvement in oxygenation at 72 hours after randomization. Secondary end points included indexes of lung mechanics and gas exchange, number of ventilator free days, length of ICU stay, and death at 28 days and 180 days.

Results

The study reached its stopping criterion and was terminated after 61 patients had been enrolled. The ratio of the partial pressure of arterial oxygen to the fraction of inspired oxygen at 72 hours was 88 mmHg higher in the esophageal-pressure-guided group than in the control group (95% confidence interval, 78.1 to 98.3; P = 0.002). This effect was persistent over the entire follow-up time (at 24, 48, and 72 hours; P = 0.001 by repeated-measures analysis of variance). Respiratory-system compliance was also significantly better at 24, 48, and 72 hours in the esophageal-pressure-guided group (P = 0.01 by repeated-measures analysis of variance).

Conclusions

As compared with the current standard of care, a ventilator strategy using esophageal pressures to estimate the transpulmonary pressure significantly improves oxygenation and compliance. Multicenter clinical trials are needed to determine whether this approach should be widely adopted. (ClinicalTrials.gov number, NCT00127491.)     

Postoperative hypoxemia for patients undergoing Stanford type A aortic dissection

Clinically, it is widely recognized that surgical treatment is the preferred and reliable option for Stanford type A aortic dissection. Stanford type A aortic dissection is an emergent and serious cardiovascular disease characterized with an acute onset, poor prognosis, and high mortality. However, the incidences of postoperative complications are relatively higher due to the complexity of the disease and its intricate procedure. It has been considered that hypoxemia, one of the most common postoperative complications, plays an important role in having a worse clinical prognosis. Therefore, the effective intervention of postoperative hypoxemia is significant for the improved prognosis of patients with Stanford type A aortic dissection.     

呼气末正压对急性呼吸窘迫综合征绵羊内脏器官灌注的影响

目的　观察呼气末正压 (PEEP)对急性呼吸窘迫综合征 (ARDS)绵羊内脏器官灌注的影响。方法　内毒素 (LPS)静脉注射复制绵羊ARDS模型 ,维持心脏最佳前负荷 ,依次调整PEEP为 5、 10、15cmH2 O ,观察不同PEEP对血流动力学、呼吸力学、氧代谢及内脏器官灌注的影响。结果　与基础值(PEEP =0cmH2 O)比较 ,PEEP 5、 10、 15cmH2 O组心率、平均动脉压、肺动脉压、中心静脉压、肺动脉嵌顿压及心输出量差异无显著性意义 ,但PEEP 10、 15cmH2 0组动脉氧分压和动脉氧饱和度均同步明显增加 ,氧合指数也从 ( 10 4 6 4± 2 5 2 1)mmHg提高到 ( 136 2 5± 38 5 4 )和 ( 135 37± 37 5 6 )mmHg (P <0 0 5 ) ,PEEP 5、 10、 15cmH2 O组肠黏膜pH值 (pHi)与基础比较 ,差异无显著性意义 (P >0 0 5 )。各组肠黏膜与动脉二氧化碳分压差 (Pg aCO2 )也无明显差异。全身氧输送、血乳酸无明显改变 (P >0 0 5 )。与基础值比较 ,PEEP各组平均气道压、气道平台压及肺动态顺应性显著增加 ,PEEP 15cmH2 O组气道峰压也明显增高(P <0 0 5 )。结论　维持心脏最佳前负荷状态下 ,血流动力学和氧输送可保持稳定 ,PEEP在 15cmH2 O以下对ARDS绵羊内脏灌注无明显影响     

肺复张治疗对纠正深低温停循环主动脉术后低氧血症的疗效观察

目的 评价肺复张对深低温停循环主动脉术后低氧血症的治疗作用及安全性.方法 前瞻性随机对照研究.2010年11月至2011年11月行深低温停循环主动脉手术术后发生低氧血症患者40例,随机分为两组:对照组(n=20),行常规机械通气治疗;试验组(n=20),行肺复张治疗.对比两组患者机械通气时间及肺复张前后呼吸和循环参数的变化.结果 肺复张组患者氧合明显改善(PaO2/FiO2:94.0±2.9 vs.180.4±31.8,P<0.001);肺复张期间对血管活性药物剂量进行调整后,患者的平均动脉压、心率、中心静脉压均可维持稳定状态;肺复张组较常规治疗组的机械通气时间缩短,但差异无统计学意义[(25.4±16.4)h vs.(21.8±12.6)h,P=0.493].结论 肺复张可改善深低温停循环主动脉术后的氧合状态,且患者耐受性良好,是一种安全有效的治疗手段.     

Experts’ opinion on management of hemodynamics in ARDS patients: focus on the effects of mechanical ventilation

Rationale

Acute respiratory distress syndrome (ARDS) is frequently associated with hemodynamic instability which appears as the main factor associated with mortality. Shock is driven by pulmonary hypertension, deleterious effects of mechanical ventilation (MV) on right ventricular (RV) function, and associated-sepsis. Hemodynamic effects of ventilation are due to changes in pleural pressure (Ppl) and changes in transpulmonary pressure (TP). TP affects RV afterload, whereas changes in Ppl affect venous return. Tidal forces and positive end-expiratory pressure (PEEP) increase pulmonary vascular resistance (PVR) in direct proportion to their effects on mean airway pressure (mPaw). The acutely injured lung has a reduced capacity to accommodate flowing blood and increases of blood flow accentuate fluid filtration. The dynamics of vascular pressure may contribute to ventilator-induced injury (VILI). In order to optimize perfusion, improve gas exchange, and minimize VILI risk, monitoring hemodynamics is important.

Results

During passive ventilation pulse pressure variations are a predictor of fluid responsiveness when conditions to ensure its validity are observed, but may also reflect afterload effects of MV. Central venous pressure can be helpful to monitor the response of RV function to treatment. Echocardiography is suitable to visualize the RV and to detect acute cor pulmonale (ACP), which occurs in 20–25 % of cases. Inserting a pulmonary artery catheter may be useful to measure/calculate pulmonary artery pressure, pulmonary and systemic vascular resistance, and cardiac output. These last two indexes may be misleading, however, in cases of West zones 2 or 1 and tricuspid regurgitation associated with RV dilatation. Transpulmonary thermodilution may be useful to evaluate extravascular lung water and the pulmonary vascular permeability index. To ensure adequate intravascular volume is the first goal of hemodynamic support in patients with shock. The benefit and risk balance of fluid expansion has to be carefully evaluated since it may improve systemic perfusion but also may decrease ventilator-free days, increase pulmonary edema, and promote RV failure. ACP can be prevented or treated by applying RV protective MV (low driving pressure, limited hypercapnia, PEEP adapted to lung recruitability) and by prone positioning. In cases of shock that do not respond to intravascular fluid administration, norepinephrine infusion and vasodilators inhalation may improve RV function. Extracorporeal membrane oxygenation (ECMO) has the potential to be the cause of, as well as a remedy for, hemodynamic problems. Continuous thermodilution-based and pulse contour analysis-based cardiac output monitoring are not recommended in patients treated with ECMO, since the results are frequently inaccurate. Extracorporeal CO₂ removal, which could have the capability to reduce hypercapnia/acidosis-induced ACP, cannot currently be recommended because of the lack of sufficient data.