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1、Chicago, Illinois理解临床血流动力学understanding clinicial hemodynamics原文:Micharel F. OConnor, M.D. FCCM翻译:福建医科大学附属协和医院麻醉科规培住院医师 陈静The physiologic paradigm that clinicians reference in their attempts to explain and understand the biology of both healthy and critically ill patients has been in evolution for m
2、ore than 100 years.(临床医师尝试着阐述和了解健康和危重症患者而借助的生理学范式已经发展100多年了。)Interestingly, our understanding of the clinical circulation has always been thought of as complete, (有趣的是,人们对临床循环的理解一直被视为“很完整”,)with creative clinicians invoking a variety of reasons to explain away apparent discrepancies between commonly
3、 used mental models and the realities of clinical medicine.(而富有创新性的临床医师则希望通过种种解释消除常用思维模式和临床医学现实之间显著的差异。)The most primitive formulation of the circulation entails simple conservation of matter:(最原始的循环公式蕴含着简单的物质守恒:) Cardiac Output = Stroke Volume x Heart Rate = Qt = SV x HR (心输出量(CO)=每博量心率=Qt = SVHR)
4、This statement, while obviously always true, offers sapient practitioners little insight into why the circulation in a articular patient might be unacceptable, and how they might rationally intervene. (很显然,该表述很正确,却几乎没有为智慧的工作者深入了解为何个别患者的循环可能不稳定以及如何进行合理的干预提供帮助。)During the mid-20th century, a relativel
5、y complete paradigm for understanding the role of the enous return in controlling the cardiac output was refined by Guyton and his co-workers, and has been repetitively validated since it was first described (refs Jacobsohn, Magder, Guyton, Sylvester).在20世纪中叶,Guyton及其同事修订了一个相对完善、关于了解静脉回心血量在控制心输出量中的作
6、用的范式,该范式从首次被描述就进行了反复验证。Although not complete, this theory was powerful in thehands of those who understood it.尽管该理论还不完善,却对已理解该理论的人群产生了很大的作用。The balloon-tipped, flow directed, thermistor equipped pulmonary artery catheter heralded the subsequent era of the understanding of the clinical circulation.装备
7、有末端套囊、血流导向以及热敏电阻的肺动脉导管,预示着理解临床循环时代的到来。This device, coupled with a deep understanding of themechanics of left ventricular function heralded the era in which the circulation and all of its pathology wereunderstood from the perspective of the left-ventricle which some now refer to as the LV centered vi
8、ew of thecirculation (Sagawa).对肺动脉导管及左心室力学功能的深入了解预示着从左心室的视角来理解循环以及循环病理学时代的来临。Nevertheless, the LV centered view of the circulation focused on preload, afterload, and contractility, and was frustrated by a variety of obstacles.然而,以左室为中心观察循环主要以前负荷、后负荷和收缩力为主要研究对象,但若遇到一些障碍,则结果就相形见绌了。 The most important
9、was the poor correlation between measured filling pressures and left ventricular end-diastolic volumes as assessed by echocardiography (refs Kumar,Hofer, Kramer).最重要的是,通过超声心动图进行评估发现,充盈压和左心室舒张末容积之间的相关性较差。Echocardiography has documented that LV compliance is far more dynamic than anyone believed prior
10、 to itswidespread clinical use (Coriat).通过超声心动图证实,左心室顺应性比之前认为已广泛应用于临床的任一参数更优越。The other, more insidious problem with the LV centered world-view is that adherents tend to regard RAP almost exclusively as an index of circulatory volume, forgetting that it is the downstream hydrostatic resistance to ve
11、nous return in the model of Guyton:另一方面,以左心室为中心观察循环存在的潜在问题为,支持者更趋向于认为,RAP几乎为循环容量唯一的指标,而遗忘了在Guyton模型中,RAP为下游流体静力学阻力: VR = CO = Pms RAP RVR(Where VR = Venous Return, RAP = Right Atrial Pressure, and RVR = Resistance to Venous Return)(VR=静脉回心血量,RAP=右心房压,RVR=静脉回心阻力)The circulation in any patient at any
12、moment in time is the product of the interaction of the venous circuit with the heart (the pump). The RAP is a product of that interaction.对于任一患者的任一时刻,循环都是心脏(泵)和静脉回路相互作用的产物。RAP即为该相互作用的产物。While shock is classically associated with hypotension, there is increasing acceptance of the contention that hyp
13、otension is a relatively late indicator of shock, and that clinicians should be more attuned to organ system dysfunction as evidence of shock.虽然休克通常与低血压有关,然而有越来越多的观点认为,低血压已是休克相对“晚期”的指标,临床医师更应习惯于以器官系统功能失调作为休克的证据(表1)。Signs of Shock: - altered mentation- oliguria- decreased mixed venous or central veno
14、us saturation- hypotension, abnormal heart rate- lactic acidosis- peripheral cyanosis (variable)In both the critical care and trauma literature, the endpoints for resuscitation have also evolved.Whiletraditional endpoints such as mean arterial pressure and central venous pressure are still regarded
15、as important,increasing emphasis is being placed on the mixed/central venous oxygen saturation (Ladakis) and lactate levels in the blood.在重症监护和创伤医学文献中,复苏终点也已不断演变。虽然传统的复苏终点(如,平均动脉压和中心静脉压)仍然很重要,但越来越强调混合/中心静脉氧饱和度和血乳酸水平。The combination of inexpensive and readily available serum lactates and increasing a
16、ppreciation of theprevalence of hyperchloremic acidosis in the setting of large volume resuscitation has led to the near abandonment of the base excess/deficit as a guide to the adequacy of resuscitation.在大容量复苏的过程中,作为复苏适度的风向标,方便快捷的血清乳酸测定结合日益受宠的高氯血症酸中毒已经逐渐取代碱过量/缺失。Several publications over the past s
17、everal years have dampened enthusiasm for the use of central venous oxygenation (Chawla, Sander, Varpula), but it nevertheless remains a very useful indicator of the adequacy of oxygen delivery.在过去数年中,许多论文已经降低了对使用中心静脉氧饱和度的热情,但对于氧供充足与否而言,其仍然为非常有用的指标之一。Importantly, as oxygen delivery to the tissues fa
18、lls, oxygen extraction rises, and continues until the tissues are nolonger able to extract more oxygen. When this happens, crisis ensues.重要的是,当组织氧供下降时,氧解离增加,直至组织再没有能力摄取更多的氧。当发生这种情况时,危机就随之而来。In the left figure, oxygen extraction increases as oxygen delivery decreases. When the tissues reach the limit
19、s of their ability to extract oxygen (the critical extraction ratio ERc), the critical oxygen delivery has been reached (Qo2c), and further decreases in oxygen delivery will be associated with a decline in oxygen consumption.From Physics : V = I x R Substituting produces: BP Pra = Qt x SVR物理学:V = IR
20、 替代公式:BP Pra = QtSVRHypoperfusion (shock) can arise from: - low cardiac output - low SVR - the combination of a low cardiac output and high SVR灌注不足(休克)可由以下因素引起:低心排低SVR低排高阻(低心排和高体循环阻力)As demonstrated by the above figure, we can superimpose the Starling curve from above left upon the venous return cur
21、ve from the above right and generate a graphical representation of the state of the circulation. The cardiac output is represented by the Y projection of the intersection of these curves, and the CVP we measure clinically is represented by the X projection of the intersection of these curves.将左侧的Sta
22、rling曲线图和静脉回心血量图叠加,生成循环状态的图示。心排出量则是通过这些曲线的交叉点Y轴的投影表示的,临床监测的CVP通过曲线交叉点的X轴投影表示的。Diastolic dysfunction is a generally underappreciated and very important contributor or cause of shock states.舒张功能不全为一项被普遍低估、却非常重要的休克状态的诱因或病因。In animal models of hemorrhagic shock, even small reductions in pleural pressure
23、s from reduced levels ofPEEP or reduced respiratory rates can produce dramatic improvements in survival (Herff).在失血性休克动物模型中,即使由PEEP水平降低或呼吸频率减少导致胸腔压力细微的下降都可使动物模型的存活状况显著改善(Herff)。This data, coupled with similar data from animal models of CPR, are generating increased interest in ventilation strategies
24、 associated with the lowest possible airway pressures in patients with shock.基于该数据及从心肺脑复苏动物模型中得到的相似数据,人们越来越对以尽可能最小的气道压力对休克患者进行通气的模式感兴趣。Bedside Assessment of the patient with shock休克患者的床旁评估The following questions constitute an orderly way to assess the patient with inadequate circulation:1. Is the Ca
25、rdiac Output Reduced?2. Is the heart “too full”?3. What doesnt fit?以下几个问题形成了一个有序的方法,可用于循环容量不足患者的评估: 心输出量是否减少 心脏是否“太满” 什么方法不适合Is the cardiac output reduced?No Vasodilated ShockYes Hypovolemic shock, Cardiogenic Shock, or Obstruction to Venous Return心输出量是否减少不是血管扩张性休克(血流分布性休克)是的低血容量性休克、心源性休克、静脉回心受阻The
26、above figure demonstrates the sentinel feature of vasodilated or high cardiac output shock:the wide pulsepressure.血管扩张性或高心排性休克的标志性特征为:脉压差大。Patients with vasodilated shock almost invariably have a pulse pressure which is greater than half of their systolic pressure, whereas patients with low cardiac
27、output shock typically have a pulse pressure which is substantially lower than normal.对于血管扩张性休克患者,脉搏压力大于收缩压的一半的状态几乎始终存在,总体而言,低心排性休克患者的脉压则低于正常人。A patient with a blood pressure of 80/30 almost certainly has vasodilated shock,whereas a patient with a blood pressure of 80/60 will have one of the causes
28、of low cardiac output.当患者血压为80/30 mmHg时,几乎可以确定存在血管扩张性休克,而血压为80/60 mmHg时,则为引起低心输出量的原因之一。Differential Diagnosis of Vasodilated Shock:- Sepsis, Sepsis, Sepsis- Systemic Inflammatory Response Syndrome (SIRS) (e.g. pancreatitis)- Hepatic failure- Anaphylaxis- Adrenal insufficiency- AV fistula- Others血管性休
29、克的鉴别诊断:-脓毒血症,败血症,菌血症-全身炎症反应综合征SIRS(如胰腺炎)-肝衰竭-过敏反应-肾上腺功能不全-动静脉血管瘘-其他Is the heart too full? If the cardiac output is low, the differentiation of hypovolemic and cardiogenic shock is accomplished through the review of pertinent historical, physical examination, and laboratory data.Historical informatio
30、n is often compelling in its support for the conclusion that hypovolemia is the cause of an unacceptable circulation.如果合并低心输出量,低血容量性休克和心源性休克的鉴别可通过相关病史的回顾、体格检查和实验室检查来实现。既往信息常常在得出低血容量为导致循环不稳定的原因这一结论时才引起人们的注意。 Cardiogenic shock is most readily assessed with echocardiography. The differential diagnosis
31、of cardiogenic shock includes acute LV infarction, acute on chronic LV failure, RV infarction, RV failure from some cause of increased pulmonary vascular resistance, and previously undiagnosed valvular lesions such as aorticstenosis, mitral stenosis, and mitral regurgitation. 通过超声心动图最容易对心源性休克进行评估。心源
32、性休克的鉴别诊断包括急性左心梗死、慢性左心衰急性期、右心梗死、由某些因素造成肺血管阻力增加导致的右心衰以及先前未确诊的瓣膜疾病,如主动脉瓣狭窄、二尖瓣狭窄和二尖瓣关闭不全。Echocardiography has supplanted the Swan-Ganz catheter as the method of choice for assessing the patientwith suspected cardiogenic shock.超声心动图已经取代Swan-Ganz导管成为评估疑似心源性休克患者的首选。Reasons for this include increasing reco
33、gnition that practitioner understanding of how to utilize data from a Swan-Ganz catheter is generally poor (Iberti), difficulty demonstrating that these catheters improve outcomes (Sandham), and increasing acceptance that central venous gases correlate well with mixed venous gases.其原因包括进一步认识到医师对如何应用
34、Swan-Ganz导管知识的贫乏,导管难以改善预后的阐释以及对中心静脉气体与混合静脉气体之间的良好的相关性的认同性增加。Perhaps most importantly, echocardiographic studies have documented surprisingly poor correlation between filling pressures as measured by invasive monitors and left ventricular end-diastolic volume (Osman). Evidence impeaching the use of c
35、entral venous pressure measurements continues to accumulate, and is now being summarized in colorful review articles(Marik).可能更重要的是,超声心动图研究已经证明,行有创监测获得的充盈压与左心室舒张末容积之间的相关性极差。关于中心静脉压监测的质疑证据也不断积累,并被总结成了丰富多彩的综述文章。As a consequence of these insights, experts are increasingly advocating the use of arterial
36、 pulse pressurevariation as a guide to administering fluid, with a difference of 10-15% with respiration strongly associated with a favorable response to fluid administration (Michard, 2005).鉴于以上观点,专家越来越主张将动脉脉压变异度作为液体管理的一项指南,当呼吸相关性动脉脉搏压力变异度10%15%时,液体治疗往往会产生比较好的反应。The two most commonly used metrics a
37、re Systolic Pressure Variation (SPV) and Delta Pulse Pressure (PP). Systolic Pressure Variation is easier to estimate from conventional monitors, but is slightly inferior to delta Pulse Pressure (also referred to as Pulse Pressure Variation PPV).最常用的两种监测指标为收缩压变异度(SPV)和PP。收缩压变异度更容易通过应用传统监护仪来评估,但略逊于PP
38、(也被称为,脉搏压力变异PPV)。SPV and/or PPV outperform both CVP and Pcwp as predictors of volume responsiveness in septic patientsand cardiac patients, including patients undergoing OPCAB and post-op CABGs (Auler, Hofer, Kramer).对于败血症和心脏病患者,包括进行OPCAB以及CABG术后的患者,将SPV和/或PPV作为容量反应的预测指标优于CVP和PCWP。Newer monitors int
39、ended for use in either the ICU or the OR incorporate software that facilitates the evaluation of these parameters.通过应用ICU或OR中的较新的监护仪整合了便于分析这些参数的软件。Other technologies, including Stroke Volume Variation (SVV)(Lahner, Machare-Delgado), and the PICCO derived Intrathoracic Blood Volume Index (ITBV) are
40、being explored as alternatives to the CVP inpredicting volume responsiveness (Muller), but do not yet match the performance of either PPV or SPV. There is agrowing literature regarding the use of pulse-oximeter derived plethysmography as a less-invasive alternative toSPV or PPV(e.g. Pizov)作为CVP预测容量反
41、应能力的替代指标,其他技术(包括每博量变异度(SVV)以及由胸内血容量指数(ITBV)演变而来的PICCO)正在研发中,但其性能不如PPV或SPV。Systolic pressure variation is useful as a guide to the management of the patient in shock in another way:patients with minimal or no variation in the blood pressure and pulse pressure are very unlikely to respond to volume ad
42、ministration.另一方面,对休克患者进行管理时,收缩压变异度为一个非常有用的指标:患者血压和脉压出现极小或无变异时,几乎不可能对容量治疗作出反应。The initial efforts to resuscitate such patients should therefore be directed at pharmacologicor mechanical interventions, which are much more likely to be effective. Because this strategy minimizes theunnecessary administ
43、ration of fluid to critically ill patients, it may improve outcomes.因此,对此类患者进行复苏时,最初的努力应着眼于使用药物或机械方法干预,这样或许会更有效。由于该方案最大限度的减少了对危重患者实施的不必要的液体治疗,因而可能会改善预后。What doesnt fit?Most patients with hypovolemic shock, LV shock, and sepsis respond to appropriate therapy. Failure to respond should raise red flags
44、, and drive an evaluation for obstructive shock.大多数低血容量性休克、LV休克(左心室相关性休克)以及败血症患者对恰当的治疗均有反应。对于无反应者,应该停止治疗并评估是否发生阻塞性休克。Obstructive shock is shock caused by an obstruction to venous return. Obstructions to venous return are often insidious. While volume resuscitation and therapy with vasoactives might
45、produce a transient minor improvement in the circulation, the definitive treatment consists of relieving the obstruction if this is possible.阻塞性休克由静脉回心受阻引起。静脉回心受阻一般较为隐匿。虽然容量复苏和应用血管活性药物治疗可能会产生短暂轻微的循环改善,但如果可能,恰当的治疗应当包括减轻静脉回心阻力。Causes of Obstructive Shock (Obstructions to Venous Return)- pericardial ef
46、fusion- restrictive pericardium- tension pneumothorax- high levels of PEEP or intrinsic PEEP- massive pleural effusion- abdominal tamponade- venous occlusion (clot, air, tumor, pregnancy)- atrial occlusion (clot, air, tumor)阻塞性休克的病因(静脉回心受阻):-心包积液-心包缩窄-高PEEP或固定PEEP-大量胸腔积液-腹腔填塞-静脉闭塞(血块、气体、肿物、羊水)-动脉闭塞(血块、气体、肿物)Interestingly, as a group, obstructions to venous return produce the kinds of variations in pulse pressure described above (Magder 2004, 2005). More recent clinical studies have
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