1、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 more 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 h
2、as 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 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 f
3、ormulation 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）This statement,while obviously always true,offers sapient practitioners little insight into why the circulation in a articular patient
4、 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 relatively complete paradigm for understanding the role of the enous return in controlling the cardiac output was refined by Guyton and his co-worke
5、rs,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 b
6、alloon-tipped,flow directed,thermistor equipped pulmonary artery catheter heralded the subsequent era of the understanding of the clinical circulation.装备有末端套囊、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 i
7、n 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 view 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。For those who trained in that paradigm,preload,afterload,and contractili
8、ty were the determinants of cardiac output:接受该范式培训的人群应该了解，前负荷、后负荷以及收缩力都是心输出量的决定因素：Cardiac Output=CO=MAP-RAP SVR(Where MAP=Mean Arterial Pressure,RAP=Right Atrial Pressure and SVR=Systemic Vascular Resistance)（MAP=平均动脉压，RAP=右心房压，SVR=体循环阻力）Some patients have a right heart limited circulation,which can
9、 be formulated using a very similar equation:有些患者存在右心循环受限，可以用一相似的方程式计算心输出量：_ CO=PA-LAP _ PVR(Where PA=Mean Pulmonary Artery Pressure,LAP=Left Atrial Pressure,and PVR=Pulmonary Vascular Resistance).（PA=平均肺动脉压，LAP=左心房压，PVR=肺血管阻力）。Nevertheless,the LV centered view of the circulation focused on preload,
10、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 was the poor correlation between measured filling pressures and left ventricular end-diastolic volumes as assessed by echocardiography(refs Kumar,Hofer,Kr
11、amer).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 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 adhere
12、nts tend to regard RAP almost exclusively as an index of circulatory volume,forgetting that it is the downstream hydrostatic resistance to venous 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
13、=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 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。R
14、AP即为该相互作用的产物。All of this has produced the present understanding of clinical hemodynamics,which is predicated on a synthesis of venous return and cardiac physiology(Sylvester,Jacobsohn).当前对临床血流动力学的理解综合了静脉回心量和心脏生理学。This model can be used to generate a series of questions that can guide the assessment
15、of a patient in shock.该模型可以解释一系列问题以指导休克患者的评估。What is Shock？Shock is globally inadequate perfusion of tissues sufficient to produce both tissue hypoxia and organ dysfunction.休克为全身组织灌注不足导致组织缺氧和器官功能失调。While shock is classically associated with hypotension,there is increasing acceptance of the contentio
16、n that hypotension 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
17、 venous 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 a
18、s 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 appr
19、eciation 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 seve
20、ral 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。It is helpful to understand the modern incarnation of th
21、e Fick Equation of the relationship between oxygenconsumption,cardiac output,arterial oxygen content,and mixed venous oxygen content.这有助于理解Fick方程的现代演变，即有关氧耗量、心输出量、动脉血氧含量以及混合静脉氧含量之间的关系。This algebraicrearrangement emphasizes that the mixed venous saturation is adequate only when the delivery of oxygen
22、 to the peripheral tissues is well matched to their needs:这种代数重组过程强调，只有当输送到外周组织的氧与外周组织的氧耗契合良好时，混合血氧饱和度才充足：SvO2(CvO2)=CaO2 VO2 Qt(Where SvO2 is the mixed venous oxygen saturation,CvO2 is the mixed venous oxygen content,CaO2 is the arterial oxygen content,VO2 is the oxygen consumption,and Qt is the ca
23、rdiac output)(SvO2为混合静脉氧饱和度，CvO2为混合静脉氧含量，CaO2为混合静脉氧含量，VO2为氧耗，Qt为心输出量）Importantly,as oxygen delivery to the tissues falls,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
24、而来。In the left figure,oxygen extraction increases as oxygen delivery decreases.When the tissues reach the limits 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
25、a decline in oxygen consumption.Arterial hypoxemia,anemia,hyper-metabolism,and a low cardiac output all lower the mixed venous and central venous saturation.动脉低氧血症、贫血、高代谢以及低心排都可降低混合静脉和中心静脉氧饱和度。Increasingly,practitioners are utilizing protocols which include as one of their endpoints a central venous
26、 oxygen saturation above a certain level(Ladakis,Rivers).越来越多的临床医师开始参照指南，包括将一定水平的中心静脉氧饱和度作为复苏终点之一。This strategy of forward defense is in part based on the increasing recognition that hypotension is a relatively late indicator of shock,and that resuscitating a patient to a marginal blood pressure may
27、 leave them with an inadequate physiologic reserve.这一“早期防御”策略部分基于将低血压视为休克相对晚期的指标的认同感增加，而且复苏患者达到临界血压，其可能处于不适当的生理储备。From Physics:V=I x R Substituting produces:BP Pra=Qt x SVR物理学：V=IR 替代公式：BP Pra=QtSVR Hypoperfusion(shock)can arise from:-low cardiac output -low SVR -the combination of a low cardiac out
28、put 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 curve from the above right and generate a graphical representation of the state of the circulation.The cardiac output is represente
29、d 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Starling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 underappreciate
30、d 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 pressures 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
31、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 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
32、。Bedside Assessment of the patient with shock休克患者的床旁评估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 Cardiac 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
33、 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 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
34、：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 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
35、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 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。On examination,patients with vasodilated shock
36、will have brisk capillary refill while patients with low cardiac output shock will have delayed capillary refill.通过检查可以发现，血管扩张性休克患者会出现快速的毛细血管再充盈，而低心输出量性休克患者则出现毛细血管再灌注延迟。运用脉压差区分是血管扩张性休克和低心输出性休克运用脉压差区分是血管扩张性休克和低心输出性休克Differential Diagnosis of Vasodilated Shock:-Sepsis,Sepsis,Sepsis-Systemic Inflammato
37、ry Response Syndrome(SIRS)(e.g.pancreatitis)-Hepatic failure-Anaphylaxis-Adrenal insufficiency-AV fistula-Others血管性休克的鉴别诊断：-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 accomp
38、lished through the review of pertinent historical,physical examination,and laboratory data.Historical information 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
39、定的原因这一结论时才引起人们的注意。Causes of Hypovolemia:-Hemorrhage-insensible losses-redistribution to extravascular space-GI losses-renal losses-vasodilation(venodilation)引起低血容量休克的原因：-出血-意识丧失-血管外腔再分布-血糖指数下降-肾损伤-血管损伤Supportive of Cardiogenic Shock:-jugular venous distention-extra heart sounds-pulmonary edema in as
40、sociation with narrow PP-signs or symptoms of myocardial ischemia-new heart murmurs-cardiomyopathy or myocarditis心源性休克的支持依据：心源性休克的支持依据：-颈静脉怒张颈静脉怒张-额外心音额外心音-和窄脉压有关的肺水肿和窄脉压有关的肺水肿-心肌缺血的标志和症状心肌缺血的标志和症状-新的心脏杂音新的心脏杂音-心肌梗死和心肌炎心肌梗死和心肌炎 Cardiogenic shock is most readily assessed with echocardiography.The dif
41、ferential diagnosis 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
42、对心源性休克进行评估。心源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 in
43、creasing recognition 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
44、识到医师对如何应用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 us
45、e of central 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 arte
46、rial 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
47、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（也被称为，
48、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 intended for
49、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 being explored a
50、s 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预测容量反应能力的替代指标，其他技术（包括每博量变
