1、Chicago, Illinois理解臨床血流動力學understanding clinicial hemodynamics原文：Micharel F. OConnor, M.D. FCCM翻譯：福建醫科大學附屬協和醫院麻醉科規培住院醫師 陳靜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.（臨床醫師嘗試著闡述和了解健康和危重癥患者而借助的生理學范式已經發展100多年了。）Interestingly, our understanding of the clinical circulation has always been thought of as complete, （有趣的是，人們對臨床循環的理解一直被視為“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.（而富有創新性的臨床醫師則希望通過種種解釋消除常用思維模式和臨床醫學現實之間顯著的差異。）The most primitive formulation of the circulation entails simple conservation of matter:（最原始的循環公式蘊含著簡單的物質守恒：） Cardiac Output = Stroke Volume x Heart Rate = Qt = SV x HR （心輸出量（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. （很顯然，該表述很正確，卻幾乎沒有為智慧的工作者深入了解為何個別患者的循環可能不穩定以及如何進行合理的干預提供幫助。）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世紀中葉，Guyton及其同事修訂了一個相對完善、關于了解靜脈回心血量在控制心輸出量中的作

6、用的范式，該范式從首次被描述就進行了反復驗證。Although not complete, this theory was powerful in thehands of those who understood it.盡管該理論還不完善，卻對已理解該理論的人群產生了很大的作用。The balloon-tipped, flow directed, thermistor equipped pulmonary artery catheter heralded the subsequent era of the understanding of the clinical circulation.裝備

7、有末端套囊、血流導向以及熱敏電阻的肺動脈導管，預示著理解臨床循環時代的到來。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).對肺動脈導管及左心室力學功能的深入了解預示著從左心室的視角來理解循環以及循環病理學時代的來臨。Nevertheless, the LV centered view of the circulation focused on preload, afterload, and contractility, and was frustrated by a variety of obstacles.然而，以左室為中心觀察循環主要以前負荷、后負荷和收縮力為主要研究對象，但若遇到一些障礙，則結果就相形見絀了。 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，通過超聲心動圖進行評估發現，充盈壓和左心室舒張末容積之間的相關性較差。Echocardiography has documented that LV compliance is far more dynamic than anyone believed prior

10、 to itswidespread clinical use (Coriat).通過超聲心動圖證實，左心室順應性比之前認為已廣泛應用于臨床的任一參數更優越。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，以左心室為中心觀察循環存在的潛在問題為，支持者更趨向于認為，RAP幾乎為循環容量唯一的指標，而遺忘了在Guyton模型中，RAP為下游流體靜力學阻力： VR = CO = Pms RAP RVR(Where VR = Venous Return, RAP = Right Atrial Pressure, and RVR = Resistance to Venous Return)（VR=靜脈回心血量，RAP=右心房壓，RVR=靜脈回心阻力）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.對于任一患者的任一時刻，循環都是心臟（泵）和靜脈回路相互作用的產物。RAP即為該相互作用的產物。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.雖然休克通常與低血壓有關，然而有越來越多的觀點認為，低血壓已是休克相對“晚期”的指標，臨床醫師更應習慣于以器官系統功能失調作為休克的證據（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.在重癥監護和創傷醫學文獻中，復蘇終點也已不斷演變。雖然傳統的復蘇終點（如，平均動脈壓和中心靜脈壓）仍然很重要，但越來越強調混合/中心靜脈氧飽和度和血乳酸水平。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.在大容量復蘇的過程中，作為復蘇適度的風向標，方便快捷的血清乳酸測定結合日益受寵的高氯血癥酸中毒已經逐漸取代堿過量/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.在過去數年中，許多論文已經降低了對使用中心靜脈氧飽和度的熱情，但對于氧供充足與否而言，其仍然為非常有用的指標之一。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，當組織氧供下降時，氧解離增加，直至組織再沒有能力攝取更多的氧。當發生這種情況時，危機就隨之而來。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物理學：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（低心排和高體循環阻力）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.將左側的Sta

22、rling曲線圖和靜脈回心血量圖疊加，生成循環狀態的圖示。心排出量則是通過這些曲線的交叉點Y軸的投影表示的，臨床監測的CVP通過曲線交叉點的X軸投影表示的。Diastolic dysfunction is a generally underappreciated and very important contributor or cause of shock states.舒張功能不全為一項被普遍低估、卻非常重要的休克狀態的誘因或病因。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).在失血性休克動物模型中，即使由PEEP水平降低或呼吸頻率減少導致胸腔壓力細微的下降都可使動物模型的存活狀況顯著改善（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.基于該數據及從心肺腦復蘇動物模型中得到的相似數據，人們越來越對以盡可能最小的氣道壓力對休克患者進行通氣的模式感興趣。Bedside Assessment of the patient with shock休克患者的床旁評估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?以下幾個問題形成了一個有序的方法，可用于循環容量不足患者的評估： 心輸出量是否減少 心臟是否“太滿” 什么方法不適合Is the cardiac output reduced?No Vasodilated ShockYes Hypovolemic shock, Cardiogenic Shock, or Obstruction to Venous Return心輸出量是否減少不是血管擴張性休克（血流分布性休克）是的低血容量性休克、心源性休克、靜脈回心受阻The

26、above figure demonstrates the sentinel feature of vasodilated or high cardiac output shock:the wide pulsepressure.血管擴張性或高心排性休克的標志性特征為：脈壓差大。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.對于血管擴張性休克患者，脈搏壓力大于收縮壓的一半的狀態幾乎始終存在，總體而言，低心排性休克患者的脈壓則低于正常人。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.當患者血壓為80/30 mmHg時，幾乎可以確定存在血管擴張性休克，而血壓為80/60 mmHg時，則為引起低心輸出量的原因之一。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、克的鑒別診斷：-膿毒血癥，敗血癥，菌血癥-全身炎癥反應綜合征SIRS（如胰腺炎）-肝衰竭-過敏反應-腎上腺功能不全-動靜脈血管瘺-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.如果合并低心輸出量，低血容量性休克和心源性休克的鑒別可通過相關病史的回顧、體格檢查和實驗室檢查來實現。既往信息常常在得出低血容量為導致循環不穩定的原因這一結論時才引起人們的注意。 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. 通過超聲心動圖最容易對心源性休克進行評估。心源

32、性休克的鑒別診斷包括急性左心梗死、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導致的右心衰以及先前未確診的瓣膜疾病，如主動脈瓣狹窄、二尖瓣狹窄和二尖瓣關閉不全。Echocardiography has supplanted the Swan-Ganz catheter as the method of choice for assessing the patientwith suspected cardiogenic shock.超聲心動圖已經取代Swan-Ganz導管成為評估疑似心源性休克患者的首選。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.其原因包括進一步認識到醫師對如何應用

34、Swan-Ganz導管知識的貧乏，導管難以改善預后的闡釋以及對中心靜脈氣體與混合靜脈氣體之間的良好的相關性的認同性增加。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，超聲心動圖研究已經證明，行有創監測獲得的充盈壓與左心室舒張末容積之間的相關性極差。關于中心靜脈壓監測的質疑證據也不斷積累，并被總結成了豐富多彩的綜述文章。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).鑒于以上觀點，專家越來越主張將動脈脈壓變異度作為液體管理的一項指南，當呼吸相關性動脈脈搏壓力變異度10%15%時，液體治療往往會產生比較好的反應。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).最常用的兩種監測指標為收縮壓變異度（SPV）和PP。收縮壓變異度更容易通過應用傳統監護儀來評估，但略遜于PP

38、（也被稱為，脈搏壓力變異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).對于敗血癥和心臟病患者，包括進行OPCAB以及CABG術后的患者，將SPV和/或PPV作為容量反應的預測指標優于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.通過應用ICU或OR中的較新的監護儀整合了便于分析這些參數的軟件。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)作為CVP預測容量反

41、應能力的替代指標，其他技術（包括每博量變異度（SVV）以及由胸內血容量指數(ITBV）演變而來的PICCO）正在研發中，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，對休克患者進行管理時，收縮壓變異度為一個非常有用的指標：患者血壓和脈壓出現極小或無變異時，幾乎不可能對容量治療作出反應。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，對此類患者進行復蘇時，最初的努力應著眼于使用藥物或機械方法干預，這樣或許會更有效。由于該方案最大限度的減少了對危重患者實施的不必要的液體治療，因而可能會改善預后。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.大多數低血容量性休克、LV休克（左心室相關性休克）以及敗血癥患者對恰當的治療均有反應。對于無反應者，應該停止治療并評估是否發生阻塞性休克。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.阻塞性休克由靜脈回心受阻引起。靜脈回心受阻一般較為隱匿。雖然容量復蘇和應用血管活性藥物治療可能會產生短暫輕微的循環改善，但如果可能，恰當的治療應當包括減輕靜脈回心阻力。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（靜脈回心受阻）：-心包積液-心包縮窄-高PEEP或固定PEEP-大量胸腔積液-腹腔填塞-靜脈閉塞（血塊、氣體、腫物、羊水）-動脈閉塞（血塊、氣體、腫物）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