病例讨论 CSA09_全国麻醉学年会讲者文稿

2009 年中华麻醉年会投稿作者姓名：童传耀, 医学博士(Name in English: Chuanyao Tong, MD.)工作单位：美国威克大学麻醉科Dept. of AnesthesiologyWake Forest University Health ScienceMedical Center Blvd,Winston-Salem, NC 27157, USA邮编： 2715719107 USA (美国)美国联系电话： (336) 716-4498电子邮件地址： cyt970@论文标题：围术期严重肺栓塞的诊断和抢救治疗Intraoperative massive pulmonary embolism-diagnosis and resuscitation论文分类：临床麻醉病例讨论(PBLD-problem based clinical discussion）Intraoperative massive pulmonary embolism: diagnosis and resuscitationChuanyao Tong, MD, Dept. of Anesthesiology, Wake Forest University Health Science, Winston-Salem, NC 27157, USAObjective:After attending this case, the participants will be able to:1. Understand the circulatory changes associated with intraoperative acute massive pulmonary embolism.2. Learn the diagnosis modalities for intraoperative pulmonary embolism.3. Understand the optimal hemodynamic management, the vasopressors and fluids to maximize the survival possibility.4. Discuss other treatment options and prevention strategy.Stem Case:A 77 years old white female fell 3 days ago and was scheduled for left humeral open reduction and internal fixation (ORIF) and left hip replacement.PMH: hypertension, type 2 diabetes, hyperlipidemia, hypothyroidism.SH: living with dementia husband, active and golfing regularly. Nonsmoker.PE (in ER): BP126/63, HR67, RR22, T95.3, SaO298% in room air.X-ray remarks: 1) complex humeral head and neck fracture with anterior displacement, and 2) mild displaced left femoral neck fracture.Labs: HH 13.4/38.9, Platelet 309; electrolytes were normal, Glucose 194. EKG: SR 80, borderline LAD (left axis deviation). Stress echocardiogram was negative in 1997.Disposition: the patient was admitted to orthopedic floor, continuing her chronic medications, and heparin 5000 u was started, sc bid.On the day of surgery, a left interscalene brachial plexus catheter and a lumbar plexus block were performed with total of 0.5% bupivacaine 55 ml for postoperative analgesia. General anesthesia was induced by iv propofol (100 mg), fentanyl (150 mcg), and rocuronium (50 mg). The patient’s intubation (7.0 ETT) was confirmed by ETCO2 and equal bilateral breath sounds, and maintained with 0.5% isoflurane in O2/air. Shortly after induction, her blood pressure was trending down to 80/45 mmHg, no changes in heart rate and SaO2, which responded to ephedrine (10 mg) and phenylephrine (120 mcg), then iv hetastarch 500 ml was started.•Is this common in elderly patient?•What could be the differential diagnosis?As planned preoperatively, a 2nd iv and a radial arterial line were placed, the patient was moved from stretcher to OR table, turned to right lateral position (20 min later). Arterial BP was again decreased to 75/40 mmHg with HR 95. This time, it did not respond to ephedrine (35 mg) and phenylephrine (600 mcg). The resident was watching the vital signs, noticed SaO2 was 80% with an ill looking ETCO2 waveform (22-27 mmHg). Immediately gave epinephrine (100 mcg, iv) and started hand bagging with 100% O2…•What would be the differential diagnosis again?•Which therapy should be initiated?Breath sounds and ETT position were re-checked, a chest x-ray ordered immediately, and TEE called. Meanwhile, the patient was turned to a supine position and started neophenylephrine and epinephrineinfusion, with both iv fluids wide open. MAP was kept >60 mmHg so as SaO2>90%, but no improvement of ETCO2 waveform.•What would be the findings from TEE?TEE showed a significant dilated right atrium and ventricle with decreased contractility (sluggish or hypokinesia), a rather small LV chamber with good contractility (EF 55%), and deviated sepetal wall towards left, moderate to severe tricuspid regurgitation and evident a frail mitral valve prolapsed. Surprisingly, a patent PFO with left to right shunting was found. There was an estimated pulmonary hypertension (~55 mmHg), but no visible clot.•Do you consider the TEE findings supportive for the diagnosis of PE?•Was this also possible of acute right heart infarction?•If TEE were not available, how could ABG, CXR, EKG, PAC, and CVP help for diagnosis?In next 75 min of continuing resuscitation, the patient’s condition was relatively stabilized, withPaO2>110 mmHg and MAP in range of 70-85 mmHg. Troponin was negative in 2 measurements. EKG later showed junctional tachyarrhythmia (110/min), low voltage QRS (suggesting new pulmonary disease), and new abnormality of nonspecific ST and T changes. At this point, a diagnosis of pulmonary embolism (PE) was made, the original surgery was canceled and the patient was transported to ICU for continue resuscitation and treatments...Discussion:1.Risk factors for PE and the differential diagnosis for hypoxia: Bone fracture and bed resting is the most common cause of deep venous thrombosis (DVT) formation in the low extremities, which has a potential risk of PE when the clot dislodged. The differential diagnosis includes fat embolism syndrome (FES) which is manifested by continues release fatty tissue causing pulmonary vasculature inflammatory responses. Others included pneumothorax, tension pneumothorax from multi-rib fracture or interscalene block, pulmonary contusion, endobronchial intubation, anaphylactic reaction to drugs or latex. All of these could cause sudden unstable hemodynamic and hypoxia, and should be rapidly ruled out for effective management.2.The value of TEE in diagnosis and treatment of PE: a massive PE causes the right ventricle outflow obstruction by its mass and/or inflammatory reaction, results in severe decrease of preload and afterload (hypotension and left heart failure), severe pulmonary hypertension and right ventricle failure, and compromising coronary perfusion; these changes could be instantly characteristically revealed by TEE as dilated right ventricle with impaired contractility and small left chamber volume with preserved function initially. In addition, it may show some unknown preexisting cardiac anomaly, as the finding of a patent PFO with right to left shunt in this patient. The presence of visible clot in the pulmonary arterial confirms the PE diagnosis immediately. TEE is helpful in guiding resuscitation and providing immediately feedbacks concerning the treatments.3.ACLS (Advance Cardiac Life Support) for managing cardiovascular collapse: When encountered such a scenario, the first is checking the airway to ensure a patent airway (intubation and ventilation with 100% oxygen). The administration of inotropics and volume are aimed to rapidly restore the patient’s cardiovascular function. Two-thirds of the mortality following massive PE occurs within one hour of the onset of hemodynamic instability. Generally, there is no rule regarding the dose range (mcg to mg), drug choice (ephedrine, phenylephrine, epinephrine, or norepinephrine), rather how faster and effectively bring the MAP back to baseline. There is no evidence of the value of steroid (dexamethasone). CPR should be initiated if no response to inotropics in 3-5 min or the presence of PEA (puleless electrical activity). Defibrillation should be delivered immediately if presence of ventricle tachycardia or fibrillation.4.Prevention and treatment options: the stabilization and fixation of long bone fractures should take place within 72 hrs, the patient should be resuming ambulation early, starting anticoagulation(subcutaneous heparin or lovenox), placing low extremity compression cuff or/and the inferior vena cava filter; all these measures have been shown some effectiveness in decreasing DVT. The definitive emergency treatment is aimed to remove the clot and restore the cardiovascular stability. Medically, thrombolytic therapy is started with administration of thromboplastin activator (tPA) in adjunction with heparinization. Surgically, embolectomy is achieved by extracting the clot through thoracotomy or interventional radiological procedures. Numerous reports showed an immediate ECMO (extracorporeal membrane oxygenation) could be life saving and create an opportunity for definitive therapy. REFERENCES:1.Wood KE. Major pulmonary embolism: review of a pathophysiologic approach to the GoldenHour of hemodynamically significant pulmonary embolism. Chest 2002;877-905.2.Rosenberger P, Shernan SK, Shekar PS, et al: Acute hemodynamic collapse after induction ofgeneral anesthesia for emergent pulmonary embolectomy. Anesth Analg 2006;102:1311-5.3.Goldhaber SZ. Pulmonary embolism. N Engl J Med 1998;339:93-104.4.Memtsoudis SG, Rosenberger P, Loffler M, et al: The usefulness of transesophagealechocardiography during intraoperative cardiac arrest in noncardiac surgery. Anesth Analg2006;102:1653-7.5.Guidelines on the diagnosis and management of acute pulmonary embolism: the Task Force forthe Diagnosis and Management of Acute Pulmonary Embolism of the European Society ofCardiology (ESC). Eur Heart J. 2008; 29 (18):2276-315.6.Stein PD, Yaekoub AY, Matta F, Kleerekoper M: Fat embolism syndrome. Am J Med Sci. 2008;336(6): 472-7.7.Barrett JA, Baron JA, Beach ML: Mortality and pulmonary embolism after fracture in the elderly.Osteoporos Int. 2003; 14(11):889-94.8.Konstantinides S: Clinical practice. Acute pulmonary embolism. NEJM 2008; 359(26):2804-13.fere TB, Sprung J, Case KA, et al: Predicators of mortality following symptomaticpulmonary embolism in patients undergoing noncardiac surgery. Can J Anaesth 2007; 54(8):634-41.2009 年中华麻醉年会投稿作者姓名：夏云, 医学博士，哲学博士(Name in English: Yun Xia, MD, PhD)工作单位：美国俄亥俄州立大学医学中心Dept. of AnesthesiologyOhio State University Medical CenterN-416 Doan Hall410 West Tenth AvenueColumbus, Ohio 43210-1228, USA邮编： 43210-1228 USA (美国)(美国)联系电话：(614) 766-4048电子邮件地址：yun.xia@论文标题：子痫前期产妇的麻醉管理Anesthetic Considerations of a Parturient with Multiple Co-existing Diseases论文分类：临床麻醉病例讨论(PBLD-problem based clinical discussion）Anesthetic Considerations of a Parturient with Multiple Co-existing DiseasesYun Xia, MD, PhD, Ohio State University Medical Center, Columbus, Ohio OBJECTIVESAt the conclusion of this PBLD session, the participants will be able to:1. Know current classification, pathophysiology, diagnosis, and anesthetic consideration of preeclampsia2. Describe anesthetic managements of preeclampsia in an evidence based approach.3. Learn the managements of labor analgesia and Cesarean section in the US.4. Prepare for parturients with multiple co-existing diseases.STEM CASE - KEY QUESTIONSThe patient was a 34 year-old Caucasian female, G2, P0010, 34 weeks gestation, premature rapture of membrane (PROM). She had a VAS score of 4/10 during regular uterine contractions at 3-4 minutes apart. She was admitted for preterm labor. Fetal heart rate (FHT) was 140’s/minute with good variability.She presented complaints of elevated blood pressure (BP) and shortness of breath over the last month. She received corticosteroids a week ago. Her platelet account was105,000 at her last office visit, two weeks ago.Her past medical history was also remarkable with hypertension (HTN), retinopathy, hypercholesterolemia, diabetes mellitus type I (DMI) class H, hypothyroidism, gatroesophageal reflux disease, and smoking. She was diagnosed with antithrombin III deficiency due to an episode of deep venous thrombosis (DVT) at 19 weeks gestation. She has been placed on lovenox (enoxaparin) 60 mg SQ bid since then and her last injection was 24 hours ago. Four years earlier, she experienced a myocardial infarction (MI) with subsequent placement of a single sirolimus-elutung stent (SES) (Cypher TM Cordis) in the proximal left anterior descending coronary artery that was 70% stenosed. On physical examination, she was noted to be a morbid obese patient (Wt. 93.6 kg, Ht. 152 cm, BMI 40.5) with an admission BP 191/107 mmHg. The patient was having increased swelling in her upper and lower extremities; Airway: Malampatti II. Admission medication included levothyroxine, famotidine, and insulin via a Paradigm 7000 series indwelling pump (Medronic). She had been taking clopridogrel 75 mg and aspirin 81 mg for 1 year post placement of the SES.Significant initial laboratory results were a platelet 107,000, Hgb A1c 6.7%, glucose 246 mg/dL, and three plus proteinuria. Cardiac enzymes were negatives times three. Electrocardiogram was normal. Echocardiogram showed a normal left ventricle (LV) systolic function, LV ejection fraction (EF) 65%, normal wall motion, and a mild mitral regurgitation.Initial treatments included: intravenous (IV) labetalol, hydralazine, and magnesium infusion.Her BP was reduced and maintained at150s/90s mmHg. HR 84/min, RR 18/min, Hct 35%. Cervix dilation was 2 cm.1. What is the classification of Hypertensive Disorders in Pregnancy?2. Did this patient have preeclampsia (diagnosis)?3. What is the clinical significance of DM class H?4. What are the anesthetic considerations of this patient?5. What are the factors that contribute to an increased risk of epidural hematoma?6. What other information would you need to formulate your anesthetic plan?7. Can regional techniques be used for this patient’s labor analgesia? If so, when?After discussion among obstetricians, anesthesiologists, and pediatricians, epidural labor analgesia was chosen. After oral administration of sodium citrate, an epidural catheter with a flexible-tip was placed at L3-4 with no noticeable problems. After a negative testing dose, 0.125% bupivacaine 10 mL was given to the patient in three separate doses. Continuous infusion of 0.0625% of bupivacaine and fentanyl 4 mcg/ml was started at 10 mL/hour with a PCEA (dose 5 mL, delay 20 minutes, and lockout 25mL/hour). The patient had a sensory blockage of T10 level and was comfortable in bed and had minimal motor block. Oxytocin was started on the recommendations of obstetricians.7. How would you monitor this patient for the signs and symptoms of epidural hematoma?8. When can the anticoagulation therapy be re-started?Nine hours later, obstetricians noticed a fetal bradycardia which was determined as late decelerations. Despite left uterine displacement, oxygen administration, and stopping oxytocin infusion, the fetal bradycardia during each contraction progressively worsened, so a stat C-section was called.9. What is late deceleration?10. What is your anesthetic plan?After negative aspiration of epidural catheter, a five mL of 1.5% lidocaine was injected via epidural catheter. The patient immediately complained that she could not move both of her legs and she had difficulty of breathing.11. What was happening?12. What is your anesthetic plan now?13. What is the incidence of epidural catheter migration?After oral sodium citrate, intravenous (IV) pepcid (famotidine), and reglan (metoclopramide), general anesthesia was induced and endotracheal intubation wasperformed with cricoid pressure. The patient was hemodynamically stable. A vigorous baby with apgar scores of 9 (1minute) and 9 (5 minute) was delivered 2 minutes after skin incision. Oxytocin IV drip was used to manage uterine tone and estimated total blood loss was 700 mL. At the end of the surgery, epidural catheter aspiration was positive with CSF. Post-operatively, the patient remained hemodynamically stable throughout her hospitalization without any cardiac or neurological issues.14. What could be done to manage her post-operative pain?P ROBLEM B ASED L EARNING D ISCUSSIONThis patient posed a great challenge to our anesthesiologists for her anesthetic management during her labor and delivery. She not only had preeclampsia, but also significant other co-existing diseases, namely, chronic HTN, retinopathy, hypercholesterolemia, diabetes mellitus type I class H, hypothyroidism, gatroesophergeal reflux disease, coagulopathy, CAD, and a history of smoking.Preeclampsia occurs in the United States about 2.3-7.6%, on average about 5%, of all pregnancies. The incidence of preeclampsia is 23.6 cases per 1,000 deliveries in the United States. The global incidence of preeclampsia has been estimated at 5-14% of all pregnancies. Preeclampsia is the third leading pregnancy-related cause of death, after hemorrhage and embolism. Preeclampsia is the cause of an estimated 790 maternal deaths per 100,000 live births.Parturients with hypertensive disorders can be classified into the following four categories: (1) gestational hypertension; (2) chronic hypertension; (3) preeclampsia; and (4) chronic hypertension with superimposed preeclampsia.The etiology of preeclampsia is unknown. The hypotheses associated with the etiology are: (1) abnormal trophoblast invasion; (2) vascular endothelial damage; (3) immunologic abnormality; (4) genetic predisposition; and (5) dietary irregularity. Some authors believe that coagulation abnormalities and cardiovascular maladaptation may also play roles in preeclampsia.Morbidity and mortality are related to systemic endothelial dysfunction; vasospasm and small-vessel thrombosis leading to tissue and organ ischemia; CNS events such as seizures, strokes, and hemorrhage; acute tubular necrosis; coagulopathies; and placental abruption in the mother. In the fetus, ischemic encephalopathy, growth retardation, and the various sequelae of premature birth can occur.Current criteria for diagnosis of preeclampsia include hypertension and proteinuria. There are two subtypes of preeclampsia: mild preeclampsia (BP>140/90 and proteinuria > 300 mg/24 hours) and severe preeclampsia (BP>160/110 and proteinuria > 2 g/24 hours).Delivery is still believed to be the cure for preeclampsia. However, early prenatal detection, fetal and maternal surveillance, necessary hospitalization, antihypertension therapy, seizure prevention and treatment, and proper peripartum managements are also important for the treatment of preeclampsia.We believe that knowing the pathophysiological changes in preeclampsia and knowing the nature and severity of preeclampsia in each patient will enable us to formulate the optimal anesthetic plan for our patients with preeclampsia. If there is no contraindication, regional analgesia has many advantages to offer and has the potential to be the superior choice for labor analgesia and obstetric anesthesia. However, general anesthesia provides the shortest time from induction of anesthesia to fetus delivery. Therefore, in certain situations, general anesthesia can be life-saving for parturients and their babies. We will discuss these in detail during our PBLD.Through evidence-based approaches, we hope this discussion will help our participants to (1) achieve knowledge of current classification, pathophysiology, diagnosis, and anesthetic consideration of preeclampsia; (2) achieve the ability to describe anesthetic managements of preeclampsia; (3) learn the management of labor analgesia and Cesarean section in the US; and (4) prepare for paturients with multiple co-existing diseases.R EFERENCES[1] ACOG Practice Bulletin. Clinical Management Guidelines for Obstetrician-Gynecologists. Number 33, January 2002. (In: 2007Compendium, Volume II: pp 640-648. 2007). 2002.[2] Ananth CV, et al. Trends in preterm birth and perinatal mortality among singletons: United States, 1989 through 2000. ObstetGynecol. 105: 1084-1091. 2005.[3] Aya AGM, et al. Patients with severe preeclampsia experience less hypotension during spinal anesthesia for elective cesareandelivery than healthy parturients: a prospective cohort comparison. Anesth Analg. 97:867-872. 2003.[4] Sibai BM. Hypertension. In: Obstetrics: Normal and Problem Pregnancies (Eds. Gabbe S., et al). pp 863-912. 2007[5] Cunningham FG, et al. Hypertensive disorders in pregnancy. In: Williams Obstetrics (22th Edition). McGraw-Hill. pp759-808.2005.[6] Fischer T et al. Vascular reactivity in patients with preeclampsia and HELLP syndrome. Am J Obstet Gynecol 183: 1489-1494.2000.[7] Gambling DR. Hypertensive disorders. In: Obstetric Anesthesia 3rd edition (Chestnut DH ed). pp794-845. 2004.[8] Matchaba P and Moodley J. Corticosteroids for HELLP syndrome in pregnancy. Cochrane Database Syst Rev CD002076. 2004[9] Villar J, et al. Heterogeneity of perinatal outcomes in the preterm delivery syndrome. Obstet Gynecol. 104: 78-87. 2004.[10] Wang Y, et al. Evidence of endothelial dysfunction in preeclampsia. Am J Obstet Gynecol. 190: 817. 2004[11] Xia Y. Progress in Preeclampsia. Chinese Journal of Practical Gynecology and Obstetrics. 23 (7): 573-574. 2007.2009 年中华麻醉年会投稿作者姓名: 刘虹, 医学博士(Name in English: Hong Liu, M.D.)工作单位: 美国, 加利福尼亚州, 萨克拉门托市, 加州大学戴维斯分校 University of California Davis Health System4150 V Street, Suite 1200Sacramento, CA 95817, USA联系地址: 5424 Cowell Blvd.Davis, CA 95618, USA邮编: 95618 USA (美国)联系电话: (530)-848-5895电子邮件地址：hualiu@论文标题: 术中液体评估和管理的新概念论文分类：临床麻醉病例讨论(PBLD-problem based learning discussion)Intra-operative Volume AssessmentHong Liu, MD, Associate Professor, Department of Anesthesiology and Pain Medicine University of California Health System, Sacramento, California, USAObjectives:At the conclusion of this session the participant will have a better understanding the new concept of patient intraoperative fluid assessment and management.Stem Case:Patient details:64 years old, female, height: 162cm, weight: 65kg, 40 pack/year smoking history. Medical history:Hypertension, type II diabetics, peripheral vascular disease (PVD), hypercholesteremia, hypothyroidismCase Notes:The patient was scheduled for an exploratory laparotomy and Whipple procedure. Her medical history is significant for hypertension, PVD, hypercholesteremia, diabetics, and hypothyroidism. Her electrocardiogram showed some non-specific ST-T depression. Pre-operative stress echocardiography showed a left ventricular ejection fraction between 50 to 55%.Patient was taken to the operating room at 3:00 pm. One 18G intravenous (IV) catheter was placed in the left hand. Thoracic epidural catheter was placed prior to induction of general anesthesia. General anesthesia was induced with 2 mg of versed, 140 mg of propofol, and 70 mg of rocuronium. After induction, endotracheal tube was placed and verified for correct positioning.You are her anesthesiologist.1. How do you estimate her fluid deficit?2. How are you going to monitor her fluid status?3. What kind of monitor are you going to use?4. With patient’s past medical history, any special monitor you going to use? The surgeon suggested for a central line placement.5. What is your response to the surgeon’s request?6. What evidence are you going to use to backup your argument?7. Is an arterial line indicated in this case?8. Is a Vigileo/FloTrac system indicated in this case?Because of her PVD status, a central venous pressure (CVP) catheter was placed for IV access and an intra-arterial catheter with a Vigileo/FloTrac system was used for cardiac output (CO), SVV, and continues blood pressure (Bp) monitoring. Patient’s heart rate (HR) was 82/min, Bp was 128/72 mmHg, CVP: 10 cmH20,CO: 5.3 L/min and SVV: 10%.9. What are the numbers tell you?10. What is the normal range SVV?After the general anesthesia and at the early stage of surgery the patient’s SVV and CO was very stable throughout this period. Fifty minutes into surgery, the surgeon encountered some bleeding and the anesthesiologist noticed that about 500 ml of blood were lost. At the same time the SVV was increased from 11% to 41% and CO decreased from 4.6 to 3.2 L/min. The patient’s HR increased to 105/min, CVP 8 mmHg and an acute decrease in BP (90/50 mmHg).11. What is this SVV number telling you?12. What do you think of the CO?13. Are there connections between SVV and APCO?After immediate transfusion of 500 ml of colloid solution the patient’s HR went to 85/min, CVP: 10 mmHg, BP: 120/70 mmHg, the SVV to 13%, CO: 5.2 L/min. Due to the location of the tumor, it was difficult to control the bleeding. In order to completely control the bleeding, the surgeon decided to resect the tumor first. During next 10 minutes while the surgeon was resecting the tumor, the anesthesiologist was replacing the blood volume with packed red blood cell and colloid solution. The SVV was again increased and CO decreased during this time. After the bleeding was controlled, the SVV and CO went back to the baseline. The rest of the surgical procedure and hospital cause was uneventful. The patient was discharged home 6 days after surgery.14. Which is more sensitive to blood loss, SVV or CVP?15. Do you think SVV is a good indicator for circulatory volume status in yourdaily practice?16. What are the indications for the use of SVV/APCO?Discussion:Hemodynamic monitoring and fluid status assessment are essential for cardiovascular care in the patient undergoing major surgeries. Knowing when a patient’s hemodynamic instability comes from hypovolemia or other causes is imperative in providing a safe patient care. Adequate volume replacement to achieve optimal cardiac performance is a primary goal of hemodynamic management in those patients. However, in only half of such patients the CO increases after a fluid challenge and thus only these can be considered as responders to fluid therapy. Therefore, physicians need reliable criteria to distinguish those two patient populations to avoid any deleterious consequences of fluid overload.There are several parameters the clinicians use to guide fluid management in their everyday patient care. CVP and pulmonary artery pressure (PAP) are most commonly used in major hemodynamic instability cases. However, these standard preload index(CVP, PAP) values nor their changes in response to fluid challenges reflected their respective ventricular end diastolic volumes or changes in patients receiving a fluid challenge for hemodynamic instability, and are not capable of predicting cardiac response to fluid therapy. Therefore, they could not serve as the standards for the patient’s volume status.Believe or not, we still use formula to calculate the fluid need simply based on patient’s weight, the length of NPO, types and length of surgery to guide intra-operative fluid management. Let’s use this case as an example. The deficient from NPO overnight for 10 hrs: 1050 ml; maintenance for 4.5 hour surgery: 8 ml /kg/hr for 3rd spacing: 2340 ml; insensitive loss for 4.5 hours: 2ml/kg/hr: 585 ml; blood loss: 600 ml and you can give colloid or blood 1:1 ratio or you can use crystalloid at 1:3 ratio. The total amount of fluid the patient would receive during 4.5 hours of surgery could be about 6000 ml.The accuracy of about preload index and the method of calculation have been challenged in recent years. Studies have shown that they do not accurately reflect the left ventricular end diastolic area and volume values, even when trends are followed after the administration of a fluid challenge during hemodynamic instability. As the minimal invasive technology becoming more mature, stroke volume (SV), SVV or pulse pressure variation (PVV) in conjunction with APCO have been used more and more in recent years by clinicians to guide intra-operative fluid therapy. We hope the goal-directed intraoperative fluid management by using SVV/PVV or other parameters will replace the old methods and be the choice to guide fluid therapy in hemodynamic instable patients. References1.Kumar A, Anel R, Bunnell E, Habet K, Zanotti S, Marshall S, Neumann A, Ali A,Cheang M, Kavinsky C, Parrillo JE. Pulmonary artery occlusion pressure andcentral venous pressure fail to predict ventricular filling volume, cardiacperformance, or the response to volume infusion in normal subjects. Crit. CareMed. 2004;32: 691-992.Hamilton-Davies C, Mythen MG, Salmon JB, Jacobson D, Shukla A, Webb AR.Comparison of commonly used clinical indicators of hypovolaemia withgastrointestinal tonometry. Intensive Care Med. 1997 Mar;23(3):276-813.Bouchard MJ, Denault A, Couture P, Guertin MC, Babin D, Ouellet P, Carrier M,Tardif JC. Poor correlation between hemodynamic and echocardiographic indexes of left ventricular performance in the operating room and intensive care unit. .Crit. Care Med. 2004;32: 644-484.Michard F. Changes in Arterial Pressure during Mechanical Ventilation.Anesthesiology 2005;103: 419-285.Reuter DA, Bayerlein J, Goepfert MS, Weis FC, Kilger E, Lamm P, Goetz AE.Influence of tidal volume on left ventricular stroke volume variation measured by pulse contour analysis in mechanically ventilated patients. Intensive Care Med.2003 Mar;29(3):476-80。