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1、第一页，讲稿共四十三页哦Definition正常人肺动脉压力为1530/510mmHg，平均为15 mmHg。静息状态下，若肺动脉收缩压30 mmHg，或平均压20 mmHg，即为肺动脉高压。WHO规定：海平面状态下，静息时，右心导管检查肺动脉收缩压30 mmHg，和/或肺动脉平均压25 mmHg，或运动时肺动脉平均压30 mmHg，即为肺循环高压。诊断肺动脉高压，尚需PCWP50第三页，讲稿共四十三页哦Classification of Pulmonary Hypertension1975 WHO Classification Primary pulmonary hypertension(P
2、PH)Secondary pulmonary hypertension1998 Evian Classification Clinical classification systemDifferent categories sharing similarities in pathophysiological mechanisms,clinical presentations,therapeutic options2003 Revised Clinical Classification of Pulmonary Hypertension第四页，讲稿共四十三页哦Clinical Classific
3、ation of Pulmonary HypertensionVenice 2003Evian 1998第五页，讲稿共四十三页哦Functional ClassificationClass I-Patients with pulmonary hypertension but without resulting limitation of physical activity.Ordinary physical activity does not cause undue dyspnoea or fatigue,chest pain,or near syncope.B.Class II-patien
4、ts with pulmonary hypertension resulting in slight limitation of physical activity.They are comfortable at rest.Ordinary physical activity causes undue dyspnoea or fatigue,chest pain,or near syncope.C.Class III-patients with pulmonary hypertension resulting in marked.Limitation of physical activity.
5、They are comfortable at rest.Less than ordinary activity causes undue dyspnoea,fatigue,and chest pain or near syncope.D.Class IV-patients with pulmonary hypertension with inability to carry out any physical activity without symptoms.these patients manifest signs of right heart failure.Dyspnoea and/o
6、r fatigue may be present even at rest.Discomfort is increased by any physical activityWHO肺动脉高压患者功能分级第六页，讲稿共四十三页哦Mechanisms of pulmonary hypertension 肺动脉高压的细胞机制 肺血管结构重构是肺动脉高压重要的病理基础 内皮细胞、平滑肌细胞、成纤维细胞、血小板和血栓形成、炎症细胞第七页，讲稿共四十三页哦第八页，讲稿共四十三页哦Mechanisms of pulmonary hypertension肺动脉高压的分子机制 多种血管活性物质，正常情况下它们之间
7、处于动态平衡，维持肺血管的正常生理结构和功能气体信号分子 NO、CO、H2S 血管活性肽及其他血管活性物质依前列醇(前列环素，eroprostenol，prostacyclin，PGI2)肾上腺髓质素(ADM)内皮素-1(endothelin一1，ET一1)：血管紧张素 5一羟色胺(5一HT)血管活性肠肽钾通道第九页，讲稿共四十三页哦Injury to endothelial cells leads to overproduction of endothelin key cause of blood vessel scarring and spasm&to reduced production
8、 of nitric oxide and prostacyclins 2 key body chemicals which keep blood vessels relaxed and open.第十页，讲稿共四十三页哦肾上腺髓质素(ADM)ADM 是1993年由日本学者在嗜铬细胞瘤中发现的一种新型血管活性多肽 具有舒张血管、降低血压、利尿排钠和抑制血管平滑肌迁移增殖等多种生物学作用。持续给予低氧大鼠ADM，能够缓解肺血管结构重构和肺动脉高压的形成第十一页，讲稿共四十三页哦5-HT in pulmonary hypertensionMacLean(1999)TIPS 20:490Blood v
9、esselalveolar lumen第十二页，讲稿共四十三页哦K+channel abnormalities in Primary PH(PPH)Archer&Rich(2000)Circulation 102:2782Decreased Kv1.5 in PPHImpaired K+current in PPHSPH secondary PHDonor and NPH-normals第十三页，讲稿共四十三页哦Mechanisms of pulmonary hypertension 肺动脉高压的遗传机制 IPAH为常染色体显性遗传，但是不完全外显，相关突变的携带者中只有10 20有明显的肺动
10、脉高压表 目前认为骨形成蛋白型受体(bone morphogenetic protein receptor II，BMPR2)基因突变是IPAH的重要致病原因第十四页，讲稿共四十三页哦According to the hypothesis,vascular abnormalities characteristic of PPH are triggered by accumulation of genetic and/or environmental insults in a susceptible individual.A combination of germline BMPR2 mutat
11、ion(first hit)and the ingestion of appetite suppressants(second hit)were used to generate the clinical disease.第十五页，讲稿共四十三页哦第十六页，讲稿共四十三页哦PathophysiologyAcute:RV afterload,EDV,EF,SV of RVChronic:progressive systolic pressure overload of RV that dilates and hypertrophies,gradual RV dysfunctionvenous r
12、eturn compromises RV preload and pulm blood flowresults from positive intrathoracic pressure(ex.PEEP)which also causes alveolar overdistension which PVR and pulm blood flow第十七页，讲稿共四十三页哦Pathophysiology-PVR limits RV SV and the volume for LV filling-LV compressed by intraventricular septum during syst
13、ole,LV volume/filling,CO/BP-BP leads to coronary perfusion which can lead to myocardial ischemia/R sided failure-coronary blood flow to RV usually occurs during diastole and systole but is decreased if RV pressures are equal to or higher than systemic pressures-hypoxemia from CO/pulm blood flow or f
14、rom R to L intracardiac shunt(if RA pressures higher than LA)第十八页，讲稿共四十三页哦Signs of Disease Severity Dyspnea at restLow cardiac output with metabolic acidosisHypoxemiaSigns of right heart failure(large V wave on jugularis vein,periph edema,hepatomegaly)Syncope(poor prognosis)Chest pain(RV ischemia)第十
15、九页，讲稿共四十三页哦Physical Exam Loud P2(increases PAP)Left parasternal heave(R sided overload)Pulm valve regurgitation(dilatation of pulm valve annulus)S3 gallop(advanced RV failure)第二十页，讲稿共四十三页哦Recommended Tests before AnesthesiaECG:RV/RA enlargementCXR:enlarged central and R/L pulmonary arteries,cardiac
16、silhouetteABGECHO:?TR,?PFO,estimation of pulm pressure,RV hypertrophy,dilatation of RV with impairment of LV filling,paradoxical mvmt of IV septumCardiac Catheterization:pulm pressures,CO,response to vasodilators,?PFO,status of coronary circulation第二十一页，讲稿共四十三页哦Anesthetic Considerations:Pre-opMainta
17、in all pulm vasodilators ex.prostacyclin,Ca2+antagonists,phosphodiesterase-5-inhibitors(sildenafil,dypiridamole),endothelin receptor antagonists(Bosentan)and O2If pulm HTN diagnosed immediately pre-op and OR cant be delayed,start sildenafil(0.1mg/kg daily up to 0.5mg/kg q6hrs,adults 50-100mg daily,I
18、V 0.2mg/kg/hr)and l-arginine(15gm daily)if clinical signs of pulm HTN or poor ex toleranceHeparin should replace indirect anticoagulant(ie.Coumadin)until ORPremed:slight midaz OK as long as resp acidosis/BP not induced第二十二页，讲稿共四十三页哦Anesthetic Considerations:Goals Maintain NSR Avoid tachycardia Avoid
19、 hypotension/hypertension Avoid all factors that increase PVR:Hypoxia Hypercarbia Acidosis Pain/noxious stimuli Low lung volumes/overdistension第二十三页，讲稿共四十三页哦Anesthetic Considerations:InductionFew studies showing effect on vasoreactivityOpioids used at a dose to block the cardioresp response of intub
20、ation,they have no direct effect on pulm vesselsLidocaine(1mg/kg)can help suppress response to intubationPropofol,pentothal or etomidate may be usedDepolarizing or nondepolarizing muscle relaxants could be used(avoid MR releasing histamine)第二十四页，讲稿共四十三页哦Anesthetic Considerations:MaintenanceVolatiles
21、(iso-most common,des,sevo)can be usedDesfluranePotentiates pulm vasoconstriction to adrenoceptor activationIsofluraneAttenuates magnitude of hypoxic pulm vasoconstrictionPotentiates vasodilator response to B1 adrenoceptor activationNo effect on alpha 1 vasoconstrictionMaintain opioids at a surgical
22、analgesic levelMaintain muscle relaxation第二十五页，讲稿共四十三页哦MonitoringArt lineCVP or PACTEE if available第二十六页，讲稿共四十三页哦Treatment of Pulm HTN During SurgeryInhaled NO(20-40 ppm)Milrinone(50ug/kg bolus then 0.5-0.75ug/kg/min)Dypiridamole(0.2-0.6 mg/kg IV over 15min q 12hrs)Inhaled prostacyclin(nebulized or
23、IV 2-20 mcg/kg/min)Mg:smooth muscle relaxant,attenuates the effect of hypoxia on PVR(serum conc 3-5mmol/L)第二十七页，讲稿共四十三页哦Nitric Oxide Selective pulmonary vasodilation,improves oxygenation cGMP Used in ARDS,PPHN,cardiogenic shock,post CPB Risks:methemoglobinemia and carboxyhemoglobinemia,rebound pulm
24、HTN when stopped Requires closed inhalational circuit第二十八页，讲稿共四十三页哦Phosphodiesterase inhibitors Inhibition of nitric oxide degradation Sildenafil(PDE-5 inhibitor):PAP/PVR Min effects on systemic vasculature Synergistic with NO Reduction in RV mass:role in prevention or reversal of remodeling of RV M
25、ilrinone(PDE-3 inhibitor):PVR/PAP/SVR in setting of CV shock Nebulized minimizes systemic vasodilation第二十九页，讲稿共四十三页哦Prostacyclins Potent pulm and systemic vasodilators with antiplatelet properties Epoprostenol(IV):PVR,better CO/ex.Tolerance s/e:BP,need for central line(risk of infection)Beraprost(PO
26、):Longer duration Iloprost(nebulized)第三十页，讲稿共四十三页哦Endothelin receptor antagonists Endothelin-1:neurohormone that causes pulm vasoconstriction,smooth muscle proliferation,fibrosis Stimulates endothelin receptors A&B A:vasconstriction B:vasodilation Nonselective:Bosentan A selective:sitaxsentans/e:hep
27、atic toxicity第三十一页，讲稿共四十三页哦Ca channel blockers Chronic pulm HTN Rx s/e:hypotension causing reflex tachycardia Only 15-25%of pts respond Need to undergo vasoreactivity testing prior to starting第三十二页，讲稿共四十三页哦Post-opICUOptimal analgesia with continuous epidural,regional block or parenteral opioidsAvoid
28、,hypoxemia,BP,hypovolemiaRisk of acute pulm vasospasm,arrhythmia,fluid shifts,sympathetic tone,pulm vasc toneWean any pulmonary vasodilators progressively第三十三页，讲稿共四十三页哦麻醉医师围术期工作 正确评估肺高压及肺血管病变的可逆程度 围术期肺的保护 预防和避免引起/加重肺高压的因素 针对肺高压、右心衰治疗第三十四页，讲稿共四十三页哦正确评估肺高压及肺血管病变 评估目的：对肺高压中可逆和不可逆的两种成分比重进行判断 方法：用一系列肺血管扩
29、张药物治疗后，进行重复、动态地肺循环参数测定来识别肺高压中可逆和不可逆的两种成分的比重第三十五页，讲稿共四十三页哦肺动脉高压严重程度的评估 肺动脉压：PADP越高肺血管阻力越大（肺、主动脉瓣关闭不全时，不能反映）肺/体血流比值：3时，无明显肺血管阻力升高 肺动脉血氧饱和度：较好反映肺血流和PVR 吸氧反应及血管扩张药物反应 肺活检：估计肺血管病变的性质和程度第三十六页，讲稿共四十三页哦血管扩张试验 方法：吸入NO1020ppm,10min 吸入依洛前列素810ug,15min IV前列环素2ng/(kg.min)并逐渐增加至不能耐受，30min IV腺苷50ug/(kg.min)并逐渐增加至不
30、能耐受，10min 试验阳性定义（欧洲心脏协会）：mPAP至少降低10mmHg,并且绝对值 40mmHg，伴CO增加或不变第三十七页，讲稿共四十三页哦针对肺高压右心衰治疗 基本治疗 提高吸氧浓度改善缺氧 过渡通气，保持PaCO2在30-35mmHg,避免呼酸 纠正代酸 加强呼吸管理，避免Q/V失调 适当镇静、镇痛，避免过度应激导致EA释放 维持体温37，避免寒战第三十八页，讲稿共四十三页哦针对肺高压右心衰治疗 特殊处理 降低右室后负荷 血管扩张药 维持和支持心肌收缩 儿茶酚胺类正性肌力药 磷酸二酯酶抑制剂 增加右冠灌注压 1受体激动药苯肾上腺素第三十九页，讲稿共四十三页哦 钙离子拮抗试剂 前列环素类药物 内皮素受体拮抗剂 5型磷酸二酯酶抑制剂 NO 联合治疗血管扩张药第四十页，讲稿共四十三页哦静脉注射血管扩张药物的副作用 体循环血管扩张致低血压 冠脉灌注减少 导致并加重右心衰 Q/V失调，加重低氧血症第四十一页，讲稿共四十三页哦弥补方法 采用选择性扩张肺动脉的药物 改变用药途径 吸入法代替静脉给药 代表药物：一氧化氮（Nitric Oxid）依洛前列素（IIoprost）西地那非（Sildenafil）双心给药：肺动脉给扩血管药，同时经左心给缩血管药第四十二页，讲稿共四十三页哦感谢大家观看感谢大家观看第四十三页，讲稿共四十三页哦