（醫(yī)學(xué)課件）肺高壓患者圍術(shù)期處理.ppt

1、專用術(shù)語說明,肺循環(huán)高壓（Pulmonary hypertension） 整個(gè)肺循環(huán)，任何系統(tǒng)或者局部病變而引起肺循環(huán)血壓增高。包括：肺動(dòng)脈高壓、肺靜脈高壓、混合性肺動(dòng)脈高壓。 肺動(dòng)脈高壓（Pulmonary arterial hypertension） 肺動(dòng)脈壓力增高, 而肺靜脈壓力正常 特發(fā)性肺動(dòng)脈高壓 (Idiopathic Pulmonary arterial hypertension) 無任何原因（遺傳、病毒、藥物等）發(fā)生的肺動(dòng)脈高壓,1,Definition,正常人肺動(dòng)脈壓力為1530/510mmHg，平均為15 mmHg。 靜息狀態(tài)下，若肺動(dòng)脈收縮壓30 mmHg，或平均壓20

2、mmHg，即為肺動(dòng)脈高壓。 WHO規(guī)定：海平面狀態(tài)下，靜息時(shí)，右心導(dǎo)管檢查肺動(dòng)脈收縮壓30 mmHg，和/或肺動(dòng)脈平均壓25 mmHg，或運(yùn)動(dòng)時(shí)肺動(dòng)脈平均壓30 mmHg，即為肺循環(huán)高壓。診斷肺動(dòng)脈高壓，尚需PCWP 15 mmHg,2,Severity of Pulmonary Hypertension,Degree of disease Mild Moderate Severe,Mean PAP (mmHg) 20 - 30 30 - 50 50,3,Classification of Pulmonary Hypertension,1975 WHO Classification Prima

3、ry pulmonary hypertension (PPH) Secondary pulmonary hypertension 1998 Evian Classification Clinical classification system Different categories sharing similarities in pathophysiological mechanisms, clinical presentations, therapeutic options 2003 Revised Clinical Classification of Pulmonary Hyperten

4、sion,4,Clinical Classification of Pulmonary Hypertension,Venice 2003,Evian 1998,5,WHO肺動(dòng)脈高壓患者功能分級(jí),6,Mechanisms of pulmonary hypertension,肺動(dòng)脈高壓的細(xì)胞機(jī)制 肺血管結(jié)構(gòu)重構(gòu)是肺動(dòng)脈高壓重要的病理基礎(chǔ) 內(nèi)皮細(xì)胞、平滑肌細(xì)胞、成纖維細(xì)胞、血小板和血栓形成、炎癥細(xì)胞,7,8,Mechanisms of pulmonary hypertension,肺動(dòng)脈高壓的分子機(jī)制 多種血管活性物質(zhì)，正常情況下它們之間處于動(dòng)態(tài)平衡，維持肺血管的正常生理結(jié)構(gòu)和功能 氣體信號(hào)分子 N

5、O 、CO、 H2S 血管活性肽及其他血管活性物質(zhì) 依前列醇(前列環(huán)素，eroprostenol，prostacyclin，PGI2) 腎上腺髓質(zhì)素(ADM) 內(nèi)皮素-1(endothelin一1，ET一1)： 血管緊張素 5一羥色胺(5一HT ) 血管活性腸肽 鉀通道,9,Injury to endothelial cells leads to overproduction of endothelin key cause of blood vessel scarring and spasm & to reduced production of nitric oxide and prostac

6、yclins 2 key body chemicals which keep blood vessels relaxed and open.,10,腎上腺髓質(zhì)素(ADM),ADM 是1993年由日本學(xué)者在嗜鉻細(xì)胞瘤中發(fā)現(xiàn)的一種新型血管活性多肽 具有舒張血管、降低血壓、利尿排鈉和抑制血管平滑肌遷移增殖等多種生物學(xué)作用。 持續(xù)給予低氧大鼠ADM，能夠緩解肺血管結(jié)構(gòu)重構(gòu)和肺動(dòng)脈高壓的形成,11,5-HT in pulmonary hypertensionMacLean (1999) TIPS 20:490,Blood vesselalveolar lumen,12,K+ channel abnorm

7、alities in Primary PH (PPH)Archer & Rich (2000) Circulation 102:2782,Decreased Kv1.5 in PPH Impaired K+ current in PPH,SPH secondary PH Donor and NPH - normals,13,Mechanisms of pulmonary hypertension,肺動(dòng)脈高壓的遺傳機(jī)制 IPAH為常染色體顯性遺傳，但是不完全外顯，相關(guān)突變的攜帶者中只有10 20有明顯的肺動(dòng)脈高壓表 目前認(rèn)為骨形成蛋白型受體(bone morphogenetic protein

8、receptor II，BMPR2) 基因突變是IPAH的重要致病原因,14,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 mutation (first hit) and the ingestion of appetite suppr

9、essants (second hit) were used to generate the clinical disease.,15,WHAT IS PH?,MECHANISMS OF PH,TREATMENT OF PH,16,Pathophysiology,Acute: RV afterload, EDV, EF, SV of RV Chronic: progressive systolic pressure overload of RV that dilates and hypertrophies, gradual RV dysfunction venous return compro

10、mises RV preload and pulm blood flow results from positive intrathoracic pressure (ex. PEEP) which also causes alveolar overdistension which PVR and pulm blood flow,17,Pathophysiology,-PVR limits RV SV and the volume for LV filling -LV compressed by intraventricular septum during systole, LV volume/

11、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 from R to L

12、 intracardiac shunt (if RA pressures higher than LA),18,Signs of Disease Severity,Dyspnea at rest Low cardiac output with metabolic acidosis Hypoxemia Signs of right heart failure (large V wave on jugularis vein, periph edema, hepatomegaly) Syncope (poor prognosis) Chest pain (RV ischemia),19,Physic

13、al Exam,Loud P2 (increases PAP) Left parasternal heave (R sided overload) Pulm valve regurgitation (dilatation of pulm valve annulus) S3 gallop (advanced RV failure),20,Recommended Tests before Anesthesia,ECG: RV/RA enlargement CXR: enlarged central and R/L pulmonary arteries, cardiac silhouette ABG

14、 ECHO: ? TR, ?PFO, estimation of pulm pressure, RV hypertrophy, dilatation of RV with impairment of LV filling, paradoxical mvmt of IV septum Cardiac Catheterization: pulm pressures, CO, response to vasodilators, ?PFO, status of coronary circulation,21,Anesthetic Considerations: Pre-op,Maintain all

15、pulm vasodilators ex. prostacyclin, Ca2+ antagonists, phosphodiesterase-5-inhibitors (sildenafil, dypiridamole), endothelin receptor antagonists (Bosentan) and O2 If 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 d

16、aily, IV 0.2mg/kg/hr) and l-arginine (15gm daily) if clinical signs of pulm HTN or poor ex tolerance Heparin should replace indirect anticoagulant (ie. Coumadin) until OR Premed: slight midaz OK as long as resp acidosis/BP not induced,22,Anesthetic Considerations: Goals,Maintain NSR Avoid tachycardi

17、a Avoid hypotension/hypertension Avoid all factors that increase PVR: Hypoxia Hypercarbia Acidosis Pain/noxious stimuli Low lung volumes/overdistension,23,Anesthetic Considerations: Induction,Few studies showing effect on vasoreactivity Opioids used at a dose to block the cardioresp response of intu

18、bation, they have no direct effect on pulm vessels Lidocaine (1mg/kg) can help suppress response to intubation Propofol, pentothal or etomidate may be used Depolarizing or nondepolarizing muscle relaxants could be used (avoid MR releasing histamine),24,Anesthetic Considerations: Maintenance,Volatile

19、s (iso-most common, des, sevo) can be used Desflurane Potentiates pulm vasoconstriction to adrenoceptor activation Isoflurane Attenuates magnitude of hypoxic pulm vasoconstriction Potentiates vasodilator response to B1 adrenoceptor activation No effect on alpha 1 vasoconstriction Maintain opioids at

20、 a surgical analgesic level Maintain muscle relaxation,25,Monitoring,Art line CVP or PAC TEE if available,26,Treatment of Pulm HTN During Surgery,Inhaled 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

21、 or IV 2-20 mcg/kg/min) Mg: smooth muscle relaxant, attenuates the effect of hypoxia on PVR (serum conc 3-5mmol/L),27,Nitric Oxide,Selective pulmonary vasodilation, improves oxygenation cGMP Used in ARDS, PPHN, cardiogenic shock, post CPB Risks: methemoglobinemia and carboxyhemoglobinemia, rebound p

22、ulm HTN when stopped Requires closed inhalational circuit,28,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 Milr

23、inone (PDE-3 inhibitor): PVR/PAP/SVR in setting of CV shock Nebulized minimizes systemic vasodilation,29,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):

24、 Longer duration Iloprost (nebulized),30,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: he

25、patic toxicity,31,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,32,Post-op,ICU Optimal analgesia with continuous epidural, regional block or parenteral opioids Avoid, hypoxemia, BP, hypovolemia Risk of acute pulm vasospasm, arrhythmia, fluid shifts, sympathetic tone, pulm vasc tone Wean any pulmonary vasodilators progressively,33,麻醉醫(yī)師圍術(shù)期工作,正確評(píng)估肺高壓及肺血管病變的可逆程度 圍術(shù)期肺的保護(hù) 預(yù)防和避免引起/加重肺高壓的因素 針對(duì)肺高壓、右心衰治療,34,正確評(píng)估肺高壓及肺血管病變,評(píng)估目的：對(duì)肺高壓