《颈动脉支架成型术后血流动力学改变及防治措施.ppt课件》由会员分享，可在线阅读，更多相关《颈动脉支架成型术后血流动力学改变及防治措施.ppt课件（21页珍藏版）》请在金锄头文库上搜索。
1、文献回顾文献回顾颈动脉支架成型术后血流动力学改变及防治措施四川省资阳市第一人民医院 陈艳2008-10-06Periprocedural hemodynamic instability with carotid angioplasty and stenting颈动脉支架成型术后血流动力学不稳定文献一：Surgical NeurologyBackground:Background: Carotid angioplasty and stenting is used for treatment of carotid stenosis. Stentdeployment may induce HDI a
2、nd thereby cause systemic or neurologic deficits. This study defines characteristics and predictors of HDI with CAS.Methods: A total of 132 patients who had undergone CAS were evaluated for periprocedural and postprocedural HDI (hypertension, systolic blood pressure 160 mm Hg; hypotension, systolic
3、blood pressure 90 mm Hg; or bradycardia, heart rate 60 beats per minute).Results: Frequencies of HDI were 6.8% for hypertension, 32.6% for hypotension, and 15.9% for bradycardia.文献二：Stroke October 1999F requency and D eterm inants of P o stp ro c e d u ra l H em odynam ic In s ta b ility A fte r C a
4、 ro tid A n g io p la s ty a n d S te n tin g颈动脉支架成形术后血流不稳定因素Background and PurposeHemodynamic instability can occur acutely after carotid angioplasty and stent placement (CAS). We performed this study to determine the frequency of hemodynamic instability in a series of patients who underwent CAS an
5、d to analyze factors associated with development of postprocedural hemodynamic events.MethodsWe reviewed medical records and angiograms in a series of 51 patients (mean age 68.3+8.9 years) who underwent CAS for symptomatic (n=29) or asymptomatic (n=22) carotid artery stenosis. Any episodes of hypote
6、nsion (systolic blood pressure160 mm Hg), or bradycardia (heart rate60 bpm) that occurred in the acute postprocedural period were recorded. The effect of demographic, clinical,intraprocedural, and angiographic factors on subsequent development of hemodynamic instability was analyzed by logistic regr
7、ession.ResultsThe frequency of postprocedural hemodynamic complications in our patient series was as follows: hypotension,22.4%; hypertension, 38.8%; and bradycardia, 27.5%. Intraprocedural hypotension (odds ratio OR 14.6, P50.024) andhistory of myocardial infarction (OR 14.1, P50.04) independently
8、predicted postprocedural hypotension. Postproceduralhypertension was predicted by intraprocedural hypertension (OR 7.6, P50.01) and previous ipsilateral carotidendarterectomy (OR 7.6, P50.02). Postprocedural bradycardia was associated with intraprocedural hypotension (OR 74,P50.001) and intraprocedu
9、ral bradycardia (OR 12, P50.008). All events had resolved at the conclusion of the intensivecare unit monitoring period (mean 25.7 hours, range 18 to 43 hours).ConclusionsPostprocedural hemodynamic instability is frequent after CAS and supports the need for monitoring in settings suited to expeditio
10、us management of cardiovascular emergencies. Patients who have evidence of hemodynamicinstability during the procedure are at highest risk. (Stroke. 1999;30:2086-2093.)文献三：Neurosurgery, October 2001Prevention of Carotid Angioplasty-induced Bradycardia and Hypotension with Temporary Venous Pacemakers
11、使用临时起搏器预防颈动脉血管成形术后心动过缓及血压下降OBJECTIVE:Carotid angioplasty with stent placement is becoming an established treatment modality for patients with high-risk carotid stenosis. Unlike carotid endarterectomy, angioplasty causes direct mechanical dilation of the stenotic carotid artery and bulb. Stimulation
12、of the sinus baroreceptors （压力感受器）induces a reflexive response that consists of increased parasympathetic（副交感神经 ）discharge and inhibition of sympathetic tone（交感紧张）, which results in bradycardia （心动过缓）and subsequent cardiogenic hypotension（继发心源性低血压）.METHODS:At a single institution, the experience wit
13、h 43 patients treated from November 1994 to January 2000 with 47 angioplasty and stent procedures for occlusive carotid artery disease was retrospectively reviewed（回顾性研究）.Prophylactic（预防性） temporary venous pacemakers were used to prevent hypotension from possible angioplasty-induced bradycardia. Pac
14、emakers were set to capture a heart rate decrease below 60 beats per minute. Variables analyzed included demographics（人口统计）, etiology （病因）of disease, side of the lesion, the presence of symptoms, history of coronary artery disease, percent stenosis, type of stent used, number of dilations, pressure
15、of dilation, and angioplasty balloon diameter.RESULTS:Ten patients were excluded because pacemakers were not used during their angioplasty procedures,and these included three emergencies and a lesion that was unrelated anatomically to the carotid sinus (petrous carotid). The remaining 37 procedures
16、were performed in 33 patients with a mean age of 67 years,and consisted of 17 men, 16 women, 20 right and 17 left-sided lesions. The pacemakers maintained a cardiac rhythm in 23 (62%) of the 37 procedures and in no case did the pacemaker fail to respond when activated.Recurrent (56%; 10 of 18), radi
17、ation-induced (78%; 7 of 9), and medically refractory carotid stenosis (67%;6 of 9) required intraprocedural pacing. Two patients with recurrent stenosis became hypotensive despite the aid of the pacing device but were not symptomatic. Seventy-nine percent (15 of 19) of symptomatic lesions and 57% (
18、8 of 14) of nonsymptomatic lesions required pacing, which was statistically significant (P 0.049). No patient experienced an operative morbidity or mortality as a consequence of the temporary pacing devices.CONCLUSION:Angioplasty-induced bradycardia is a common condition, and it is more prevalent in
19、 radiationinduced stenosis and with symptomatic lesions. Temporary venous demand pacing is a safe procedure and mayprevent life-threatening, baroreceptor（压力感受器）-induced hypotension. T he blood pressure variability is related to postoperative changes in the m echanical property of the carotid sinus w
20、 all (1). U nlike carotid endarterectom y,the use of an g io p lasty in v o lv es d irect m echanical dilation of the carotid artery and bulb, and this reflex cannot be inhibited w ith the use of local anesthesia. S tretching th e sin u s c a u se s in c re a se d parasym pathetic discharge and a re
21、duction of system ic arterial sm ooth m uscle tone, w hich results in h y p o ten sio n . T h erefo re, p a tie n ts a t o u r in stitu tio n received prophylactic tem porary venous pacem akers to prevent angioplasty-induced bradycardia an d su b seq u en t h y p o ten sio n.Neuronal circuits regula
22、te systemic blood pressure andparticipate in a feedback loop that controls heart rate, cardiac output, and sympathetic tone. In the carotid artery, these nerve fibers are located in the wall of the carotid sinus, classified as mechanoreceptors(机械感受器） or baroreceptors（压力感受器）, and are principally affe
23、cted by distention of the carotid sinus. The stretching of the carotid vessel stimulates and activates the afferent fibers（传入纤维） that project to the nucleus tractus solitarius（孤束核） via the glossopharyngeal nerve (舌咽神经）(Fig. 1). Second-order solitary nucleus neurons excite cells in the dorsal motor n
24、ucleus of theNeuronal circuitry （神经传导通路）involved during carotid angioplasty that results in hypotension and bradycardia. The glossopharyngeal（窦房结） nerve transmits impulses from the carotid sinus baroreceptors （压力感受器）to the nucleus solitarius（孤束核）. Collateral nerve fibers are sent to the nucleus ambi
25、guous, dorsal motor nucleus of the vagus, and red nucleus. The vagus nervecarries parasympathetic signals to the heart, which produce bradycardia when activated. Collateral fibers from the reticulospinal（网状脊髓束） and solitariospinal tract synapse on the lateral horn of the thoracic spinal cord inhibit
26、 sympathetic fibers（交感神经纤维）, producing vasodilation and decreased heart rate. These effects may be synergistic and result in symptomatic hypotension .Pathophysiology of carotid sinus-induced hypotensionCASE1: 患者，男性，患者，男性，4646岁，因岁，因“一过性晕厥一过性晕厥1 1月，右侧肢体无月，右侧肢体无力半月力半月”第一次入院。第一次入院。 DSADSA提示双侧颈内动脉起始重度狭窄，
27、提示双侧颈内动脉起始重度狭窄，MRIMRI提示双侧半卵提示双侧半卵圆中心腔隙性梗塞。圆中心腔隙性梗塞。 既往有既往有HT10HT10年，年，DM10DM10年，有高血脂病史及烟酒嗜好。术年，有高血脂病史及烟酒嗜好。术前血压前血压150/90mmHg,HR72150/90mmHg,HR72次次/ /分，行左侧颈动脉支架置入分，行左侧颈动脉支架置入术，术后病情稳定术，术后病情稳定BP120/80mmHg,HR62BP120/80mmHg,HR62次次/ /分。分。 术后一月行右侧颈动脉支架成形术，术后术后一月行右侧颈动脉支架成形术，术后2 2小时发生血小时发生血压下降，压下降，80/40mmHg8
28、0/40mmHg，心率，心率35-4535-45次次/ /分，患者诉心慌，分，患者诉心慌，全身大汗，颦死感，经使用阿托品、多巴胺、扩容等症全身大汗，颦死感，经使用阿托品、多巴胺、扩容等症状状1 1小时缓解，心率小时缓解，心率45-5045-50次次/ /分，血压升至分，血压升至100 -100 -110/50mmHg,110/50mmHg,多巴胺持续泵入多巴胺持续泵入4848小时停用，无自觉症状。小时停用，无自觉症状。 HolterHolter提示窦性心动过缓提示窦性心动过缓。术前术前术前术前：双侧颈内动脉近段重度狭窄，右侧：残双侧颈内动脉近段重度狭窄，右侧：残余管径余管径/ /原始管径原始管
29、径=1.0/5.5mm;=1.0/5.5mm;左侧左侧=1.2/4.3mm=1.2/4.3mm第二次术后DSA片CASE2:患者，男性，患者，男性，7272岁，因岁，因“发作性意识丧失伴跌发作性意识丧失伴跌倒倒1010月月”入院。入院。DSADSA发现发现LVLV开口重度狭窄，开口重度狭窄，RICARICA起始段重度狭窄起始段重度狭窄并行并行LVLV开及开及RICARICA起始段支架成形术，入院时起始段支架成形术，入院时ECGECG提示房室传导延搁，提示房室传导延搁，PRPR间期间期0.270.27秒。术中（球秒。术中（球囊扩张时）患者出现心率下降囊扩张时）患者出现心率下降32-4332-43次次/ /分，无分，无自觉症状，行临时起搏器安置，术后自觉症状，行临时起搏器安置，术后5 5天心率升天心率升至至45-5245-52次次/ /分，拔出起搏器，无症状出院，分，拔出起搏器，无症状出院，HolterHolter提示提示2 2度房室传导阻滞，偶发室早，短阵度房室传导阻滞，偶发室早，短阵室速。术后室速。术后1 1月发生心悸，心率月发生心悸，心率35-4535-45次次/ /分，安分，安置永久起搏器置永久起搏器。
