短期应用高渗盐水对重症蛛网膜下腔出血患者颅内压、脑血流量的影响

目的 探讨23.4%高渗盐水(HTS)对重症蛛网膜下腔出血(SAH)患者颅内压、脑灌注压、脑血流量(CBF)的影响.方法 16例重症SAH患者(GCS≤8分)在颅压升高时接受静脉输注23.4%HTS,监测用药前及用药后30、60、90、120、150、180 min的颅内压(ICP),平均动脉压(MAP),脑灌注压(CPP)及脑血流速度(FV).结果 用药后30 min可见ICP显著降低,同时MAP、CPP及FV显著升高(P<0.05),ICP显著降低可持续180 min,CPP和FV的改善持续约90 min(P<0.05).结论 HTS能显著降低重症SAH患者的ICP,改善脑组织灌注,可用来纠正脑缺血引起的病生理变化.     

小剂量氯胺酮对颅脑手术患者颅内压的影响

目的观察小剂量氯胺酮对颅脑手术患者颅内压的影响。方法选择20例需行开颅手术的颅内肿瘤患者,随机分为氯胺酮组(K组)和对照组(C组),每组10例:K组在麻醉诱导后给予氯胺酮0.2mg/kg静脉注射,然后以6μg/(kg·min)泵入维持至缝皮,C组给予等量生理盐水。于麻醉前、诱导、插管、切皮、钻孔、去骨瓣以及手术结束时测定两组颅内压(ICP)、平均动脉压(MAP)、脑灌注压(CPP)和心率(HR)。结果两组比较ICP、MAP、CPP、HR差异无显著性(P>0.05);组内较比,去骨瓣及术毕时两组ICP都显著低于麻醉前(P<0.05)。两组各时点CPP均维持在9.3kPa(70mmHg)以上。结论小剂量氯胺酮不升高ICP,可应用于颅脑外科手术麻醉。     

23.4%高张盐水用于治疗顽固性颅内高压

作者报告了23.4％高张盐水用于治疗顽固性颅内高压(RIH)的效果。本组共8例病人,其中动脉瘤蛛网膜下腔出血(SAH)5例,脑外伤、脑肿瘤及自发性基底神经节出血各1例。7例经脑室内置管,1例蛛网膜下腔放置测压螺栓以监测颅内压(ICP),同时监测平均动脉压(MAP)、脑灌注压(CPP),中心静脉压(CVP)和其他重要指标。当采用包括过度通气、甘露醇、呋塞米和巴比妥酸盐等常规措施不能使增高的ICP最大值下降50％以上者,即诊断为RIH,并决定接受高张盐水治疗。     

异丙酚和普鲁卡因对颅内压及脑灌注压的影响

目的观察异丙酚、普鲁卡因对颅内压(ICP)和脑灌注压(CPP)的影响。方法25例脑肿瘤病人随机分成异丙酚组(D组)和普鲁卡因组(P组)。局麻下钻孔于颅骨及脑膜间安置SP-2000型颅内压监护仪，连续监测ICP，同时用Colin508连续监测MAP、HR及PETCO2。静注异丙酚2mg／kg后，输注异丙酚100～150pg·kg     

大量输血后硫喷妥钠对MAP、ICP、CPP的影响

硫喷妥钠能降低颅脑压,减少脑耗氧量,降低脑代谢,宜用于颅内压增高的脑神经外科手术的麻醉,近些年来很多报告此药用于脑复苏有良好作用。临床上危重病人特别是大出血休克和心跳骤停复苏时常需较大量输血,为此本实验观察了大量输血后硫喷妥钠对平均动脉压(MAP)、中心静脉压(CVP)、颅脑压(ICP)、脑灌流压(CPP)和心电图的影响。     

置入喉镜和气管内插管期间颅内压增高的预防——硫喷妥钠第二个剂量的应用

据文献报道,置入喉镜和气管内插管期间颅内压(ICP)和平均动脉压(MAP)急剧增加,ICP增高的神经外科病人其增加更显著。为预防置入喉镜和气管内插管时ICP和MAP增加,许多作者推荐在这些操作前使用硫喷妥钠或三甲噻方,以及预先用β-肾上腺素能受体阻滞剂和利多卡因治疗。本研究的目的在于评价应用第二个剂量应喷妥钠后,在置入喉镜和气管内插管期间动脉压、ICP和脑灌注压(CPP)的变化。方法:选择9例预定做开颅术,术前行ICP监测的病人进行研究。心肺无主要疾病。术前2小时口服安定10mg,诱导前10分钟测定动脉压和ICP做为对照值,CPP根据MAP和平均ICP之差算出。随后的处理可分为三期:Ⅰ期—静注阿托品0.6mg,1分钟内注入硫喷妥钠(5mg/kg),随后注入潘侃罗宁(1mg/kg,)用笑气-氧(2:1)采用非重复吸入系统进行过度通气3分钟,而后在30秒钟内注入硫喷妥钠(2.5mg/kg)。Ⅱ期—注射上述第     

持续颅内压监护和脑灌注压监护在重型颅脑损伤中的临床应用

目的探讨持续颅内压（intracranial pressure,ICP）监护和脑灌注压（cerebral perfusionpressure,CPP）监护在重型颅脑损伤患者诊疗中的临床作用。方法临床上采用脑实质内ICP探头置入术,对60例重型颅脑损伤患者进行了持续ICP监护和CPP监护,根据ICP和CPP的变化给予相应治疗。结果根据GOS评分,随访发现预后良好24例（40%）;中残8例（13.3%）,重残4例（6.7%）,植物状态2例（3.3%）,死亡22例（36.7%）。结论持续ICP监护和CPP监护有利于颅脑损伤患者的病情观察,指导脱水药的使用,提高疗效,减少并发症。     

甘露醇对颅脑手术患者脑氧供需平衡的影响

目的：探讨颅脑手术麻醉期间静脉输注甘露醇对脑氧供需平衡的影响。方法：选择静脉全麻醉上开颅行幕上肿瘤切除术患者14例，分别检测静脉输液25％甘露醇1g/kg输液前和输注后，30，60分钟时的颅内压（ICP），颈内静脉和桡动脉的血气，计算脑灌注压（CPP），动－颈静氧含量差（C(a-j)O2)和脑氧摄取率（CEO2）。结果：甘露醇输注后30分钟，ICP和心率（HR）较输注前显著降低（P＜0．05），但CPP，C(a-j)O2和CEO2虽呈下降趋势，但与输液前比较均无统计学差异。结论：颅脑手术麻醉期间输注甘露醇，不仅可降低ICP，对MAP和CPP无明显影响，而且能改善脑血流代谢耦联，对开颅手术的病人有利。     

3%高渗盐水治疗重型颅脑损伤脑水肿的临床研究

目的研究3%高渗盐水治疗重型颅脑损伤的临床疗效。方法在颅内压监护下对13例患者使用3%的高渗盐水脱水治疗,与同期15例使用甘露醇脱水患者进行对比研究,观察两组患者用药后6小时内,连续监测患者颅内压(ICP)、平均动脉压(MAP)、中心静脉压(CVP)、血脑灌注量(CPP)。记录起效时间以及治疗后至ICP恢复用药前水平所间隔的时间。结果 3%高渗盐水的脱水效果与甘露醇比较差异无统计学意义,远期疗效及死亡率相当。结论 3%的高渗盐水脱水效果确切,对重型颅脑损伤患者可作为临床一线脱水药物。     

高渗氯化钠羟乙基淀粉40注射液对外伤性颅内血肿伴失血性休克患者术中颅内压的影响

目的 探讨高渗氯化钠羟乙基淀粉40注射液(HH40)对外伤性颅内血肿伴失血性休克患者术中颅内压(ICP)的影响.方法 外伤性颅内血肿伴失血性休克患者40例,急诊行颅内血肿清除术,随机均分为HH40组(H组)和4.2%高渗盐水组(C组).麻醉诱导后,分别在15 min内快速静脉输入HH40 5ml/kg或4.2%高渗盐水5 ml/kg.在输注HH40或4.2%高渗盐水前即刻(T0)、输注后15 min(T1)、30 min(T2)、60 min(T3)、90 min(T4)、120 min(T5)记录MAP、HR、CVP、尿量,采集桡动脉血测定血浆Na+、K+浓度进行血气分析,并计算各时点脑灌注压(CPP):CPP=MAP-ICP.结果 与T0时比较,T1～T5时两组MAP、CVP、CPP升高,HR减慢,T2～T5时ICP降低(P＜0.05).与C组比较,T4、T5时H组HR减慢和T5时MAP升高(P＜0.05);H组降低ICP幅度与其相似,而降ICP作用维持时间较长(P＜0.05).结论 HH40可安全地用于外伤性颅内血肿伴失血性休克手术患者,能有效地纠正其休克,降低其ICP.     

不同体位对危重患者腹内压及腹腔灌注压的影响

【摘要】〓目的〓观察不同体位对腹内压及腹腔灌注压的影响。方法〓对2013年1月~2013年12月收治ICU的有腹内压监测适应征的78位患者分别在0°、15°、30°、45°采用测量膀胱压的方法监测腹内压,并计算腹腔灌注压。结果〓在腹内高压者,30°(21.46±3.91 mmHg, P=0.001)及45°(25.69±4.09 mmHg, P<0.001)时腹内压比0°(16.31±3.38 mmHg)时明显升高,而腹腔灌注压45°(51.92±10.05 mmHg,P=0.03)时明显低于0°(60.54±9.86 mmHg);在腹内压正常者30°(11.17±3.24 mmHg,P=0.002)及45°(15.59±4.13 mmHg, P=0.001)时腹内压比0°(7.23 ±2.14 mmHg)时明显升高,而腹腔灌注压45°(60.78±9.13 mmHg, P=0.004)时明显低于0°(71.28±8.86 mmHg)。结论〓危重病人不同体位对腹内压及腹腔灌注压有影响,床头角度越高,腹内压越高,腹腔灌注压越低,提示测量时应考虑体位的因素。     

Effect of head elevation on intracranial pressure, cerebral perfusion pressure, and regional cerebral oxygen saturation in patients with cerebral hemorrhage

OBJECTIVE: To study the effects on cerebral dynamics and regional oxygenation (rSO2) of the semi-sitting position, with the head at either 30 degrees or 45 degrees, in surgery for cerebral hemorrhage. PATIENTS AND METHODS: We performed a prospective study of 10 patients undergoing surgery for cerebral hemorrhage under sedation and analgesia and with mechanical ventilation. Intracranial pressure (ICP), mean arterial pressure (MAP), cerebral perfusion pressure (CPP), and rSO2 measured using near-infrared spectroscopy were recorded with the head in the supine position (0 degrees) and elevated to an angle of 30 degrees and then 45 degrees, following a stabilization period of 5 minutes. RESULTS: Mean (SD) ICP values were significantly lower in both semi-sitting positions than in the supine position: 2.8 (1.4) mm Hg lower at 30 degrees and 4.4 (1.4) mm Hg lower at 45 degrees. Mean CPP values were fell slightly when the head was elevated to 30 degrees (3.5 [3.1] mm Hg, P=.048); a greater reduction was achieved when the head was elevated 45 degrees (7.1 [4.8] mm Hg, P<.01). The greatest reduction in mean MAP values also occurred with the head elevated to 45 degrees (11.8 [4.6] mm Hg, P<.001). Mean rSO2 values fell when the head was elevated to 30 degrees and 45 degrees; the greatest reduction occurred when the head was elevated to 45 degrees (7% [2%], P<.001). There was a moderate correlation between CPP values and changes in rSO2 (r2=0.45, P<.001). CONCLUSION: Head elevation significantly reduces ICP and CPP in patients with cerebral hemorrhage. Head elevation also reduces rSO2, to a greater or lesser extent depending on the degree to which the head is elevated.     

Cerebral perfusion pressure, intracranial pressure, and head elevation

Previous investigations have suggested that intracranial pressure waves may be induced by reduction of cerebral perfusion pressure (CPP). Since pressure waves were noted to be more common in patients with their head elevated at a standard 20 degrees to 30 degrees, CPP was studied as a function of head position and its effect upon intracranial pressure (ICP). In 18 patients with varying degrees of intracranial hypertension, systemic arterial blood pressure (SABP) was monitored at the level of both the head and the heart. Intracranial pressure and central venous pressure were assessed at every 10 degrees of head elevation from 0 degree to 50 degrees. For every 10 degrees of head elevation, the average ICP decreased by 1 mm Hg associated with a reduction of 2 to 3 mm Hg CPP. The CPP was not beneficially affected by any degree of head elevation. Maximal CPP (73 +/- 3.4 mm Hg (mean +/- standard error of the mean] always occurred with the head in a horizontal position. Cerebrospinal fluid pressure waves occurred in four of the 18 patients studied as a function of reduced CPP caused by head elevation alone. Thus, elevation of the head of the bed was associated with the development of CPP decrements in all cases, and it precipitated pressure waves in some. In 15 of the 18 patients, CPP was maintained by spontaneous 10- to 20-mm Hg increases in SABP, and pressure waves did not occur if CPP was maintained at 70 to 75 mm Hg or above. It is concluded that 0 degree head elevation maximizes CPP and reduces the severity and frequency of pressure-wave occurrence. If the head of the bed is to be elevated, then adequate hydration and avoidance of pharmacological agents that reduce SABP or prevent its rise are required to maximize CPP.     

Is cerebral perfusion pressure a major determinant of cerebral blood flow during head elevation in comatose patients with severe intracranial lesions?

OBJECT: Head elevation as a treatment for lower intracranial pressure (ICP) in patients with intracranial hypertension has been challenged in recent years. Therefore, the authors studied the effect of head position on cerebral hemodynamics in patients with severe head injury. METHODS: The effect of 0 degrees, 15 degrees, 30 degrees, and 45 degrees head elevation on ICP, cerebral blood flow (CBF), systemic arterial (PsaMonro) and jugular bulb (Pj) pressures calibrated to the level of the foramen of Monro, cerebral perfusion pressure (CPP), and the arteriovenous pressure gradient (PsaMonro - Pj) was studied in 37 patients who were comatose due to severe intracranial lesions. The CBF decreased gradually with head elevation from 0 to 45 degrees, from 46.3+/-4.8 to 28.7+/-2.3 ml x min(-1) x 100 g(-1) (mean +/- standard error, p<0.01), and the PsaMonro - Pj from 80+/-3 to 73+/-3 mm Hg (p< 0.01). The CPP remained stable between 0 degrees and 30 degrees of head elevation, at 62+/-3 mm Hg, and decreased from 62+/-3 to 57+/-4 mm Hg between 30 degrees and 45 degrees (p<0.05). A simulation showed that the 38% decrease in CBF between 0 degrees and 45 degrees resulted from PsaMonro - Pj changes for 19% of the decrease, from a diversion of the venous drainage from the internal jugular veins to vertebral venous plexus for 15%, and from CPP changes for 4%. CONCLUSIONS: During head elevation the arteriovenous pressure gradient is the major determinant of CBF. The influence of CPP on CBF decreases from 0 to 45 degrees of head elevation.     

超声观察不同偏头位对右颈内静脉和颈总动脉解剖关系的影响

目的观察右颈内静脉(right internal jugular vein,RIJV)与颈总动脉(common carotid artery,CAA)解剖关系以及不同偏头位对其的影响。方法选择择期全麻手术患者131例,男55例,女76例,年龄18~74岁,ASAⅠ或Ⅱ级。分别在0、15、30、45°偏头位,于甲状软骨喉结平面(喉结平面)和胸锁乳突肌三角顶点平面(三角平面)进行超声扫描并测量RIJV安全穿刺横径、RIJV与CAA横径重叠率、RIJV与CAA连线与水平轴夹角(α角),并根据α角将RIJV与CAA位置关系分为前外侧位、外侧位、后外侧位、偏后外侧位。结果安全穿刺横径在0°~30°偏头范围内,随着偏头角度的增加而递增(P0.05),在任一偏头位,三角平面安全穿刺横径均明显高于喉结平面(P0.05);横径重叠率在喉结平面0°~30°偏头范围内,随偏头角度增加而递减(P0.05),而在三角平面各偏头位之间差异均无统计学意义;在0°、15°偏头位,三角平面横径重叠率低于喉结平面(P0.05);RIJV位置分布以外侧位和后外侧位为主,并且随着偏头角度的增加,外侧位呈现升高趋势,同时后外侧位比例表现为降低(P0.05)。结论 30°~45°偏头位时RIJV安全穿刺范围较大、重叠程度较小;RIJV与CAA位置关系以外侧位和后外侧位为主,随偏头角度的增加外侧位比例增加而后外侧比例降低;三角平面穿刺条件优于喉结平面。     

High intracranial pressure effects on cerebral cortical microvascular flow in rats

To manage patients with high intracranial pressure (ICP), clinicians need to know the critical cerebral perfusion pressure (CPP) required to maintain cerebral blood flow (CBF). Historically, the critical CPP obtained by decreasing mean arterial pressure (MAP) to lower CPP was 60?mm Hg, which fell to 30?mm Hg when CPP was reduced by increasing ICP. We examined whether this decrease in critical CPP was due to a pathological shift from capillary (CAP) to high-velocity microvessel flow or thoroughfare channel (TFC) shunt flow. Cortical microvessel red blood cell velocity and NADH fluorescence were measured by in vivo two-photon laser scanning microscopy in rats at CPP of 70, 50, and 30?mm Hg by increasing ICP or decreasing MAP. Water content was measured by wet/dry weight, and cortical perfusion by laser Doppler flux. Reduction of CPP by raising ICP increased TFC shunt flow from 30.4±2.3% to 51.2±5.2% (mean±SEM, p<0.001), NADH increased by 20.3±6.8% and 58.1±8.2% (p<0.01), and brain water content from 72.9±0.47% to 77.8±2.42% (p<0.01). Decreasing CPP by MAP decreased TFC shunt flow with a smaller rise in NADH and no edema. Doppler flux decreased less with increasing ICP than decreasing MAP. The decrease seen in the critical CPP with increased ICP is likely due to a redistribution of microvascular flow from capillary to microvascular shunt flow or TFC shunt flow, resulting in a pathologically elevated CBF associated with tissue hypoxia and brain edema, characteristic of non-nutritive shunt flow.     

Effect of head elevation on intracranial pressure, cerebral perfusion pressure, and cerebral blood flow in head-injured patients.

The traditional practice of elevating the head in order to lower intracranial pressure (ICP) in head-injured patients has been challenged in recent years. Some investigators argue that patients with intracranial hypertension should be placed in a horizontal position, the rationale being that this will increase the cerebral perfusion pressure (CPP) and thereby improve cerebral blood flow (CBF). However, ICP is generally significantly higher when the patient is in the horizontal position. This study was undertaken to clarify the issue of optimal head position in the care of head-injured patients. The effect of 0 degree and 30 degrees head elevation on ICP, CPP, CBF, mean carotid pressure, and other cerebral and systemic physiological parameters was studied in 22 head-injured patients. The mean carotid pressure was significantly lower when the patient's head was elevated at 30 degrees than at 0 degrees (84.3 +/- 14.5 mm Hg vs. 89.5 +/- 14.6 mm Hg), as was the mean ICP (14.1 +/- 6.7 mm Hg vs. 19.7 +/- 8.3 mm Hg). There was no statistically significant change in CPP, CBF, cerebral metabolic rate of oxygen, arteriovenous difference of lactate, or cerebrovascular resistance associated with the change in head position. The data indicate that head elevation to 30 degrees significantly reduced ICP in the majority of the 22 patients without reducing CPP or CBF.     

四种卧位局部体表压力特点及影响因素分析

目的测量不同卧位压疮好发部位的体表压力,探索体表压力的分布特点及影响因素,为临床压疮防护提供参考。方法抽取200名健康志愿者取仰卧位、45°半侧卧位、90°侧卧位或45°半坐卧位,运用简易测压装置测量压疮好发部位的体表压力。结果不同性别志愿者不同卧位时体表压力分布差异有统计学意义(均P<0.01),男性体表压力普遍高于女性;不同卧位时,体表相同受压部位的压力存在统计学差异(P<0.05,P<0.01),半坐卧位时的骶尾部压力最大。志愿者取不同卧位时,身高、体质量及BMI与局部体表压力呈显著正相关(均P<0.01)。结论各种卧位男性体表压力均高于女性,半侧卧位各受压点压力相对较轻。护理人员可根据体表压力分布特点选用适当卧位,以减少压疮的发生。     

Effects of head posture on cerebral hemodynamics: its influences on intracranial pressure, cerebral perfusion pressure, and cerebral oxygenation

OBJECTIVE: Severely head-injured patients have traditionally been maintained in the head-up position to ameliorate the effects of increased intracranial pressure (ICP). However, it has been reported that the supine position may improve cerebral perfusion pressure (CPP) and outcome. We sought to determine the impact of supine and 30 degrees semirecumbent postures on cerebrovascular dynamics and global as well as regional cerebral oxygenation within 24 hours of trauma. METHODS: Patients with a closed head injury and a Glasgow Coma Scale score of 8 or less were included in the study. On admission to the neurocritical care unit, a standardized protocol aimed at minimizing secondary insults was instituted, and the influences of head posture were evaluated after all acute necessary interventions had been performed. ICP, CPP, mean arterial pressure, global cerebral oxygenation, and regional cerebral oxygenation were noted at 0 and 30 degrees of head elevation. RESULTS: We studied 38 patients with severe closed head injury. The median Glasgow Coma Scale score was 7.0, and the mean age was 34.05 +/- 16.02 years. ICP was significantly lower at 30 degrees than at 0 degrees of head elevation (P = 0.0005). Mean arterial pressure remained relatively unchanged. CPP was slightly but not significantly higher at 30 degrees than at 0 degrees (P = 0.412). However, global venous cerebral oxygenation and regional cerebral oxygenation were not affected significantly by head elevation. All global venous cerebral oxygenation values were above the critical threshold for ischemia at 0 and 30 degrees. CONCLUSION: Routine nursing of patients with severe head injury at 30 degrees of head elevation within 24 hours after trauma leads to a consistent reduction of ICP (statistically significant) and an improvement in CPP (although not statistically significant) without concomitant deleterious changes in cerebral oxygenation.     

Relationship between intracranial pressure and critical closing pressure in patients with neurotrauma

BACKGROUND: The driving pressure gradient for cerebral perfusion is the difference between mean arterial pressure (MAP) and critical closing pressure (CCP = zero flow pressure). Therefore, determination of the difference between MAP and CCP should provide an appropriate monitoring of the effective cerebral perfusion pressure (CPP(eff)). Based on this concept, the authors compared conventional measurements of cerebral perfusion pressure by MAP and intracranial pressure (CPP(ICP)) with CPP(eff). METHODS: Simultaneous synchronized recordings of pressure waveforms of the radial artery and blood flow velocities of the middle cerebral artery were performed in 70 head trauma patients. CCP was calculated from pressure-flow velocity plots by linear extrapolation to zero flow. RESULTS: Intracranial pressure measured by intraventricular probes and CCP ranged from 3 to 71 and 4 to 70 mmHg, respectively. Linear correlation between ICP and CCP was r = 0.91. CPP(ICP) was 77 +/- 20 mmHg and did not differ from CPP(eff); linear correlation was r = 0.92. However, limits of agreement were only +/- 16.2 mmHg. Therefore, in 51.4% of the patients, CPP(ICP) overestimated CPP(eff) by 19.8 mmHg at most. CONCLUSION: Assuming that CPP(eff) (MAP - CCP) takes into account more determinants of cerebral downstream pressure, in individual cases, the actual gold standard of CPP determination (MAP - ICP) might overestimate the CPP(eff) of therapeutic significance.