体位变化以及护理干预对重型颅脑损伤病人颅内压和脑灌注压的影响

目的探讨体位变化以及护理干预对重型颅脑损伤病人颅内压和脑灌注压的影响。方法选取本院2015年9月-2017年9月收治的重型颅脑损伤患者73例作为研究对象。采取3种体位,即仰卧位、左侧卧位和右侧卧位,结合头部抬高15°和30°,保持每种姿势15 min后监测颅内压和脑灌注,同时实施护理干预。结果仰卧位和左侧卧位头部抬高15°颅内压升高而脑灌注压下降,但无统计学差异(P0.05);而右侧卧位头部抬高15°颅内压升高和灌注压下降均有统计学差异(P0.05);仰卧位、左侧卧位和右侧卧位头部抬高30°颅内压下降而脑灌注压升高,但无统计学差异(P0.05)。护理干预后不同体位颅内压下降而脑灌注压升高,均有统计学差异(P0.05)。73例患者护理总满意率为97.3%。结论重型颅脑损伤患者不同体位变化颅内压及脑灌注压存在差异,护理干预可降低颅内压和升高脑灌注压,并能提高护理满意度。     

体位及头高位对重型颅脑损伤病人颅内压和脑灌注压的影响

[目的]探讨体位及头高位对重型颅脑损伤病人颅内压和脑灌注压的影响。[方法]收集2016年10月—2017年12月某三级甲等医院颅脑外伤病区50例住院病人为研究对象。在静息状态下,依次将病人置于仰卧位合并头位抬高0°、30°、45°,左半侧卧位合并头位抬高0°、30°、45°,右半侧卧位合并头位抬高0°、30°、45°,每种体位保持15 min。记录每种体位保持15 min时的颅内压、平均动脉压、心率、血氧饱和度,并计算得出相应脑灌注压。[结果]同一头高位,病人三种卧位下颅内压、平均动脉压、脑灌注压比较差异无统计学意义(P0. 05);同一体位,病人颅内压、平均动脉压、脑灌注压随头部抬高角度增加呈下降趋势,除脑灌注压在头高位30°与45°时差异无统计学意义(P0. 05)外,其余指标同一卧位不同头高位数据两两比较,差异均有统计学意义(P0. 05)。同一体位,病人头高位0°与45°相比,心率差异有统计学意义(P0. 05),同一体位不同头高位、同一头高位不同体位,病人血氧饱和度比较差异均无统计学意义(P0. 05)。[结论]重型颅脑损伤病人床头抬高30°,有利于控制颅内压、平均动脉压,保持脑灌注压水平的稳定,且对病人生命体征没有影响。     

体位护理联合床头抬高角度干预对重症颅脑损伤病人颅内压及脑灌注压的影响

[目的]探讨体位护理联合床头抬高角度干预对重症颅脑损伤病人颅内压及脑灌注压的影响。[方法]选择2015年2月—2017年3月就诊于我院的40例重症颅脑损伤病人为研究对象,分别观察病人在0°、10°、20°、30°床头高度时平均动脉压、脑灌注压、颅内压变化情况。[结果]平均动脉压和颅内压水平随着床头角度的抬高逐渐降低,差异具有统计学意义(P0.05);当床头抬高至30°时,颅内压≥25mmHg组病人不同床头抬高角度的脑灌注压比较差异具有统计学意义(P0.05);不同颅内压水平病人的颅内压、平均动脉压会随着床头角度的抬高逐渐降低,差异具有统计学意义(P0.05)。[结论]体位护理联合床头抬高角度干预对重症颅脑损伤病人的脑灌注压、颅内压有重要影响,床头抬高30°时能明显降低颅内压及平均动脉压,保证有效的脑灌注,减少不必要的治疗干预。     

体位对颅脑损伤患者颅内压、脑灌注压的影响

颅内压（ICP）增高是一个复杂的病理生理过程,是重型颅脑损伤的主要并发症。颅内高压如不能及早发现并解除,可引起脑代谢障碍、脑灌注压下降和脑疝形成等严重后果,难以控制的颅内高压病死率达到92％～100％［1-2］。目前脑室内放置 ICP 监测管是临床上常用的方法,被称为ICP 监测的“金标准”［3-4］。颅脑损伤后脑水肿早期,通过实时监测患者的颅内压（ICP）及脑灌注压（CPP）等重要指标,可保证脑组织有足够的血液供应,从而确保脑组织的氧供和糖分需要［5］。研究认为临床护理可影响这些指标的变化,其中患者的体位维持尤为重要［6］。本组选择了复旦大学附属华山医院神经外科急救中心2015年5月至12月期间收治的51例重型颅脑损伤行脑室内 ICP 监测的患者,分别观察其头轴位平卧、头偏位平卧、头轴位床头抬高30°、头偏位床头抬高30°对患者 ICP、CPP 的影响。现报道如下。     

基于脑血流监测的高血压脑出血患者体位管理

目的:探讨基于脑血流监测的高血压脑出血患者体位管理。方法:选取2017年8月至2019年5月扬州大学附属医院收治的高血压脑出血患者80例,在经颅多普勒(transcranial Doppler,TCD)脑血流监测下,对患者实施体位管理,逐渐改变患者的床头抬高角度(0°,15°,30°,45°)。观察比较患者在不同体位下的颅内压(intracranial pressure,ICP)及、脑灌注压(cerebral perfusion pressure,CP P)以及各生命体征的变化。结果:TCD脑血流监测结果显示:床头抬高1 5°和3 0°的I CP和CP P水平均显著低于床头抬高0°,而床头抬高45°的ICP和CPP水平则高于抬高0°,差异均有统计学意义(P0.05)。不同床头抬高角度下,患者的心率(heart rate,HR)、收缩压(systolic pressure,SP)、舒张压(diastolicpressure,DP)、平均动脉压(meanar ter ialpressure,M AP)以及脉搏血氧饱和度(pulse oximetry saturation,Sp O2)水平变化差异均无统计学意义(P0.05)。结论:TCD为目前准确监测脑出血患者ICP和CPP的可行有效方法。对高血压脑出血术后患者实施抬高体位15°～30°干预能够显著降低患者的CPP和ICP,降低脑组织二次损伤的发生率,使患者获得最佳护理效果,值得临床上广泛推广。     

肝硬化大量腹腔积液病人的两种体位护理效果比较

[目的]探讨肝硬化大量腹腔积液病人最适宜的体位。[方法]选择60例肝硬化大量腹腔积液病人随机分成对照组和观察组,分别采取半卧位和床头抬高30°左侧卧位,观察两组压疮及腰部疼痛的发生率。[结果]平卧位压疮发生率26.7%,床头抬高30°左侧卧位压疮发生率6.7%（P〈0.05）;平卧位腰背部疼痛发生率36.7%,床头抬高30°左侧卧位,腰背部疼痛发生率10%（P〈0.05）,差异具有统计学意义。[结论]床头抬高30°左侧卧位为肝硬化大量腹腔积液病人最适宜的体位。     

体位对醋氨酚中毒后暴发性肝肾衰竭病人颅内压及脑灌流压的影响

以往的研究已表明,抬高头部能降低增高的颅内压力。因此,对患有神经外科、神经内科疾患的病人冒着颅内压不断增高的危险,接受头部抬高体位的常规护理。急性肝衰竭所致的肝性脑病患者因脑水肿仍然是主要死亡原因,有些作者建议,对此类病人也应采取头部向上抬高30～60°体位护理。本文作者试图通过试验证实是否头高位能通过改变ICP来改善脑灌流压(CPP),或是头抬高后的体位使平均动脉压(MAP)降低,从而明显地降低了大脑的灌流量。作者测量了8例自服醋氨酚中毒引起暴发性肝衰竭伴少尿型肾衰竭所致的3-4级肝昏迷病人不同体位对ICP及CPP的影响。所有病人均采用过度通气(PaCO_2维持在26-34之间〔3.15-4.5kPa〕)。     

颈内静脉氧饱和度与脑灌注压在重型颅脑损伤中的意义

目的 评估颈内静脉氧饱和度(SjvO2)作为重型颅脑损伤的预后指标及与脑灌注压(CPP)的相关性. 方法 回顾性分析2006年10月至2008年5月上海市闵行区中心医院收治的32例重型颅脑损伤患者,每6 h测定一次颈静脉搏氧饱和度,持续监测平均动脉压(MAP)及颅内压(ICP). 结果 SjvO2与重型颅脑损伤预后显著相关,SjvO2≤50%或SjvO2≥75%发作2次以上提示预后不良.在CPP＜70 mm Hg,SjvO2与CPP有显著的相关性,而CPP≥70 mm Hg组患者中,SjvO2与CPP无明显相关性. 结论 SjvO2与CPP监测相结合,能较可靠地反映脑供血及脑代谢状况,对重型颅脑损伤的治疗有指导意义.     

颅内压监测和阶梯式治疗重型颅脑外伤患者的护理

由于颅脑外伤后脑受伤机制及机体反应的差异,重型颅脑外伤患者的颅内压变化很大。近年来持续颅内压(ICP)监测对重型颅脑损伤患者的治疗的指导意义显得愈发重要,通过严密监测颅内压并有效干预颅内压增高,维持恰当的脑灌注压,已成为治疗重型颅脑外伤的最为重要的环节之一[1]。自2     

两种气管内吸痰方法对重型颅脑损伤患者颅内压的影响

患者气管内吸痰可以改善通气,减少C02潴留,是颅脑损伤患者的重要护理措施之一。颅内压( intracranial pressure,ICP)、脑灌注压(cerebral perfusion pressure,CPP)、平均动脉压(mean artery pressure,MAP)是监护重型颅脑损伤患者病情的重要指标,由于气管内吸痰( endotracheal suction,ETS)刺激气管可引起静脉系统压力升高,可能使重型颅脑伤患者处于颅内高压及脑缺血状态,致残率、致死率高。本研究分别观察开放式吸痰法(open ETS)与密闭式吸痰法(closed ETS)对重型颅脑伤患者的平均动脉压( MAP)、颅内压(ICP)、脑灌注压(CPP)以及血氧饱和度等脑代谢的影响,比较两种气管内吸痰在临床应用的合理性,报道如下。     

Systolic pressure variation and pulse pressure variation during modifications of arterial pressure

OBJECTIVE: This study was performed to investigate the effect of vasopressor therapy on systolic pressure variation (SPV) and pulse pressure variation (PPV) compared to experimentally measured left ventricular stroke volume variation (SVV). DESIGN AND SETTING: Prospective study in a university laboratory. SUBJECTS: Twelve anesthetized and mechanically ventilated pigs. INTERVENTIONS: Increase in mean arterial pressure (by 100%) using phenylephrine and decrease (by 38%) using adenosine. MEASUREMENTS AND RESULTS: SPV and PPV were calculated and compared to SVV derived from aortic blood flow measurements. SPV was significantly affected by changes in arterial pressure [4.6% (1.5) vs. 6.3% (2.1), p[Symbol: see text]<[Symbol: see text]0.05, increased vs. decreased arterial pressure], whereas PPV did not change during modifications of arterial pressure. During baseline conditions and decreased afterload, correlation with SVV was good both for SPV (r[Symbol: see text]=[Symbol: see text]0.892 and r[Symbol: see text]=[Symbol: see text]0.859, respectively) and for PPV (r[Symbol: see text]=[Symbol: see text]0.870 and r[Symbol: see text]=[Symbol: see text]0.871, respectively) (all p[Symbol: see text]<[Symbol: see text]0.001). Correlation with SVV was only moderate during increased arterial pressure (r[Symbol: see text]=[Symbol: see text]0.683 for SPV and r[Symbol: see text]=[Symbol: see text]0.732 for PPV, p[Symbol: see text]<[Symbol: see text]0.05). CONCLUSION: For guiding fluid therapy in patients under vasopressor support, PPV seems superior to SPV.     

Effect of positive end-expiratory pressure on intra-abdominal pressure

Massive elevation of intra-abdominal pressure (IAP) causes renal, cardiovascular, and respiratory dysfunction. Positive end-expiratory pressure (PEEP) markedly increases the detrimental effect of IAP on the cardiovascular system. The purpose of this study was to determine the effect of PEEP on IAP. In 15 patients requiring mechanical ventilation, IAP was measured, after 15-minute equilibration intervals, at PEEP levels of 0, 5, 10, and 15 cm H2O. Parametric analysis with multiple paired t tests and nonparametric analysis with Spearman's rho and Kendall's tau tests were used to determine correlation between PEEP and IAP. All patients were male. The mean age was 39 years (range, 18-77). Ten patients had just had laparotomy. No correlation was found between PEEP and IAP. We conclude that PEEP of 15 cm H2O or less has no effect on IAP, and we discuss the clinical implications.     

Plasma osmotic pressure and oncotic pressure

Water distribution in the body fluid is controlled by osmotic pressure and oncotic pressure of plasma. Lower plasma osmotic pressure induces intracellular edema, while lower plasma oncotic pressure induces extracellular edema. The increase in osmo-active substance in plasma induces increase in plasma volume (or extracellular fluid), and then results in extracellular edema.     

Intracranial pressure. Intracranial pressure monitoring

Based on the data on the current literature, the authors present the basic physiological and pathophysiological aspects of measurement of intracranial pressure and discuss indications for its monitoring and clinical value.     

Quantification of pressure relief using interface pressure and tissue perfusion in alternating pressure air mattresses

OBJECTIVE: To examine whether the interface pressure (IP) relief provided by alternating pressure air mattresses (APAMs) is matched with maintenance of tissue perfusion over the points of contact by measuring transcutaneous oxygen and carbon dioxide (tcPO2, tcPCO2). DESIGN: Comparative analysis of 2 APAMs with a 2-parameter continuous time-based method for quantifying pressure relief (PR) and transcutaneous gas measurement for assessing tissue perfusion. SETTING: Rehabilitation research facility in a university hospital. PARTICIPANTS: Eleven able-bodied adult postgraduate student volunteers. MAIN OUTCOME MEASURES: Two full-replacement APAM systems were used. For each mattress the mean maximum and minimum interface pressures; mean peak air pressures in the mattresses; interface pressure durations below 30, 20, and 10 mmHg over a 60-minute period; mean maximum tcPCO2 and minimum tcPO2; and mean area under the tcPO2 and tcPCO2 curves were measured for each subject. RESULTS: IP on the sacrum was held below thresholds of 30, 20, and 10 mmHg longer on a 2-cell, low pressure system than on a 3-cell, high pressure system (p < .001). Integrated over time, tcPO2 levels also indicated that the 2-cell system retained oxygen levels closer to the unloaded baseline than did the 3-cell system (p < .01). tcPCO2 levels did not rise significantly (p > 0.1) compared with the baseline measurement in both mattresses. CONCLUSIONS: PR was sensitive to the design of the APAM, especially its inflation pressure, cycle time, and inflation sequence. If future trials demonstrate that PR values and transcutaneous blood gas measurements correlate significantly with the clinical incidence of pressure sore formation, then this technique may prove useful in assessing the effectiveness of alternating pressure support surfaces.     

The effects of NG-nitro-L-arginine methyl ester on systolic pressure, diastolic pressure and pulse pressure according to the initial level of blood pressure

The objective of this study was to re-examine whether the effect of the nitric oxide synthesis inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), on blood pressure depends on peripheral vascular tone. The effects of L-NAME (10 mg/kg, i.v.) on diastolic blood pressure (DBP), systolic blood pressure (SBP), pulse pressure (PP) and heart rate (HR) were studied in pithed rats. Sal-pithed rats received 0.9% NaCl, 10 microl/kg/min. Vascular tone was step-wise increased with 3, 10 and 30 microg/kg/min intravenous phenylephrine infusion (LPhe-pithed, MPhe-pithed and HPhe-pithed rats respectively). L-NAME elicited vasopressor responses in all the animals studied. L-NAME increases in SBP and DBP in Sal-pithed rats were significantly smaller than the ones obtained in phenylephrine infused rats. The increases in DBP elicited by L-NAME were greater in LPhe-pithed rats compared with those of MPhe-pithed and HPhe-pithed rats (i.e. the step-wise rises in DBP obtained with phenylephrine were inversely related to the increases in DBP produced by L-NAME); however, the increases in SBP were similar between these experimental groups. The PP increased during L-NAME-induced pressor responses in phenylephrine-infused rats. l-NAME increases in PP showed the following order: Sal-pithed < LPhe-pithed < MPhe-pithed < or = HPhe-pithed rats. HR was not modified by L-NAME. In conclusion, the vasopressor responses produced by L-NAME in pithed rats are influenced by the pre-existing vasomotor tone in complex form. We did not find a simple positive correlation between the vascular tone or level of arterial pressure, and the magnitude of the diastolic and systolic pressor responses elicited by L-NAME. Interestingly, the increase in PP induced by l-NAME was greater in accordance with the increasing value of baseline arterial pressure. NO synthesis inhibition in the arterial endothelium may possibly explain the increase in PP caused by L-NAME, as resulting from the reduction in proximal conduit artery compliance.     

Effects of relaxation of inspiratory muscleson ventilator pressure during pressure support

OBJECTIVE: During pressure support ventilation (PS), an abrupt increase in ventilator pressure above the pre-set level is considered to signify expiratory muscle activity. However, relaxation of inspiratory muscles may also cause the same phenomenon, and this hypothesis has not been explored. The aim of this study is to examine the cause of this increase in ventilator pressure, during PS, in critically ill patients. DESIGN: Retrospective study. SETTING: In a university intensive care unit. METHODS: Fifteen patients instrumented with esophageal and gastric balloons, and in whom airway pressure (P (aw)) during PS exhibited an acute increase above the pre-set level towards the end of mechanical inspiration were retrospectively analyzed. For each breath, the time of the rapid increase in P (aw) was identified (t (Paw)) and, using the transdiaphragmatic (P (di)) and gastric (P (ga)) pressure waveforms, related to: (1) the end of neural inspiration (peak P (di)) and (2) the time at which P (ga) started to increase rapidly after the end of neural inspiration indicating expiratory muscle recruitment. RESULTS: The t (Paw) was observed 32+/-34ms after the end of neural inspiration, well before (323+/-182ms) expiratory muscle recruitment (identified in eight patients). There was a significant linear relationship between the rate of rise of P (aw) after t (Paw) and the rates of decline of P (di) and inspiratory flow. CONCLUSION: We conclude that, during PS ventilation, the relaxation of inspiratory muscles accounts for the acute increase in P (aw) above the pre-set level, in addition to the contribution made by the occurrence of expiratory muscle activity.     

Pulmonary artery pressure versus pulmonary capillary wedge pressure and central venous pressure in shock

Evidence is presented from 43 dogs and 30 patients that under conditions of severe hemorrhagic, traumatic or septic shock, there may be partial obstruction of the pulmonary microcirculation due to disseminated intravascular coagulation (DIC) particularly in the pulmonary venules. This may cause the left atrial pressure to fall and the pulmonary artery pressure to rise, in some cases drastically. Pulmonary edema may result. This dangerous rise in pulmonary artery pressure is not reflected by the wedged pulmonary artery catheter which will monitor only the status of the left heart. Central venous pressure (CVP) may remain within normal limits even after pulmonary artery pressure has risen to dangerous levels with the development of pulmonary edema. It is only with right ventricle failure against the high pulmonary pressure that CVP rises. It is concluded that pulmonary artery pressure measurements are very important in monitoring intravenous fluid administration in severe shock. Wedged pulmonary artery pressures monitor the left heart but may be misleading if taken alone. Central venous pressure gives a delayed response to fluid overload.