肾脏灌注压多少合适?

肾脏是机体供血量最丰富的器官,具有较强的血流自主调节能力,使得动脉压在一定范围内发生变化时肾血流量具有保持相对稳定的能力。多种因素如炎症反应、脓毒症、容量不足、梗阻、缺血-再灌注损伤和手术等均可以导致肾血流自主调节功能受损,此时动脉血压的较小波动就可能引起肾小球滤过率的明显波动,导致急性肾功能损伤。因此,对肾脏灌注水平的监测显得尤为重要。临床上可通过彩色多普勒、肾动脉血流频谱、肾脏增强超声造影等肾脏超声技术、近红外光谱技术、磁共振成像组织氧监测等监测肾脏灌注。由于潜在疾病和基础疾病状态不同,对于确保足够的肾灌注压而言,每个患者的最佳血压值并不一样。临床实践过程中强调越低越好的中心静脉压和肾血流灌注为导向的滴定式和个体化治疗策略来调节机体容量状态和肾脏灌注压水平。     

静脉回流:重症医学医师值得关注的心功能之外的问题

重症患者往往存在血流动力学的紊乱,而临床医师往往关注的是心功能的变化。然而,与心功能评估同样重要的是静脉回流。当静脉回流发生变化时会导致更为复杂的血流动力学变化。静脉回流不仅会受到生理因素影响,还明显受到病因和治疗的影响,导致复杂的血流动力学效应。理解静脉回流的变化及治疗对其影响,对重症患者的血流动力学治疗具有重要意义。     

重症肾脏超声:肾脏血流动力学评估

器官的血流动力学评估逐渐成为热门话题。肾脏作为最易受休克影响的器官之一,其血流动力学评估也备受重视。重症超声由于具有动态、实时、可重复的特点,能兼顾结构与血流灌注的结合,更是为重症患者的器官血流动力学评估提供了新的理念和方法。本文重点阐述重症超声在肾脏血流动力学评估中的应用及意义,主要包括脉冲多普勒肾血管阻力指数测定、彩色多普勒血流显像结合彩色血流定量技术和超声造影成像等内容。     

休克的治疗:血流动力学启示录

休克, 虽已被临床认识和治疗多年, 但仍是常见的危及生命的疾病状态。重症血流动力学为休克治疗提供了具体指导和新的启示。血流动力学是研究血液及其组成成分在机体内运动特点和规律的科学。与监测不同, 重症血流动力学治疗是以血流动力学理论为基础, 根据机体实时状态和反应, 目标导向的定量治疗过程。重症血流动力学治疗基本原则和理念时刻在影响着休克治疗方法的选择和实施。首先, 在选择反馈性指导治疗指标时, 应保证流量指标的最高优先等级, 但应注意每个血流动力学指标只要测量准确, 均具有临床应用价值; 其次, 右心功能改变在休克中具有重要意义, 右心功能管理在休克治疗中已成为不可忽视的重要环节; 再次, 休克治疗中需保持尽可能低的中心静脉压, 与传统将压力指标代替容量不同, 中心静脉压具有明确的临床指导意义; 最后, 重症血流动力学不仅仅是支持性治疗, 而是包括从休克病因到预后的全过程治疗。     

两种动脉重建方式彩超对移植肾远期影响的比较

目的 通过对5年以上供肾动脉与髂外动脉行端侧吻合（EEA）或与髂内动脉行端端吻合（ESA）的移植肾进行二维超声、多普勒血流参数及血肌酐(SCr)的比较，评价两种动脉重建方式的远期效果。方法 根据供肾动脉的不同吻合方式将64名肾移植患者分为髂内动脉端端吻合组和髂外动脉端侧吻合组，采用彩色多普勒超声进行监测，观察移植肾的大小、结构、血流灌注情况、血流动力学参数，进行对比分析。结果 两组移植肾患者的血肌酐(SCr)、移植肾体积、椎体大小、肾皮质厚度、肾动脉内径、移植肾段动脉、叶间动脉、弓形动脉血流及阻力指数差异均无统计学意义(P>0．05)。结论 供肾动脉与髂内动脉端端吻合或与髂外动脉端侧吻合5年以上的移植肾患者在肾功能、二维超声、多普勒血流上没有明显差异。     

TACE对肝癌患者门脉系统血流动力学影响

目的:探讨肝动脉灌注栓塞术(TACE)对肝癌患者门脉系统血流动力学影响。方法:运用彩超对TACE前后门脉系统血流动力学变化进行分析。结果:TACE前后门脉系统血流动力学无改变。结论:门脉系统动力学定量分析对TACE治疗具有指导作用,TACE应遵循个体化原则。     

两种动脉重建方式对移植肾远期影响的彩色多普勒超声观察

目的:通过对5年以上供肾动脉与髂外动脉端侧吻合或与髂内动脉端端吻合的移植肾进行二维超声、多普勒血流参数及血肌酐(SCr)的比较,评价两种动脉重建方式的远期效果。方法:根据供肾动脉的不同吻合方式将64例肾移植患者分为ESA组和EEA组,采用彩色多普勒超声进行监测,观察移植肾的大小、结构、血流灌注情况、血流动力学参数,进行对比分析。结果:两组移植肾患者的SCr、移植肾体积、锥体大小、肾皮质厚度、肾动脉内径、移植肾段动脉、叶间动脉、弓形动脉血流及阻力指数差异均无统计学意义(P>0.05)。结论:供肾动脉与髂外动脉端侧吻合或与髂内动脉端端吻合5年以上的移植肾患者在肾功能、二维超声、多普勒血流上没有明显差异。     

充血性心力衰竭的区域血流量

1 区域血液动力学的基础生理概念 1.1 器官的基础血流量是与器官的灌注压呈比例的。根据公式:器官血流量=器官灌注压/器官血流阻力,即等于器官动脉压—静脉压并与器官血管阻力呈反比。器官的血流量与器官灌注压水平相当。因此器官间心排血量分布是根据各种器官和区域相应血管阻力决定的。任何器官或区域血管对血流的阻     

CT灌注成像评价健脾平肝汤配合肝癌介入治疗后肝血液动力学变化

目的：肝癌介入治疗后结合中医辨证论治，如健脾理气中药配合，对治疗效果有促进作用。由于组织器官的生理性和病理性改变都与其血流变化相关，对血流变化进行研究有可能反映组织器官的病理过程和生理功能，故以研究组器官血流动力学为目的的灌注成像更显重要。肝脏CT灌注成像可计算出肝动脉灌注量（HAP）、门静脉灌注量（PVP）、总肝灌注量（TLP）、肝动脉灌注分数（HAF）、分布容积（DV）、平均通过时间（MTT）等参数，根据其中各项参数的变化来判断肝癌介入治疗后运用健脾理气中药配合治疗的效果，同时对指导临床选择更加合适的用药配方等应具有重要意义。     

不同气腹压力及截石位改变速度对妇科腹腔镜手术患者的影响

目的:探讨不同气腹压力及截石位改变速度对妇科腹腔镜手术患者血流动力学的影响。方法:将我院2014年6~12月收治的128例妇科腹腔镜患者随机等分为对照组和试验组,对照组患者CO2气腹压力12 mm Hg,变换体位速度8 s;试验组气腹压力13 mm Hg,体位改变速度大于30 s。比较两组患者实施气腹后平均动脉压、收缩压、舒张压、心率。结果:试验组患者在实施气腹前后的平均动脉压、收缩压、舒张压、心率改变幅度小于对照组(P0.05)。结论:气腹压力13 mm Hg,体位改变速度大于30 s能够达到手术所需的膨腹作用,患者血压、心率改变幅度较小,保证手术患者安全。     

Diltiazem and autoregulation of canine cerebral blood flow

Recent in vitro evidence suggests the existence of stretch-activated calcium channels in cerebrovascular smooth muscle. These channels, which may play a role in cerebral autoregulation, also appear resistant to antagonism by the benzothiazepine calcium antagonist diltiazem, an agent known to block potential-sensitive and receptor-operated calcium channels. If cerebral autoregulation involves stretch-sensitive diltiazem-resistant calcium channels, then autoregulation should remain intact during vasodilatation produced by diltiazem. The present study was conducted to test this hypothesis. Using a canine cerebral venous outflow preparation, experiments were first performed to determine the optimum dose and route of administration for diltiazem. Although continuous i.v. diltiazem (1-100 micrograms/kg/min) did not increase cerebral perfusion at any normotensive dose, i.a. (lingual artery) diltiazem at 10.0 micrograms/kg/min increased cerebral blood flow by 36% and decreased cerebrovascular resistance by 31% without significant effects on blood gas levels, cerebral oxygen uptake, cardiac output or mean arterial pressure. In autoregulation experiments, 10.0 micrograms/kg/min of diltiazem significantly attenuated but did not eliminate autoregulatory responses to increases (inflation of an aortic balloon) and decreases (hemorrhage) in cerebral perfusion pressure. Autoregulatory responses to increases and decreases in perfusion pressure were equally affected by diltiazem, but both were unaffected by i.a. saline. These data support the view that cerebral autoregulation involves both diltiazem-sensitive and diltiazem-resistant mechanisms. The diltiazem-resistant mechanisms, which may include the proposed population of stretch-sensitive calcium channels appear to account for up to one-half of the autoregulatory capacity in the cerebral circulation.     

Journal of clinical monitoring and computing 2016 end of year summary: monitoring cerebral oxygenation and autoregulation

In the perioperative and critical care setting, monitoring of cerebral oxygenation (ScO₂) and cerebral autoregulation enjoy increasing popularity in recent years, particularly in patients undergoing cardiac surgery. Monitoring ScO₂ is based on near infrared spectroscopy, and attempts to early detect cerebral hypoperfusion and thereby prevent cerebral dysfunction and postoperative neurologic complications. Autoregulation of cerebral blood flow provides a steady flow of blood towards the brain despite variations in mean arterial blood pressure (MAP) and cerebral perfusion pressure, and is effective in a MAP range between approximately 50–150 mmHg. This range of intact autoregulation may, however, vary considerably between individuals, and shifts to higher thresholds have been observed in elderly and hypertensive patients. As a consequence, intraoperative hypotension will be poorly tolerated, and might cause ischemic events and postoperative neurological complications. This article summarizes research investigating technologies for the assessment of ScO₂ and cerebral autoregulation published in the Journal of Clinical Monitoring and Computing in 2016.     

The influence of urapidil,a new antihypertensive agent,on cerebral perfusion pressure in dogs with and without intracranial hypertension

The influence of urapidil, an arylpiperazinederivate, on intracranial pressure (ICP), mean arterial pressure (MAP) and cerebral perfusion pressure (CPP) was investigated in dogs with (group II) and without (group I) intracranial hypertension. After i.v. administration of urapidil, intracranial pressure remained unchanged and cerebral perfusion pressure decreased to the same extent as mean arterial pressure (20%). As in neurosurgical patients, autoregulation of cerebral blood flow is often lost; a sudden increase in blood pressure may lead to an increase in cerebral blood flow and to a damage of the blood bain barrier with consequent cerebral edema. Urapidil seems to be suitable for treating hypertensive episodes perioperatively in neurosurgical patients.     

Vasopressin impairs brain, heart and kidney perfusion: an experimental study in pigs after transient myocardial ischemia

Introduction

Arginine vasopressin (AVP) is increasingly used to restore mean arterial pressure (MAP) in low-pressure shock states unresponsive to conventional inotropes. This is potentially deleterious since AVP is also known to reduce cardiac output by increasing vascular resistance. The effects of AVP on blood flow to vital organs and cardiac performance in a circulation altered by cardiac ischemia are still not sufficiently clarified. We hypothesised that restoring MAP by low dose, therapeutic level AVP would reduce vital organ blood flow in a setting of experimental acute left ventricular dysfunction.

Methods

Cardiac output (CO) and arterial blood flow to the brain, heart, kidney and liver were measured in nine pigs using transit-time flow probes. Left ventricular pressure-volume catheter and central arterial and venous catheters were used for haemodynamic recordings and blood sampling. Transient left ventricular ischemia was induced by intermittent left coronary occlusions resulting in a 17% reduction in cardiac output and a drop in MAP from 87 ± 3 to 67 ± 4 mmHg (p < 0.001). A low-dose therapeutic level of AVP (0.005 U/kg/min) was used to restore MAP to pre-ischemic values (93 ± 4 mmHg).

Results

AVP further impaired systemic perfusion (CO and brain, heart and kidney blood flow reduced by 29, 18, 23 and 34%, respectively) due to a 2.0-, 2.2-, 1.9- and 2.1-fold increase in systemic, brain, heart and kidney specific vascular resistances. The hypoperfusion induced by AVP was associated with an increased systemic oxygen extraction. Oxygen saturation in blood drawn from the great cardiac vein fell from 29 ± 1 to 21 ± 3% (p = 0.01). Finally, these effects were reversed 40 min after AVP was withdrawn.

Conclusion

Low dose AVP induced a pronounced reduction in vital organ blood flow in pigs after transient cardiac ischemia. This indicates a potentially deleterious effect of AVP in patients with heart failure or cardiogenic shock due to impaired coronary perfusion.     

Transcranial Doppler Assessment of Cerebral Autoregulation

Cerebral autoregulation describes the process by which cerebral blood flow is maintained despite fluctuations in cerebral perfusion pressure. The assessment of cerebral autoregulation is a key to the optimisation of cerebral perfusion pressure in patients with brain injury. This review evaluates the current evidence for transcranial Doppler in the assessment of cerebral autoregulation. The study of cerebral autoregulation classically assesses changes in cerebral perfusion pressure secondary to changes in systemic blood pressure. It is defined static autoregulation if blood pressure changes are progressive, thereby allowing a steady-state autoregulatory response to be completed. For sudden changes in blood pressure, the autoregulatory response is defined as dynamic. The static and dynamic components of cerebral autoregulation have been approached using linear mathematical models (models based in direct correlations). Over the past decade, demonstration of the nonstationary (the property of changing over time or space) behaviour of cerebral autoregulation has emphasised the benefit obtained in using nonlinear statistical models (models based on changeable functions), suggesting that these methods may improve the mathematical representation of cerebral autoregulation. Despite the multiple determinants involved in cerebral autoregulation, it appears feasible to reliably assess cerebral autoregulation through the combination of linear and nonlinear methods. Nonlinear methods appear attractive in the research setting, but the challenge is how to adopt these methods to the clinical setting. (E-mail: 30489jbr@comb.es)     

Control of skeletal muscle blood flow during postural changes in acute myocardial infarction

Central and local regulation of skeletal muscle blood flow in the leg was studied in the acute phase of myocardial infarction. Blood flow was measured by the local 133Xe washout technique in the anterior tibial muscle. The vasoconstrictor response to increase in venous transmural pressure was not present on day 1 after coronary occlusion but gradually returned during days 2, 3 and 7. A normal response to decrease in arterial perfusion pressure was observed, suggesting that intrinsic vascular reactions responsible for autoregulation of blood flow were not affected in the acute phase of myocardial infarction. Passive head-up tilt (30 degrees) induced vasoconstriction in skeletal muscle tissue. There were no differences in this response at any time during the course of acute myocardial infarction. The abolition of the vasoconstrictor response to increase in venous transmural pressure on day 1 is most likely due to centrally elicited increase in sympathetic activity as a normal vasoconstrictor response was obtained the following days. Decrease in baroreceptor activity induced by head-up tilt enabled a marked neurogenically mediated vasoconstriction in skeletal muscle tissue which was almost unaffected during the course of myocardial infarction.     

Effect of two models of portal hypertension on splanchnic organ blood flow in the rat

Splanchnic organ blood flow and cardiac output were measured by the microsphere method in fasted rats with prehepatic portal hypertension due to portal vein stenosis, in rats with intrahepatic portal hypertension due to bile duct ligation, and in unoperated normal rats. Portal venous pressure was higher in both groups of portal hypertensive rats than in normal rats. Cardiac output was significantly higher in portal hypertensive rats than in normal rats. In rats with portal vein stenosis, splanchnic blood flow was higher than in controls. This increase was caused by increased perfusion of all organs drained by the portal vein, and by increased hepatic arterial blood flow. In rats with bile duct ligation, splanchnic blood flow was not significantly higher than in normal rats: haemoperfusion of all organs contributing to the portal circulation decreased, whereas hepatic arterial blood flow increased. As cardiac output rose similarly, the differences observed between the two types of portal hypertension depend mainly on the difference in distribution of flow within the splanchnic bed.     

Regulation of myocardial oxygen delivery

In most organs, oxygen consumption is maintained at relatively constant levels as oxygen delivery decreases, until a critical level is reached. This biphasic action is not observed in the heart. Myocardial oxygen consumption is supply dependent at all levels of myocardial oxygen delivery, because changes in myocardial oxygen delivery modify ventricular loading conditions and hence myocardial oxygen consumption. Since the oxygen content of coronary sinus blood is very low, only limited increases in oxygen extraction are possible. Therefore, coronary dilation is the primary mechanism for increasing myocardial oxygen delivery. Four- to sixfold increases in coronary blood flow can occur in several animal species and in human beings. Apart from metabolic control mechanisms, the regulation of myocardial oxygen delivery is multifaceted; major factors include extravascular compressive forces, autoregulation, neural controls, and humoral factors. In situations of decreased myocardial oxygen delivery, coronary vessels dilate to increase flow, and as coronary flow reserve falls to zero, flow becomes exquisitely dependent on perfusion pressure. With onset of supply dependency, contractility falls in an effort to maintain cardiac output at a given myocardial oxygen consumption.     

Cerebral blood flow and metabolism in severe brain injury: the role of pressure autoregulation during cerebral perfusion pressure management

Objective: To ascertain if norepinephrine can be used as part of the cerebral perfusion pressure (CPP) management to increase arterial blood pressure (MAP) without causing cerebral hyperemia after severe head injury (HI).¶Design: Prospective, interventional study.¶Setting: Intensive care unit in a university hospital.¶Patients: Twelve severely HI patients; median Glasgow Coma Scale was 6 (range 3–8).¶Interventions: CPP management ( = 70 mmHg). Pressure autoregulation (assessed by norepinephrine infusion) was defined intact if %CPP/%CVR ≤ 2.¶Results: Cerebral blood flow (CBF: Xe¹³³ inhalation technique), jugular bulb oxygen saturation (SjO₂) and transcranial Doppler (TCD) were recorded during the test. Norepinephrine increased CPP by 33 % ( ± 4). Autoregulation was found to be intact in ten patients and defective in two. In the ten patients with preserved autoregulation, CBF decreased from 31 ± 3 to 28 ± 3 ml/100 g/min; in the two patients with impaired autoregulation CBF increased respectively from 16 to 35 and from 21 to 70 ml/100 g/min. SjO₂ did not change significantly from baseline. TCD remained within the normal range.¶Conclusions: During CPP management norepinephrine can be used to increase MAP without potentiating hyperemia if pressure autoregulation is preserved. The assessment of pressure autoregulation should be considered as a guide for arterial pressure-oriented therapy after HI.     

Regulation of myocardial oxygen delivery

In most organs, oxygen consumption is maintained at relatively constant levels as oxygen delivery decreases, until a critical level is reached. This biphasic action is not observed in the heart. Myocardial oxygen consumption is supply dependent at all levels of myocardial oxygen delivery, because changes in myocardial oxygen delivery modify ventricular loading conditions and hence myocardial oxygen consumption. Since the oxygen content of coronary sinus blood is very low, only limited increases in oxygen extraction are possible. Therefore, coronary dilation is the primary mechanism for increasing myocardial oxygen delivery. Four- to sixfold increases in coronary blood flow can occur in several animal species and in human beings. Apart from metabolic control mechanisms, the regulation of myocardial oxygen delivery is multifaceted; major factors include extravascular compressive forces, autoregulation, neural controls, and humoral factors. In situations of decreased myocardial oxygen delivery, coronary vessels dilate to increase flow, and as coronary flow reserve falls to zero, flow becomes exquisitely dependent on perfusion pressure. With onset of supply dependency, contractility falls in an effort to maintain cardiac output at a given myocardial oxygen consumption.