CVP对于肾衰竭的重症患者有哪些影响？
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中心静脉压（CVP）在传统意义上可以代表血容量的多少，因此，CVP通常用于临床指导重症患者的液体平衡。然而近期研究发现，高水平的CVP可能阻碍静脉回流并干扰微循环，从而导致组织淤血以及器官衰竭。即使在没有液体过负荷的情况下，通过增加肾脏的“后负荷”，升高的CVP也会严重损伤肾血流并加重AKI。特别是在感染性休克、心脏手术、机械通气和腹腔内高压的情况下，维持尽可能低的CVP应该成为预防和治疗AKI的常规方法。
Background
Acute kidney injury (AKI) is a common complication in critically ill patients with high attributable morbidity and mortality [1, 2]. Systemic and renal perfusion considerably determines the development and cour of AKI. Yet, optimal hemodynamic targets to minimize the risk of AKI are not precily defined [3, 4]. In critical care, hypotension and shock are the “rogue enemies.” Resuscitation primarily focus on optimizing mean arterial pressure (MAP) to improve renal perfusion [5]. However, there is little evidence that MAP correctly reflects organ perfusion. Moreover, aggressive fluid loading may contribute to an incread central venous pressure (CVP). By accepting high CVP levels [6, 7, 8, 9, 10], clinicians neglect that volume treatment and AKI are cloly intertwined.
CVP is traditionally ud for asssing volume status and volume responsiveness at the bedside [11]. However, CVP measurements to direct volume management in critically ill patients have repeatedly been found unreliable [12]. Whether and how CVP monitoring should be adapted to a particular patient (e.g., postsurgical, cardiac, ptic) population is topic of controversy and debate [13, 14]. Monitoring CVP also does not guarantee prervation of renal function. A recent study reported a higher incidence of AKI in patient
s undergoing CVP monitoring as compared with unmonitored subjects. A 1 cm H2O higher CVP was associated with a 1.02 (95% CI 1.00–1.03, pdarling的意思 = 0.02) risk of AKI. No association was found between pulmonary edema and AKI [13]. Till recently, the innate pressure character of CVP and its pathophysiological impact have been largely underestimated. What follows is a thorough discussion about the role of CVP, beyond its value as volume indicator, in various dias.
Main text
CVP is a pressure ud to estimate volumenwt
unisonThe CVP is the pressure recorded from the superior vena cava or right atrium which, in the abnce of tricuspid stenosis, equals right ventricular end-diastolic pressure. CVP is determined by the interaction between cardiac function and venous return which both depend on changes in total blood volume, vascular tone, cardiac output (CO), right ventricular compliance, intrathoracic and pericardial pressure [15]. CVP measurements are especially uful when followed over time and combined with a CO recording. A prop
chloe什么意思erly measured CVP can successfully guide right ventricular filling [16]. Within a certain range, CVP increas with expanding blood volume. However, excessive fluid administration may augment CVP and end-diastolic pressure without increasing end-diastolic or stroke volume. On the other hand, an incread CVP is often associated with decread right ventricular compliance. Additionally, CVP is the downstream pressure for venous return and clo to the minimum pressure in the global circulation [17].
CVP and kidney “afterload”
CVP must be lower than renal venous pressure (RVP) in order to allow an adequate venous renal blood flow (RBF) to the heart. Accordingly, the prence of a high CVP requires a much higher RVP to ensure this flow. Renal perfusion pressure (RPP) approximates the difference between renal arterial pressure and RVP. As such, a higher RVP lowers RPP. In analogy with cardiac physiology, this forms the basis for the renal “afterload” concept [18]. Recent studies focusing on kidney “afterload” have revived interest in older studies which suggested that kidney dysfunction resulted from venous co
ngestion transmitted to the renal venous compartment. Almost a century ago, it was indeed demonstrated that an hypervolemia-induced increa in RVP caud AKI independently of CO or RBF [19].
Effect of CVP on pressure and flow in the kidney家具销售技巧
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Kidney perfusion is pressure and flow dependent. If intravascular volume augments without excessive CVP elevation, the unstresd volume (i.e., the fluid volume to fill the vascular bed to the point where it exerts force on the vesl walls) may incrementally follow a CO increa and RBF will ri. When CVP is already high, however, any additional volume load may increa CVP without a subquent increa in CO and RBF. Right ventricular function then may deteriorate and evolve into acute cor pulmonale [17]. The difference between mean system filling pressure (MSFP) and CVP is the driving force behind venous return. Thus, with increasing CVP, a venous return will drop [20, 21]. With the heart functioning on the steep portion of the Starling curve, volume expansion will increa MSFP more than CVP. In contrast, changes in MSFP are approximately simidisdain
英语四级准考证号查询入口lar to CVP changes on the flat part of the Starling curve with no or minimal effects on CO [22, 23]. If fluid administration fails to obtain a higher MSFP, CVP must be kept low to enhance venous return, cardiac preload and CO. In isolated kidneys of healthy dogs, renal venous and tissue pressures were unaffected over a large range of incread venous pressures. However, RBF fell when RVP approached or exceeded renal venous and tissue pressure [24]. Critically ill patients even have a more narrow pressure autoregulation range [25]. In the cardiorenal syndrome, an elevated CVP caus lowering of RPP below the kidney autoregulation threshold, resulting in pressure-dependent renal perfusion [26]. The ri in CVP is transmitted to the renal veins, sustains the cardiorenal syndrome, and induces a detrimental feedback loop via the renin–angiotensin–aldosterone and neuroendocrine pathways that leads to refractory heart failure. Worning congestion also enhances sodium retention which exacerbates heart failure.
