The macrohemodynamics targets, such as blood mean arterial pressure (MAP), cardiac output (CO), peripheral resistance, etc., have been used to drive goal-directed therapy in case of circulatory shock. However, it has been reported that conditions of microcirculatory disfunction could persist and evolve initially in hypoperfusion and then in cryptic shock  in spite of improvement or stability of macrocirculatory parameters. In cases of circulatory shock, monitoring microcirculatory parameters could be the most important endopoint to optimize the treatment, since microcirculatory disfunction could persist despite the improvement of macrocirculatory parameters . Routine microcirculatory monitoring parameters, such as venous oxygen saturation (SvO2) and venous central oxygen saturation (SvcO2), remain fundamental but have several limits to consider . SvO2 measurement implicates a pulmonary artery catheter. Collecting a sample of blood from superior caval vein allows to obtain a value of SvcO2 that reflects the O2 saturation of the superior vascular tree, that is slightly different as compared to O2 saturation of inferior vascular tree (as the abdominal vascular district) [1, 4]. Indeed, usually oxygen consumption (VO2) is independent of oxygen delivery (DO2) until tissues can satisfy metabolic requirement increasing oxygen extraction when DO2 decreases. This mechanism has an intrinsic limit: beyond critic DO2, the compensatory increasing of O2 extraction run out and VO2 become dependent from DO2.
Bloos et al. demonstrated that in patients with protract cardiac arrest, in case of microcirculatory artero-venous shunt or cellular apoptosis due to severe tissue damage, SvO2 and SvcO2 could show normal or increased values in spite of dangerous tissue hypoxia . Consequently, tissue hypoxia develops and increased serum lactate and lactic acidosis may be observed [5,6,7].
Doppler-based renal resistive index measurement is a rapid and non-invasive tool that may be useful to detect tissue hypoperfusion and oxygenation, and to measure resistance to arterial blood flow in renal vessels in intensive care unit (ICU) patients [8, 9]. Sampling renal interlobar or arcuate arteries with pulsed wave Doppler ultrasound allows to obtain a “low resistance” profile typical of the downstream territories with high resting perfusion. Doppler waveform recorded in those territories shows a steep systolic rise that is the “early systolic peak”, followed by a decreasing component representing the diastolic flow.
RRI can be calculated as (peak systolic velocity − end diastolic velocity)/peak systolic velocity .
Evidence of a direct correlation between RRI and cardiovascular damages is more and more frequently reported; therefore, RRI has been proposed as a new tool in ICU patients monitoring [11, 12].
In normal conditions, renal artery blood flow occurs during both systolic and diastolic phase. On the contrary, in several pathologic conditions (such as shock, systemic inflammation, obstruction, etc.), renal arterial blood flow decreases and becomes even reverted during the diastolic phase consequently provoking an increase of RRI [8,9,10,11,12].
Nevertheless, RRI is the result of complex, and often not fully understood, interactions between arterial characteristics and systemic hemodynamic factors; in fact, many systemic parameters correlate with these ultrasonographic (US) measures. RRI does not always selectively indicate organ damage, but under particular conditions, it reflects systemic vascular disease. Increased values are associated with extrarenal factors such as age, vascular disease, pulse pressure, systemic vascular compliance, heart rate and cardiac function and with renal factor as end-stage renal disease and renal capillary wedge pressure. Thus, the hemodynamic factors involved have to be considered to understand RRI clinical meaning. Ageing provokes a progressive rigidity of the aorta with a great increase in the arterial pulse pressure. Pulse pressure is connected with cardiac function and systemic arterial compliance affecting the value of peak systolic velocity. The vascular compliance of large arteries determines the blood pressure pulsatility; consequently, in the condition of reduced systemic compliance, RRI results are strongly modified. The cardiac function, with its components such as heart rate and left ventricular outflow, can also strongly affect RRI.
Moreover, RRI is considered as a marker of progression of renal damage and an indicator of irreversible damage in chronic kidney failure.
Renal capillary wedge pressure develops from the combination of renal interstitial and venous pressure; therefore, conditions of systemic venous congestion could increase renal capillary wedge pressure with a subsequent elevation of RRI indexes .
Due to these confounding factors, as it has been previously suggested, it might be important to compare RRI with Splenic Doppler Resistive Index (SRI) . Corradi et al. showed that the evaluation of SRI allows the early detection of occult hemorrhagic shock and persistent occult hypoperfusion after polytrauma in adult patients .
Since SRI variations after fluid administration could be an effective tool to monitor systemic hemodynamic, also SRI may represent a useful method in the detection of organ perfusion .