Effects of Fluids on the Macro- and Microcirculations Victoria A
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Bennett et al. Critical Care (2018) 22:74 https://doi.org/10.1186/s13054-018-1993-1 REVIEW Open Access Effects of Fluids on the Macro- and Microcirculations Victoria A. Bennett*, Alexander Vidouris and Maurizio Cecconi this is lost in some disease states. This overview explores Abstract the effects of the fluid on the macro- and microcircula- This article is one of ten reviews selected from the tions and how we can monitor these effects. Annual Update in Intensive Care and Emergency Medicine 2018. Other selected articles can be found Indications for Fluid online at https://www.biomedcentral.com/collections/ Classically, the need for fluid therapy is identified using annualupdate2018. Further information about the Annual information from the clinical history, examination, Update in Intensive Care and Emergency Medicine is measurement of hemodynamic variables and markers of available from http://www.springer.com/series/8901. tissue hypoperfusion [7]. Markers of hypoperfusion may include lactate, prolonged capillary refill time and skin Background mottling [6]. A fluid challenge is given when tissue hy- Intravenous fluid administration is one of the most poperfusion is suspected [7]. Fluid is given to optimize frequently performed interventions in the intensive care cardiovascular status with the aim of ensuring adequate unit (ICU) and in hospital in general. In fact, most inpa- end-organ perfusion and improving oxygen delivery to tients will receive fluids at some point during their the tissues. Fluid is given as a fluid challenge so that re- hospital stay [1]. In critically ill patients, fluid resuscita- sponse can be assessed and the need for ongoing fluid tion is a vital component of patient management. It has therapy ascertained. To mitigate against the risk of fluid been shown that both too little and too much fluid can overload in those who do not require additional intra- be detrimental. A positive cumulative fluid balance on vascular volume, the smallest volume that provides an day four of a critical care admission has been associated effective challenge of the cardiovascular system should with increased morbidity [2, 3]. Both perioperatively and be used [8]. during sepsis, a U-shaped curve has been described for Most often, measures of the macrocirculation are used volume of fluid administered and morbidity. Higher to assess and treat hemodynamic compromise in the mortality is observed at both extremes of volume of fluid critically ill patient and measures of the microcirculation given [4, 5]. are not routinely used at the bedside. Resuscitation However, despite extensive research in the field, con- based on macrocirculatory endpoints is expected to re- troversy remains regarding the best approach to fluid sult in parallel improvement in the microcirculation [9]. therapy. The FENICE study focused on the fluid challenge and found wide disparity in practice; from fluid Macrocirculation choice to method of administration and clinician response The macrocirculatory response to intravenous fluid to the result [6]. To help guide decision making around administration is based on the principles of the Frank- fluid administration, the effects, both desirable and poten- Starling law of the heart. Venous return is always equal tially detrimental ones, need to be considered. This can be to cardiac output. The Frank-Starling principle describes considered at both the macrocirculatory and the microcir- how the heart is able to accommodate increased venous culatory level. Whilst in health coherence between the return and then eject the increased volume from the macrocirculation and microcirculation can be assumed, heart, with an increase in stroke volume. Increased venous return increases ventricular filling, which results in increased stretch of the cardiac myocyctes. This in- * Correspondence: [email protected] Department of Intensive Care Medicine, St George’s University Hospital NHS creased stretch results in increased contractility, or in Foundation Trust, London, UK other words, the increased diastolic expansion results in © Bennett et al. 2018 Bennett et al. Critical Care (2018) 22:74 Page 2 of 6 increased systolic contraction [10, 11]. Administration of this patient is fluid responsive. At C, although an ad- fluid aims to challenge this and assess whether a patient equate fluid challenge is given, as demonstrated by an can accommodate an increased preload with an in- increase in Pmsf, no significant increase in stroke creased stroke volume. volume is seen at point D – this patient is not fluid re- The hemodynamic response to a fluid challenge can sponsive. If an inadequate fluid challenge, of too small a be understood by considering the effects at different volume to increase Pmsf, is given at point A, an increase points on the cardiovascular system. The first change in stroke volume is not seen at point E and the patient seen is an expansion of the intravascular volume. Intra- would incorrectly be labeled as non-responsive to fluid. vascular volume can be divided into stressed and Cecconi et al. demonstrated that a change in the pres- unstressed volumes. The unstressed volume fills the ves- sure gradient of venous return, defined as the difference sels but does not generate any pressure. The stressed between the Pmsf and central venous pressure (CVP), volume causes stretch of the vessel walls and increases following a fluid challenge was seen in responders but the pressure within the vessels. Mean systemic filling not in non-responders. In the non-responders, the in- pressure (Pmsf) is the measurement of the pressure crease in Pmsf was mirrored by an increase in CVP [14]. when there is no flow in the vessels, or in circulatory In those that respond, the maximal change in cardiac arrest. Whilst Pmsf cannot be measured under the output is seen one minute after completion of the fluid circumstances with which it was initially described, alter- challenge. The increase in cardiac output is a transient native techniques have been validated [12]. If an effective response; a return to baseline values is seen ten minutes fluid challenge is given, it will, at least transiently, in- post-fluid administration [13]. crease the stressed volume and cause a rise in Pmsf. This The decision to give fluids should be based on whether increases cardiac preload, which ultimately increases an increase in cardiac output is likely to occur with fluid cardiac output in preload-responsive patients. The re- loading and whether it would be likely to improve tissue sponse to the increase in cardiac preload can be explained perfusion. These are clinical questions that the clinician by the Frank-Starling principle. should ask before considering giving fluids. A patient In a patient who is fluid responsive, an effective fluid who is non-responsive is unlikely to benefit from further challenge will result in a significant increase, of more fluid loading. Not all patients who are responsive to fluid than 10%, in the stroke volume or cardiac output. If a require the additional volume [8]. For example, in a fluid challenge is given, which is effective in significantly study of healthy volunteers, by definition not in shock, a increasing Pmsf, but no subsequent increase in cardiac significant increase in stroke volume was seen following output is seen, the patient is labeled as non-responsive a head down tilt (mimicking a fluid challenge). Despite [13]. This is demonstrated in Fig. 1: an adequate fluid being fluid responsive these healthy volunteers were challenge administered at point A, increases Pmsf and a unlikely to need fluid resuscitation or have evidence of significant increase in stroke volume is seen at point B – tissue hypoperfusion [15]. Fig. 1 Assessment of fluid responsiveness using a fluid challenge; effects on mean systemic filling pressure (Pmsf) and stroke volume, explained using the Frank Starling Curve. See text for explanation Bennett et al. Critical Care (2018) 22:74 Page 3 of 6 Other hemodynamic parameters, used more historically, upon smooth muscle. They respond to physical stimuli in include static endpoints, such as heart rate. However, a the microcirculation, such as increased blood pressure, change in heart rate in response to fluid administration is causing constriction in the arterioles of the microcircula- not a sensitive marker of fluid responsiveness and can be tion. Some of the molecules that are active in the vascula- influenced by numerous other factors [13]. ture of the microcirculation are released from the CVP has historically also been used to guide fluid ad- endothelial wall including prostaglandins, nitric oxide ministration. Targeting a CVP of 8–12 cmH2O was part (NO) and endothelin, which are released as a result of of several optimization protocols in the past [16, 17]. The shear stress on the vessels. NO release can also be stimu- role of CVP in predicting fluid responsiveness has since lated by other vasoactive peptides. Metabolic stimuli, such been refuted. Use of the CVP as an indicator of fluid as adenosine, hydrogen ions, carbon dioxide and oxygen responsiveness has been shown to be unreliable [18, 19]. tension, generated in tissues also control blood flow in the It does not provide accurate information about blood microcirculation via dilation of the vessels [9]. The func- volume [20]. Monitoring trends in CVP over time may tion of the microcirculation is also controlled by the per- provide information about cardiovascular function but meability of the capillaries, their structure, the osmotic should not