Passive leg raising
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- Monnet, X. & Teboul, J. Intensive Care Med (2008) 34: 659. doi:10.1007/s00134-008-0994-y
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To assess whether the passive leg raising test can help in predicting fluid responsiveness.
Nonsystematic review of the literature.
Passive leg raising has been used as an endogenous fluid challenge and tested for predicting the hemodynamic response to fluid in patients with acute circulatory failure. This is now easy to perform at the bedside using methods that allow a real time measurement of systolic blood flow. A passive leg raising induced increase in descending aortic blood flow of at least 10% or in echocardiographic subaortic flow of at least 12% has been shown to predict fluid responsiveness. Importantly, this prediction remains very valuable in patients with cardiac arrhythmias or spontaneous breathing activity.
Passive leg raising allows reliable prediction of fluid responsiveness even in patients with spontaneous breathing activity or arrhythmias. This test may come to be used increasingly at the bedside since it is easy to perform and effective, provided that its effects are assessed by a real-time measurement of cardiac output.
KeywordsFluid responsivenessPassive leg raisingVolume expansionCardiac preload
Physiological changes in hemodynamics during PLR
Lifting the legs in the event of circulatory collapse is a rescue maneuver that has been used for years by first-aid rescuers. Passive leg raising (PLR) has recently gained interest as a test for monitoring functional hemodynamic and assessing fluid responsiveness since it is a simple way to transiently increase cardiac preload. Lifting the legs passively from the horizontal plane in a lying subject obviously induces a gravitational transfer of blood from the lower part of the body toward the central circulatory compartment and especially toward the cardiac cavities. Using radiolabeled erythrocytes a physiological study in humans demonstrated that the volume of blood contained in the calves was reduced during PLR, a reduction corresponding to the transfer of approx. 150 ml blood . Thus PLR recruits a part of blood contained in the venous reservoir and converts unstressed volume to stressed volume. In turn PLR increases right cardiac preload, likely through an increase in the mean circulatory pressure which is the driving pressure for venous return. If the right ventricle is preload responsive, the increase in systemic venous return results in an increase in right cardiac output and hence in the left ventricular filling. Clinical studies conducted in various hemodynamic conditions have reported an increase in pulmonary artery occlusion pressure [2–5], left ventricular end-diastolic dimension [2, 6], E wave of the mitral flow [2, 3, 7], and left ventricular ejection time  during PLR, supporting the evidence that the volume of blood transferred to the heart during PLR is sufficient to increase left cardiac preload. Nonetheless, if the preload reserve of the right heart is limited, the increase in right cardiac preload should not result in an increased flow toward the left ventricle, and thus PLR should not increase left-side preload in such cases. The response to PLR of the markers of right preload (e. g., central venous pressure) and of left preload may therefore differ.
As a result of the increase in left ventricular preload PLR may ultimately result in an increase in cardiac output, depending on the degree of left ventricular preload reserve. Interestingly, Wong and colleagues  reported that the increase in stroke volume induced by a 45° leg lifting in healthy subjects was of larger magnitude after withdrawal of 500 ml blood, suggesting that PLR affects cardiac output differently according to the central volume status and thus the degree of cardiac preload reserve. An important point is that the PLR-induced increase in cardiac preload vanishes completely when the legs are returned to horizontal position [5, 8, 10, 11]. Therefore PLR can be considered as a brief and completely reversible “self-volume challenge”. It must also be stressed that the effect of PLR on cardiac output—when it occurs—is not always sustained when the leg elevation is prolonged. In septic shock patients capillary leak may account for this attenuation. In a study including critically ill patients with circulatory failure we observed that the increase in the blood flow of the descending thoracic aorta induced by PLR in “preload-dependent” patients occurred in few seconds and was maximal approx. 1 min after starting the PLR maneuver . In patients who did not have a sustained response to PLR the response to volume infusion also was not sustained. Thus the hemodynamic effects of PLR should be assessed during the time frame of 30–90 s after the onset of the test.
The response to PLR may also depend upon the ability of the venous reservoir to be recruited. In a patient who is vasoconstricted because of hypovolemic/cardiogenic shock the venous reservoir is likely reduced, and the volume recruited by the PLR would be expected to be less. By contrast, in a patient with a vasodilatory state such as septic shock a higher unstressed volume is expected to be recruited by PLR. Based on this hypothesis, PLR should theoretically increase right ventricle preload less in patients with hypovolemic than in those with septic shock. However, in volume-depleted patients with high volume responsiveness even a moderate increase in preload can result in a significant change in cardiac output. In support of this, the increase in cardiac output in normal subjects in response to PLR has been shown to be increased after blood removal .
PLR for testing fluid responsiveness in the critically ill
Predicting fluid responsiveness solely on the basis of measures of preload must be discouraged. Not only one but a family of Frank–Starling curves rely cardiac preload and stroke volume according to individual factors such as cardiac contractility (Fig. 2). Accordingly, a given value of preload could be associated with preload reserve in patients with normal cardiac contractility but with absence of preload reserve in the case of patients with profoundly impaired contractility because they are on the steep part of their cardiac function curve. Numerous studies now support the evidence that static measures of cardiac preload are not appropriate to assess preload reserve [14, 15]. In this regard cardiac filling pressures such as central venous pressure and pulmonary artery occlusion pressure cannot differentiate between patients responding and patients not responding to fluid administration . Fluid responsiveness assessment must be rather based on the response to dynamic tests which induce transient changes in cardiac preload .
Since mechanical ventilation is able to induce cyclic changes in cardiac preload, the respiratory variation in stroke volume has been proposed to assess preload reserve . Accordingly, the respiratory variations in surrogates of stroke volume such as arterial pulse pressure , Doppler subaortic flow , pulse contour derived stroke volume [20, 21], descending aortic blood flow , and even pulse oximetry wave  have been demonstrated to predict fluid responsiveness in the critically ill. Nonetheless, such heart–lung interaction indices can be used in only specific conditions, such as regular sinus cardiac rhythm and full adaptation of the patient to the ventilator as during deep sedation or coma. If not, the irregularity of the cardiac rhythm or of the respiratory cycle also account for variability in stroke volume such that fluid responsiveness can no longer be predicted by the variations in stroke volume [8, 24]. In patients with spontaneous ventilation respiratory variation in the central venous pressure has been proposed as an alternative . Conflicting results have subsequently been reported , perhaps because the test is effective only in cases of no forced expiration .
As with any method for predicting response to fluid administration, the cutoff value found for the PLR effects should not be considered as a magic number. Furthermore, sensitivity and specificity values are not absolute. They should be interpreted differently depending upon the clinical context. For instance, the risk of giving fluid unduly may be more dangerous in patients with acute lung injury or acute respiratory distress syndrome. In these cases the physician should administer fluid if the effects of PLR on the cardiac output estimate are clearly above the proposed cutoff value.
Practical aspects of the PLR test
A simple way to perform PLR is to transfer the patient from the 45° semirecumbent to the PLR position by using the automatic pivotal motion of the patient's bed  (Fig. 1; see ESM). In addition to its ease of use, this method allows PLR to be performed rapidly without inducing hip flexion and femoral catheters motion. This is important since such procedures should avoid any pain-induced sympathetic stimulation that can result in erroneous interpretation of the hemodynamic effects of PLR. Accordingly, when performed in such a way, PLR did not increase heart rate, suggesting that no confusing sympathetic alteration occurred during the test . Additionally, keeping the thorax in the horizontal position, and not lower, may avoid the risk of gastric inhalation. Nevertheless, it is reasonable to avoid PLR in patients with head trauma since it can increase the intracerebral pressure. Elastic compression stocking may also alter the venous volume recruited by the PLR .
Another important point concerns the conditions that must be fulfilled for correct measurement and interpretation of PLR effects. The first condition is that it be a real-time cardiovascular assessment able to track hemodynamic changes in the time frame of PLR effects, i. e., 30–90 s  (see ESM). The second is that the limits of precision in the technique used for assessing the response of cardiac output to PLR be far below the 10–15% increase in cardiac output found as a predicting cutoff . PLR-induced changes in arterial pulse pressure [5, 11], descending aorta blood flow [8, 31], pulse contour-derived stroke volume , and pulsed Doppler-derived velocity–time integral [11, 28] have been proposed to be used for this purpose. In patients monitored with esophageal Doppler we found that PLR-induced changes in arterial pulse pressure were less accurate than PLR-induced changes in descending aorta blood flow  in predicting fluid responsiveness in critically ill patients. This is probably explained by the fact that the descending aorta blood flow is a more direct estimate of cardiac output than arterial pulse pressure . Given the good sensitivity and specificity values reported in recent clinical studies it is likely that other real-time hemodynamic assessment methods such as transthoracic echocardiography (pulsed Doppler subaortic flow) [11, 28] and pulse contour cardiac output monitor  can be also appropriately used for quantifying the short-term hemodynamic response to PLR. The third requirement is to ensure that there is actually a change in preload in response to PLR before trying to determine whether there is an increase in cardiac output or preload. In the case of increase in cardiac preload with PLR the absence of increase in stroke volume should indicate that the patient is not fluid responsive. On the other hand, in the case of insufficient increase in preload with PLR (insufficient volume recruitment) the absence of PLR-induced increase in stroke volume cannot be interpreted. In such cases the PLR cannot be used to predict volume responsiveness. Thus it should be recommended to follow the changes in a marker of cardiac preload as a prerequisite to a correct interpretation of the PLR test . Central venous pressure, duration of the aortic flow measured by esophageal Doppler, or end-diastolic dimensions at echocardiography can be used for this purpose. Finally, the level of the intra-abdominal pressure may be important to consider since it can impede the PLR-induced blood transfer when elevated. This point may be one of those that should be addressed by further studies concerning PLR.
In summary, the physiological effects of PLR consist of an increase in venous return and cardiac preload. The PLR thus acts as a self-volume challenge which is easy-to-perform and completely reversible. It has gained an increasing interest in the field of functional hemodynamic monitoring since it can help to detect fluid responsiveness in critically ill patients even in cases of ventilator spontaneous triggering or cardiac arrhythmias. Its optimal use requires a real-time cardiovascular assessment device able to quantify accurately the short-term hemodynamic response.