This Invited Commentary accompanies the following article:
Pathil A, Stremmel W, Schwenger V, Eisenbach C. The influence of haemodialysis on haemodynamic measurements using transpulmonary thermodilution in patients with septic shock: an observational study. Eur J Anaesthesiol 2013; 30:16–20.
Debate continues as to what are the ‘best’ measured or derived parameters for assessing the volume and flow status of critically ill patients. There is a range of cardiac output technologies available that can be broadly categorised as invasive (pulmonary artery catheter), less invasive (pulse pressure analysis, transoesophageal echocardiography or Doppler) or noninvasive (transthoracic echocardiography, applied Fick principle, bioimpedance or bioreactance and plethysmographic indices).1 Some of the more familiar devices that use pulse pressure analysis require calibration with either indicator dye dilution or thermodilution. There is also a wealth of published indications for the use of cardiac output technologies both in anaesthesia and critical care.2,3 It is acknowledged that there is variability in the performances of these devices between measurements, between devices and between operators, especially in the critically ill.4–7 The article by Pathil et al.8 in this issue of the European Journal of Anaesthesiology highlights the potential for error when patients undergoing concurrent renal replacement therapy (RRT) have cardiac output measured using the PiCCO system with transpulmonary thermodilution.
Acute kidney injury is common in ICUs and may have a prevalence of up to 70% of patients using the RIFLE classification, with around 30% of these requiring RRT.9 Many of these patients will undergo estimation of cardiac output using the techniques outlined above.10 What is unclear is the very relevant question of whether concurrent renal replacement affects the results of cardiac output monitoring using transpulmonary thermodilution. Variability in haemodynamic indices measured by transpulmonary thermodilution may occur due to fluctuations in blood flow, volume or temperature that are associated with RRT.11 The RRT system increases the total circulating volume and also leads to a degree of recirculation, with a potential delay in the onset of the recirculation effect on the downslope of the thermodilution curve. Although recirculation is probably unimportant in the analysis of the first part of derived thermodilution curves (by the Stewart–Hamilton method for estimating cardiac output), more complex analyses of the decay curve are used by calibrated systems to calculate both the mean transit and the exponential downslope times. These variables are used in the estimation of other derived haemodynamic indices. Consequently, changes of this part of the curve could result in an overestimation of the mean transit time and an underestimation of the downslope time.
Initiating RRT causes changes in blood temperature, estimated at 0.05 to 0.1°C at typical flow rates.12 Although this change seems small, the injection of a bolus of cold isotonic saline for thermodilution measurements would only be expected to cause a temperature change of around 0.5°C, which could, therefore, be confounded by the ‘thermal noise’ of initiating RRT. The site of injection of the indicator bolus may also be relevant, especially if a dialysis catheter with an integrated injection port is used.11 Turbulence created in the catheter or in adjacent large vessels is poorly understood in vivo. This may vary with the catheter type and mode of RRT, influencing the flow of injectate.13 The initiation of RRT may of course lead to genuine changes in cardiac output which may be occurring due to removal or dilution of vasopressors and changes in circulating volumes.
The study by Pathil et al. has shown that slow extended daily dialysis does significantly reduce measurements of cardiac index (CI) and global end-diastolic volume index when measured by PiCCO in patients with septic shock, with or without haemodialysis. Others have argued that the changes are only clinically relevant when starting or stopping RRT and that, under steady state conditions, differences in cardiac output estimations are not clinically relevant.12 The article by Pathil et al., however, does not allow us to determine what exactly is being measured when commencing RRT. The question remains as to whether it is a true reduction in CI or simply an artefact of measurement by the thermodilution indicator with RRT? It would have been of interest if the authors had used other flow measurement technologies in addition to address this issue. Although there are currently more questions than answers, further studies in this area are welcomed, particularly, whether the use of other dilution indicators or technologies are associated with similar issues. Using a concurrent nontemperature-dependent measure of cardiac output may help elicit the nature of the measurement differences. So, in the meantime, we should continue to couple clinical assessment to measurements of cardiac output, not rely solely on isolated measurements and be wary of measurements obtained immediately after starting or stopping RRT.
Assistance with the commentary: none declared.
Financial support and sponsorship: none declared.
Conflicts of interest: none declared.
Comment from the Editor: this Invited Commentary was checked and accepted by the editors, but was not sent for external peer-review. MC is an Associate Editor of the European Journal of Anaesthesiology.
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