Haemodynamic evaluation and optimisation of brain-dead donors with oesophageal Doppler during organ harvesting (2018)

Editor, Keeping the circulatory system of brain-dead organ donors stable is challenging, and haemodynamic evaluation without advanced haemodynamic monitoring may be insufficient.1 Advanced haemodynamic monitoring is probably underused, and if used, it is rarely continued into the operating theatre for the organ procurement procedure. Donor management strategies have to be continued during organ procurement to ensure optimal organ preservation. The anaesthesiologist of the harvesting team often plays a crucial role in assessing the adequacy of fluid resuscitation and vasoactive (inotropic and/or vasopressor) medication in use. This assessment may be difficult to perform. Oesophageal Doppler is minimally invasive and has been demonstrated to improve outcome when used to guide haemodynamic therapy during several surgical procedures.2 The current study was undertaken to evaluate the adequacy of initial clinical assessments and whether haemodynamic management guided by oesophageal Doppler would be feasible and useful during organ procurement. The protocol (S-06184) was approved by the Regional Ethics Committee of Southern Norway on 22 June 2006. The requirement for written informed consent was waived. In 63 brain-dead donors, a clinical assessment of global haemodynamics was performed by the anaesthesiologist of the harvesting team on arrival using all available information from standard monitoring (invasive arterial and central venous pressures, pulse oximetry and blood gas analyses) and ongoing infusions. There were no preset criteria for the clinical evaluation. The donors were classified as haemodynamically stable or unstable, and whether they were hypoperfused, hypovolaemic, vasoconstricted or vasodilated (multiple categories possible). Subsequently, a CardioQ (Deltex Medical, Chichester, United Kingdom) oesophageal Doppler probe was inserted, and the clinical assessments were evaluated against the variables derived from the Doppler measurements with calculations of sensitivity and specificity (including 95% confidence intervals). The CardioQ device measures blood flow velocity in the descending aorta and displays a waveform of velocity plotted against time. From this waveform, several variables are measured and calculated, such as the inotropic variables peak velocity and mean acceleration, the loading variable flow time corrected for heart rate (FTc) and stroke distance, translated into cardiac index (CI).3,4 We defined hypovolaemia as the combination of FTc of 335 ms or less and systemic vascular resistance index (SVRI) of 2200 dyn s cm−5 m−2 or less. Hypoperfusion was defined as CI of 2.2 l min−1 m−2 or less, and the donor was defined as vasoconstricted if SVRI at least 2500 dyn s cm−5 m−2, and vasodilated if SVRI of 1300 dyn s cm−5 m−2 or less. The Doppler-derived variables were used to optimise therapy aiming at a mean arterial pressure (MAP) at least 65 mmHg, CI at least 2.5 l min−1 m−2, SVRI between 1300 and 1700 dyn s cm−5 m−2 and FTc at least 350 ms. To what extent the haemodynamic goals were reached was assessed after 1 h. The haemodynamic optimisation protocol included volume loading (dextran 70, max 500 ml and crystalloids), inotropic support with dopamine, and noradrenaline as a vasopressor. The Doppler probe was placed successfully in 60 donors. The clinical assessments of global haemodynamics were generally poor. In all, 47 and 13 donors were clinically assessed to be haemodynamically stable or unstable, respectively (Table 1). The donors classified as unstable had significantly higher heart rate, higher CI and higher values of the contractility variables mean acceleration and peak velocity, than those classified as stable, and they were well within the haemodynamic goals.Table 1: Haemodynamic variables at arrival in donors clinically assessed to be haemodynamically stable or unstableOnly two of 10 hypoperfused donors were detected by clinical assessment [sensitivity 0.2 (95% CI 0.04 to 0.36)], and two more donors were classified as hypoperfused despite a CI at least 4.7 l min−1 m−2. Clinical detection of hypovolaemia had a sensitivity of 0.71 (95% CI 0.32 to 0.75) (five of seven hypovolaemic donors) and a specificity of 0.60 (95% CI 0.55 to 0.64). Half of the vasodilated donors were wrongly assessed to be hypovolaemic. Detection of vasodilatation had a sensitivity of 0.38 (95% CI 0.22 to 0.51) and a specificity of 0.83 (95% CI 0.73 to 0.92). Twenty-four donors (40%) had SVRI of 1300 dyn s cm−5 m−2 or less at the start of organ procurement. Eleven donors were vasoconstricted. The sensitivity and specificity for clinical detection were 0.46 (95% CI 0.20 to 0.72) and 0.84 (95% CI 0.78 to 0.90), respectively. Doppler-guided therapy made eight of the 10 hypoperfused donors reach the preset target of CI at least 2.5 l min−1 m−2 (Table 2). The main interventions were administration of dopamine in two more donors (from four to six) and volume infusion averaging 2060 ± 1059 ml. CI increased by approximately 70%, accompanied by a reduction in SVRI.Table 2: Haemodynamic variables of the hypoperfused donors at arrival and after 1 h of oesophageal Doppler-guided therapyThe hypovolaemic donors received 2257 ± 814 ml of fluid which increased their FTc above target from 321 ± 14 to 364 ± 33 ms (P = 0.03) without significant changes in any other variable. The 11 vasoconstricted donors included eight from the hypoperfusion group and were similarly treated with volume (1782 ± 973 ml) which reduced their SVRI by approximately 40% from 3671 ± 722 to 2112 ± 898 dyn s cm−5 m−2 (P < 0.001). Their CI increased from 2.0 ± 0.4 to 3.2 ± 0.9 l min−1 m−2 (P < 0.001). Twenty-one of the 24 vasodilated donors received vasoactive medication at the initial assessment, but despite some increased use of noradrenaline, only four donors increased their SVRI above the preset lower limit of 1300 dyn s cm−5 m−2. Clinical evaluation of global haemodynamics in critically ill patients is difficult and generally poor.5 In the setting of a brain-dead donor, it can be even more difficult as the clinical signs we use for haemodynamic evaluation may be absent. The total lack of ability to separate haemodynamically stable from unstable donors was surprising and clearly demonstrates that clinical assessment of global haemodynamics is a poor basis for haemodynamic interventions and adjustments in this population. Hypoperfusion may cause damage to transplantable organs, and by not using advanced haemodynamic monitoring when indicated, the majority of hypoperfused donors will probably not be detected. Doppler-guided therapy effectively corrected hypoperfusion, hypovolaemia and vasoconstriction. In all, 40% of the donors were vasodilated, and most remained vasodilated. It seems that avoiding high doses of vasopressors had higher priority than avoiding fluid overload, and a low SVRI was accepted as long as MAP was above target. Oesophageal Doppler is easy to use, almost without complications and readily transportable, which makes it very suitable for organ harvesting teams. We conclude that clinical assessment of global haemodynamics in the brain-dead organ donor ready for organ procurement is difficult and often wrong, and that use of oesophageal Doppler to guide therapy towards preset goals is feasible and contributes to a better haemodynamic profile in most donors during organ harvesting. Acknowledgements relating to this article Assistance with the study: the anaesthesiologists of the harvesting teams participated in data collection and their contribution is greatly appreciated. Financial support and sponsorship: the study was supported by departmental funding only. Conflicts of interest: none.