Cardiac Output Monitoring and Fluid Responsiveness

Abstract

To the Editor, I appreciate the interest that Dr. Peled has taken in this review of hemodynamic monitoring in neurocritical care and thank him for his letter. Accuracy and precision of minimally invasive cardiac output (CO) monitoring devices is an important and highly debated issue [1]. Apart from the discussion on proper statistical methodology that should be used to compare a new device to a reference method [2], it should be realized that there is even a more fundamental problem, the one relating to the inherent limitations of the reference method itself. In fact, there is no bedside ‘‘gold standard’’ when it comes to the measurement of CO [3]. The widely accepted invasive bedside standard is the pulmonary artery catheter (PAC), nevertheless higher-precision tools like indwelling flow probes when used to compare the PAC with minimally invasive tools demonstrate that the PAC is as precise or imprecise [4–6]. In addition, as Dr. Peled notes, the behavior of these monitors in different hemodynamic conditions has not been elucidated and both accuracy and precision may vary greatly. Moreover, the use of AHM within the neurocritical care literature remains sparse and guidance comes by extrapolating knowledge from medical–surgical critical care populations. A relevant meta-analysis has recently been published by Peyton and Chong [4]. The authors reviewed the literature on four different minimally invasive methods (pulse contour, esophageal Doppler, partial carbon dioxide rebreathing, and transthoracic bioimpedance) to assess their bias, precision and percentage error (PE) in agreement with thermodilution. This study found all four methods achieving a similar ±40–45 % PE in agreement with thermodilution leading the authors to challenge the ‘‘standard’’ PE of ±30 % which is often considered the accepted limits of agreement as initially suggested by Critchley and Critchley [7]. Obviously more research is needed to appropriately validate the currently available CO monitors and to also develop newer, potentially better performing devices. The second point of Dr. Peled’s letter refers to the markers of fluid responsiveness. It should be clear that the property of volume responsiveness, i.e., operating on the ascending part of a Frank-Starling curve, does not mean that a patient needs fluids. The dynamic markers of fluid responsiveness including PPV, SVV, and dIVC among others should be consulted after a clinical decision has been made in augmenting a patient’s stroke volume or mean arterial pressure and in keeping with their limitations (e.g., spontaneous breathing and atrial fibrillation). A predicted non-responder should not be given a fluid bolus since his/ her SV will not increase with additional volume, alternative physiologic interventions (for e.g., inotropes or vasopressors) may be considered. As a more general comment, these markers are not meant to be ‘‘one more number to fix’’, they are devised to complement the clinical picture and assist in choosing among interventions in patients with complex physiologic derangements.