We thank Drs. Youngblood and Sondergaard for their letters regarding our recently published article.1
We agree with Dr. Youngblood1 that standard monitoring already provides substantial information about our patients’ hemodynamic status. Today, pulse pressure variation (PPV) and its corresponding noninvasive parameters are easily available and used in clinical practice.2 In recent years, PPV analysis algorithms have been integrated into different standard monitoring systems,3 and PPV can be reliably assessed on a noninvasive basis by plethysmography.4 Thus, standard monitoring evolves, and today PPV can be considered a standard hemodynamic parameter for a larger population of patients who require perioperative invasive blood pressure monitoring with an arterial line. When no arterial line is required, pulse oximetry devices, which provide the respective functional hemodynamic parameters, can be applied to assess and predict fluid responsiveness. Clearly, continuous end-tidal carbon dioxide monitoring may further support clinical decision making—but still this requires validation in large perioperative clinical studies. In addition, one has to keep in mind that the changes in end-tidal carbon dioxide, induced by a passive leg raising, cannot always be assessed during surgery.
We read with interest Dr. Sondergaard’s acerbic letter regarding our article; we thank him for the querulous interest he has shown in our work. Neither our results nor our discussion demonstrate that the PPV should replace cardiac output (CO) measurements. Dr. Sondergaard’s reference of our work when making this claim suggests that he is less familiar with our results.
We do demonstrate that when estimating CO trends, volume expansion-induced changes in PPV is superior to standard measures of arterial pressure.1,5 PPV is interesting because it identifies patients who will benefit from fluid loading and volume expansion-induced changes in PPV allows for ongoing assessment of fluid-loading efficacy. This provides the clinician with important information which then allows for CO optimization.
Does an increased CO, as a result of fluid loading, result in improved postoperative outcomes? Dr. Sondergaard will be disappointed when we affirm that we do not have the answer to this question. He may be even more disappointed when we affirm that the answer to this question can probably not be framed in his favored “YES/NO” format.
CO is only one of the components of oxygen delivery, and maximizing CO, through fluid administration, does not equate to optimization of oxygen delivery. Fluid loading always causes hemodilution, and hemoglobin concentration plays a key role in oxygen delivery. It is therefore possible that increasing CO, by administering a large fluid load, may actually decrease oxygen delivery. Oxygen delivery is the true parameter to optimize, but it remains difficult to measure and several parameters should be simultaneously optimized to achieve ideal oxygen delivery. PPV and volume expansion-induced changes in PPV are only two of the tools, which may be used to achieve this goal. Using them in isolation may be appropriate in some clinical settings, but it will always remain suboptimal.
Our aim in conducting this study was to explore the predictive performance of PPV under ideal conditions. As a result, we did not record the number of patients who were not selected because of atrial fibrillation.
May we offer a more balanced and less jejune set of conclusions than those purportedly “obvious” conclusions drawn by Dr. Sondergaard?
NO; CO measurements alone is not sufficient for optimization of oxygen delivery. Fluid loading impacts hemoglobin concentration, and neither volume expansion-induced changes in PPV nor direct CO measurements reliably reflect this.
NO; because there is no strong and definitive evidence to suggest that “validated” and calibrated dilution methods with continuous, updated arterial curve–based calculation of CO impact on postoperative outcomes, we do not have to use them (“…no monitoring tool, no matter how accurate, by itself has improved patient outcome.”)6
NO; we do not find ourselves compelled to adopt cardiovascular models from giants such as Guyton or Dr. Sondergaard. Eminence is rarely, if ever, a substitute for evidence.
YES, key opinion holders in the European intensive care community should be very cautious about promoting any device or system that has not clearly demonstrated its ability to improve postoperative outcomes.
Having matured beyond Dr. Sondergaard’s preoccupation with dreams of the conceptualization and intellectualization of endeavors past explored, we have actually evaluated PVV to understand its abilities and limitations. Although PPV informs clinicians on how fluid loading impacts on CO, there is a common misconception that fluid loading is required when PPV is high—this requires correcting.
PPV requires engagement, interpretation, and judgment. For this reason, we have developed the grey zone concept, which we offer to Dr. Sondergaard in the hope that he would evaluate it empirically in a clinical study.