To the Editor:
We congratulate Le Manach et al.1 for their demonstration of the superiority of changes in pulse pressure variation for the assessment of volume expansion–induced changes in cardiac output (CO) as compared with standard measures of arterial blood pressure. The findings clearly demonstrate the fallacy of determining the adequacy of CO based on static measurements of arterial pressure and encourage practitioners to thoughtfully reconsider how we assess patient responses to volume administration.
Certainly, many modalities exist to assess the response to volume infusion. In the current study, thermodilution, pulse contour analysis, esophageal Doppler, and transesophageal echocardiography are specifically mentioned. Although effective, each requires the addition of technology and invasiveness beyond standard monitoring, which is not universally available or necessary. Omitted from both this study and the accompanying editorial is reference to using our standard monitors in the assessment of this response.
Through citation of a 2011 survey of anesthesiologists,2 the authors state that “most anesthesiologists do not monitor CO during high-risk surgery,” a premise that is a gross oversimplification of standard monitoring. End-tidal carbon dioxide (ETco2) monitoring is a standard anesthetic practice and functions in the determination of both adequate ventilation and circulation. Low-CO states result in increased pulmonary dead-space and altered carbon dioxide elimination. In clinical practice, decreases in ETco2 have long been associated with deteriorating cardiovascular status, and the gradient between ETco2 and the partial pressure of carbon dioxide in arterial blood has been used as a surrogate for the adequacy of CO.
In 1994, Shibutani et al.3 demonstrated the strong linear correlation between changes in CO and ETco2. Recently, Monge García et al.4 demonstrated that changes in ETco2 after passive leg raising had a sensitivity of 90.5% and specificity of 93.7% to predict fluid responsiveness using a methodology similar to many of the pulse pressure variation and stroke volume variation models. We frequently use the arterial-ETco2 gradient as part of our assessment of CO and the trend of this gradient to assess the impact of therapeutic interventions, the most common of which being intravascular volume expansion.
We thank Le Manach et al. for their work and suggest that it teaches very important lessons in cardiovascular physiology and volume management. Although the authors demonstrated the use of pulse pressure variation for assessing hemodynamic responses to fluid administration, we suggest that our standard monitoring already provides substantial information about our patients’ hemodynamic status. More advanced, invasive, and expensive monitoring should continue to be applied on a case-by-case basis.