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"Attikon" University Hospital Athens, Greece Larissa University Hospital, Thessaly, Greece
Correspondence to: Petros Kopterides, MD, 28–30 Korai St, Nea Ionia, Athens 14233, Greece; e-mail: petkop{at}ath.forthnet.gr
To the Editor:
We read with interest the study by Chawla et al1 (December 2004), showing that mixed venous O2 saturation (SvO2) is consistently lower than central venous O2 saturation (ScvO2), with a mean difference of – 5.2 ± 5.1%. The authors attribute this difference to the "mixing of atrial blood with blood emanating from the coronary sinus." Even though we cannot totally exclude this possibility, we can challenge it with simple calculations.
If we assume that in a septic patient the total blood volume flowing from the right atrium to the right ventricle in 1 min is 5,000 mL (5 L) and the coronary sinus blood flow is 200 mL,2 that means that 4,800 mL of venous blood return from the rest of the body with a mean saturation (ScvO2) of 70%. Then, even if the effluent from the coronary sinus has an oxygen saturation of zero (which never happens!), the SvO2 would be 67.2% (4,800 mL x 70% + 200 mL x 0% = 5,000 mL x 67.2%), or only 2.8% lower than the ScvO2. We repeated the equation with different values of the index parameters and came to the same conclusion: coronary sinus blood desaturation cannot easily explain the difference between ScvO2 and SvO2.
We propose that this difference can be more easily explained by an inferior vena cava effluent with a lower oxygen content. In fact, Dahn et al3 showed that marked depression of regional (splanchnic) venous oxygen saturation (55.6 ± 14.4%) may coexist with normal or high SvO2 (70.5 ± 8.7%). The low values of splanchnic (gut) venous saturation may have profound implications in critically ill patients and also need to be explored more thoroughly. In the meantime, we agree with Chawla et al1 that "ScvO2 is not a reliable surrogate for SvO2 in critically ill medical or surgical patients."
References
The George Washington University Washington, DC
Correspondence to: Guillermo Gutierrez, MD, PhD, FCCP, Professor of Medicine and Anesthesiology, The George Washington University MFA, 2150 Pennsylvania Ave NW, Suite 5-404, Washington, DC 20037; e-mail: Ggutierrez{at}mfa.gwu.edu
To the Editor:
We thank Kopterides et al for their insightful and provocative comments regarding our recently published article1 on the oxygen saturation difference between central and mixed venous blood. In that article, we reported a step-down in oxygen saturation from the right atrium to the pulmonary artery (
SO2) and concluded it resulted from mixing atrial blood with blood with lower oxygen content. As possible sources of blood with lower oxygen content, we considered the inferior vena cava and the coronary venous effluent (coronary sinus and Thebesian veins). Although we leaned toward the latter explanation, we refrained from attributing causation to either possibility, since we lacked knowledge of inferior vena cava oxygen content, myocardial venous flow, or its oxygen content.
The notion that coronary effluent blood plays a significant role in the development of SO2 has been alluded to by others,2 and may not be as far-fetched as Kopterides et al imply in their letter. According to their equation, Kopterides et al calculate a maximum SO2 of 2.8% attributable to mixing with coronary sinus blood, even when they assume an unrealistic value of 100% oxygen extraction by the heart. This calculated SO2 contrasts with the mean SO2 of 5.2% noted in our study. In our opinion, however, a major flaw in their argument is the implied assumption that coronary sinus flow equals total coronary venous outflow.
In determining the concentration change of chemical species in a mass transport model, one must take into consideration the total flow from one compartment to another. We take coronary effluent blood as the total venous drainage from the heart, including that flowing through the coronary sinus and the cardiac veins. Whereas the structural mapping of the major ventricular and atrial cardiac veins is a complex, partially understood subject, it is known that in > 50% of human hearts only the great cardiac and middle cardiac veins drain into the coronary sinus. Moreover, the major epicardial veins drain into the coronary sinus in only 21% of hearts.3
Kopterides et al assumed in their calculations a coronary sinus outflow of 200 mL/min, a figure derived from the seminal work of Dhainaut et al4 on coronary hemodynamics and metabolism in septic shock. However, Cunnion et al5 reported that coronary sinus plus great vein flow in individuals with septic shock varies widely, from 135 to 994 mL/min (451 ± 118 mL/min [mean ± SE]). Furthermore, Schwitter et al6 compared coronary sinus blood flow measured by phase-contrast magnetic resonance to positron emission tomography-derived measures of myocardial blood flow in normal, resting individuals. They found coronary sinus flow to be approximately 65% the total left ventricular venous flow. Therefore, computations of SO2 based solely on measures of coronary sinus flow, not on total coronary venous drainage, are likely to underestimate the diluting effect of myocardial venous outflow on SO2.
By increasing coronary effluent to 350 mL/min and applying assumptions similar to those used by Kopterides et al in their model, we find SO2 equals 5%, a value equal to that found in our study, and greater than the weighted mean of published values for SO2 of 3.4%.1 Carrying the argument further, we assume a more realistic value for coronary venous blood oxygen saturation of 30%,47 along with a mean cardiac output of 3.7 L/min and central venous saturation of 71.9% (values taken from our postoperative group, Tables 1, 2 in our article1). Under these conditions, a coronary venous flow of only 380 mL/min results in SO2 of 4.9%, a value equal to that found in our study. Accounting for the medical group patients requires an increase in coronary flow to 580 mL/min, certainly a high value, but not an unreasonable one, given the data produced by Cunnion et al.5
While mass transport models may help us understand physical processes, by their very nature they cannot be used to prove or disprove a hypothesis, since models depend exclusively on the quality of the assumptions and boundary conditions used in their formulation. The next step should be, as proposed by Galileo many centuries ago, to do the experiment, in this case by taking measurements of coronary venous outflow and its oxygen saturation. In the meantime, we prefer to maintain an open mind and strongly consider the mixing of right atrial with coronary effluent blood as a possible mechanism leading to the development of SO2.
References
Boston, MA
Correspondence to: David H. Roberts, MD, FCCP, Pulmonary/Critical Care Division, Beth Israel Deaconess Medical Center, East Campus, 330 Brookline Ave, Boston, MA 02215; e-mail: dhrobert{at}bidmc.harvard.edu
To the Editor:
I thank Dr. Inoue1 for his thoughtful comments in the June issue of Chest. As he mentions, the exact chemoattractant factors that brought the eosinophils to the lung in this case are not known. Unfortunately, we do not have the ability to reprocess the biopsy and stain for the markers discussed (interleukin-4, interleukin-5, eotaxin). With regard to Dr. Inoue’s question about the synovial fluid, it was analyzed and no eosinophils were present. I thank Dr. Inoue for his recommendations regarding staining. In future cases, we will consider the use of this stain to better delineate the presence of eosinophils.
References
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