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Correspondence  |   November 2008
What Is Simple Is Perhaps Not Always the Truth
Author Notes
  • Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, India.
Article Information
Correspondence
Correspondence   |   November 2008
What Is Simple Is Perhaps Not Always the Truth
Anesthesiology 11 2008, Vol.109, 933-934. doi:10.1097/ALN.0b013e3181895dd0
Anesthesiology 11 2008, Vol.109, 933-934. doi:10.1097/ALN.0b013e3181895dd0
To the Editor:—  This letter is in response to the interesting article on venous physiology1 published in your journal. While the article expands on the thoughts of Arthur Guyton2 on these matters, it does not acknowledge the presence of other views3 of what makes the blood go around. The Guyton school of thought says that the loss of elastic energy in driving venous return needs to be restored by the heart.4 Guyton’s opponents opine that circulatory work5 (integral function of instantaneous pressure and volume decrement) is the elixir of venous flow. To the practicing clinician, the import of either the potential energy in the form of venous volume (Guyton) or a potential energy in the form of an energy derived from ventricular work propelling venous return is only of academic interest; in both models, venous flow ceases very soon after the pump stops! The mean circulatory filling pressure (strictly speaking, the pressure when cardiac output is zero in an experimental model) is therefore critically dependent on pump function. Even as we quibble about physiologic niceties, in the intact animal, the heart as a pump not only affects the fluid mechanics of blood flow; it also affects, and is in turn affected by, the neurohormonal milieu in which it works.6 Failure of pump function leads to an assortment of chemical mediators that can potentially affect the venous capacity and venous compliance.7 
Because teleologically the cardiopulmonary apparatus works to perfuse the systemic circulation, it also seems to make more physiologic sense that the venous circuit ends at the pulmonary vein–left atrial level. The right ventricle and the pulmonary circulation are nicely coupled, but either can play rogue (pulmonary hypertension or right ventricular myocardial infarction). The left heart may not then fill adequately. One might argue again that the VR = MSFP − RAP/Rvrelation explains this (VR = venous return, MSFP = mean systemic filling pressure, RAP = right atrial pressure, Rv= cumulative venous resistance) because the gradient for venous return is decreased when the right atrial pressure is high. I could equally argue that interventricular dependence has compromised left ventricular function and therefore resulted in less work done by it in pushing the blood around! All in all, any analysis of venous function that stops at the right atrium is seemingly not complete.
Arguably, the concept of the splanchnic circulation being a potential booster pump to the larger venous circulation outside it (on account of its large volume and high compliance) is elegant; how well does this model work in clinical practice? Although it offers an elegant explanation of the increase in filling pressure with aortic clamping8 or the ability to maintain vital perfusion early on with exsanguinating trauma, as the physiologic setting becomes complex (heart failure, septic shock) it becomes increasingly difficult to apply. The author himself points out that adrenergic stress could affect both the changes in stressed volume (the currency of the circulation, in principle) and the effect on mobilization of this very volume. This is an either/or function and it is possible that proportionate to stress, the latter effect predominates. To add to the conundrum, the dynamics of the splanchnic circulation are among the most controversy-ridden areas in our understanding of cardiovascular physiology.9,10 The circulation seems to be among the vulnerable in terms of ischemia11; one cannot imagine a situation of circulatory stress where a decreased  splanchnic arteriolar resistance with a decreased  resistance to hepatic outflow (working like an “arteriovenous fistula”) can potentially contribute to an increased  mean circulatory filling pressure. From this perspective, the two-compartment model has limited application in our understanding of most clinical situations causing a circulatory imbalance.
Increased intrathoracic pressure increases transmural central venous pressure. It is suggested that this is made up by squeezing the abdominal venous system (in effect increasing the intra-abdominal pressure) and by mobilizing blood from the gut by an increase in splanchnic arteriolar resistance. Both of these maneuvers are harmful because any  splanchnic ischemia is expected to trigger gut cell death,12 possible translocation of endotoxin from the gut, and eventual multiorgan disease. It follows that the surmise that increased intra-abdominal pressure (whatever the positive effects on mean systemic filling pressure are) is not harmful is incorrect. Most would agree that significant abdominal hypertension calls for only one therapeutic modality: early abdominal decompression.13 This alone can prevent the downward spiral of organ ischemia, acidosis, and renal failure. Because the analysis of the venous circulation stops at the right atrium, it cannot account for the effects of increased intrathoracic pressures (upward motion of diaphragm with increased intra-abdominal pressure) on the pulmonary vasculature and the downstream consequences on the right heart.
The commentary on the utility or lack thereof of measured central venous pressures is, of course, timely, considering the ever-increasing evidence base of dynamic circulatory indices. However, one might add, almost in requiem, that increased central venous pressure is still a useful clinical tool in the evaluation of right heart or pericardial disease.
Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, India.
References
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