My post on venous excess model has been much visited. My intention was to draw attention to the importance of the capillary and venous side of the circulatory equilibrium. The arterial side gets all the attention at the bedside because it is measurable; flows and pressures, oxygen delivery and consumption, and their manipulation have been the subject of hundreds of publications and thousands of FOAMEd posts. Moreover there has been so much denigration of central venous pressure that some even claim it should not be used for clinical decision-making. But it is dawning on us that such measurements and manipulations are not having much effect on patient outcomes; the venous side is harder to assess but could turn out to be the more important. If you want a teaching resource to check your comprehension of venous haemodynamics, try how the body works during acute hemorrhage by Shen & Baker at Harvard University. For a really succinct case against uncritical fluid resuscitation see Rory Spiegel of Stoneybrook Medicine. To quote Rory;
“Traditionally emergency physicians have focused on volume replacement as the primary method of augmenting preload in patients presenting in shock, regardless of initial volume status. As a result, many patients who may not be truly hypovolemic, receive large volume fluid resuscitations. We are learning that this high volume strategy may cause complications downstream in the patient’s inpatient hospital course. Early use of low dose vasopressors (norepinephrine at 5 mcg/min) will result in a venoconstrictive effect, decreasing venous compliance, and shifting fluids from the unstressed venous beds to the useable stressed volume.”
The late A. Johan Groeneveld provided valuable clinical data showing that oedema could be anticipated and thereby avoided or minimised if we STOPPED intravenous infusion once volume responsiveness on the arterial side became minimal; presumably the peak of the Starling curve. In other words, arterial side monitoring takes the patient close to the cliff edge of a spiral decline into pulmonary and systemic oedema. (1) What is needed is a better circulatory assessment for the critically-ill patient, one that finds safer ground between insufficient perfusion and tissue oedema. fluidphysiology.org advises rational prescribers to think about capillary pressure, even though we have no reliable clinical measurement of it, so that we achieve enough capillary ‘opening’ pressure to allow perfusion while avoiding capillary hypertension which invariably causes hyperfiltration and glycocalyx dysfunction, causing oedema if lymph flow cannot compensate and interstitial fluid accumulation results in interstitial fluid excess. Low dose norepinephrine as advocated by Rory Spiegel is then seen as a way to keep post-arteriolar capillary pressure down, the venous excess up, and lymph vessel contractions stimulated while fluids are given frugally. And, of course, if frugal fluid therapy fulfills its early promise, we’ll render the Hamburger – Ringer controversy an irrelevance!
- Woodcock TM, Woodcock TE. Revised Starling equation predicts pulmonary edema formation during fluid loading in the critically ill with presumed hypovolemia. Crit Care Med. 2012;40:2741-2; author reply 2742.