Fluid therapy: Finding the best options for perfusion, oxygen supply
May 01, 2008
Q: Could you review fluid therapy in dogs and cats?
A: Dr. William W. Muir III at the 2007 American College of Veterinary Internal Medicine (ACVIM) Forum in Seattle gave an excellent lecture titled: "Advances in Fluid Therapy: New Uses for Old and New Crystalloids." Here are some relevant points:
During septic shock, for example, severe hypotension may necessitate the administration of large volumes of fluid, leading to hemodilution and hypoproteinemia. Plasma albumin concentration and oncotic pressure may decrease which, with increased capillary membrane permeability, predisposes to fluid shifts into the interstitial fluid compartment.
The vasodilation associated with sepsis results in sequestration of blood cells and plasma in venules and peripheral tissues. If vascular volume is not restored and if arterial blood pressure is not returned to near normal (greater than 60 mmHg) values, tissue hypoxia and the release of additional vasoactive substances lead to the inability of cellular membrane pumps and transport mechanisms to maintain cellular and vascular integrity.
Vasoactive substances (prostaglandins, leukotrienes, platelet-activating factor, oxygen-free radicals) alter neuro-regulatory control, dilate arterioles (vascular hyporeactivity), constrict venules and increase capillary-membrane permeability. Decreases in venous return decrease cardiac output and, when coupled with hypovolemia, eventually result in a decrease in peripheral perfusion, tissue-oxygen deprivation and metabolic (non-respiratory) acidosis. Therefore, peripheral perfusion is dependent on intact autoregulatory and compensatory responses, and the exogenous administration of appropriate fluids in order to maintain vascular volume.
Catecholamines may be needed to maintain cardiac (contractile) pumping function and appropriate vascular tone.
Are pathophysiologic problems known?
Regardless of these limitations and because the goal of fluid therapy is to optimize vascular volume, restore circulatory function and tissue perfusion and ultimately deliver oxygen to tissues, the more appropriate questions should be:
What type of fluid should be administered? How much should be given? How fast?
These questions, however, are best answered if the pathophysiologic problems are known, the end point(s) of fluid administration have been decided and the methods to assess or evaluate fluid therapy defined.
The most efficacious methods available for the evaluation of fluid therapy in patients are not routinely used in veterinary practice or in veterinary institutions.
Fluid therapy is best evaluated by the ability to restore tissue perfusion, which can be assessed by circulatory function (changes in cardiac output and arterial blood pressure), but more specifically by indices that reflect oxygen transport (delivery) and oxygen consumption.
Numerous studies indicate that oxygen-transport variables (O2 delivery, O2 uptake) are the major predictors of appropriate circulatory function and are excellent predictors of survival or death. Since veterinarians do not routinely make the type of measurements required to determine oxygen-transport variables, does this mean that fluid therapy is a shot in the dark, or only partially effective at best?