Fluidoterapia

FLUID AND ELECTROLYTE THERAPY
(http://www.cvmbs.colostate.edu/clinsci/wing/fluids/fluids.htm)
Wayne E. Wingfield, MS, DVM
Diplomate, ACVS, ACVECC
Professor and Chief, Emergency and Critical Care Medicine
Department of Clinical Sciences
College of Veterinary Medicine and Biomedical Sciences
Colorado State University
Fort Collins, CO 80523
wwingfie@vth.colostate.edu

1. What is plasmaosmolality?
Plasma osmolality is a function of the ratio of body solute to body water; it is regulated by changes in water balance. Water intake is derived primarily from three sources: Ingested water, water contained in food, and water produced from oxidation of carbohydrates, proteins, and fats. Water losses occur in the urine and stool, as well as evaporation from the skin and respiratorytract. Alterations in plasma osmolality of as little as 1% - 2% are sensed by osmoreceptors in the hypothalamus. These receptors initiate mechanisms that affect water intake (via thirst) and water excretion (via antidiuretic hormone [ADH]) to return plasma osmolality to normal.
 
2. Define "effective circulating volume".
Effective circulating volume is defined as that part of the extracellularfluid (ECF) that is in the vascular space and effectively perfusing tissues. It varies directly with ECF volume and also with total body sodium, since sodium salts are the primary ECF solutes holding water in the extracellular space. Therefore, regulation of sodium balance, by changes in renal sodium ion, and the maintenance of effective circulating volume, are closely related.
 
3. What are themajor effectors of effective circulating volume?
Three major effectors alter effective circulating volume: 1) The sympathetic nervous system, 2) angiotensin II, and 3) renal sodium excretion. Volume depletion, sensed by arterial baroreceptors as hypotension, causes an increase in peripheral sympathetic tone. Increased sympathetic tone returns volume to normal by initiating specific compensatorychanges. These compensatory changes include the following:
* Venous constriction: Increased venous return
* Increased myocardial contractility and heart rate: Increased cardiac output
* Arterial vasoconstriction: Increases systemic vascular resistance and blood pressure
* Increased renin secretion: Increases levels of angiotensin II which is a potent vasoconstrictor* Increased renal tubular sodium resorption (due to increased levels of angiotensin II and aldosterone).
Sympathetic tone induced changes in effective circulating volume are transient and compensatory; appropriate changes in renal sodium excretion are required to restore normal volume.
 
4. What is the body’s main defense against hyperosmolality?
The major defense againsthyperosmolality (accumulation of solute in excess of body water) is increased thirst. Although the kidney can minimize water losses via the action of ADH, water deficits can be corrected only by increased dietary intake.
 
5. When can hypo-osmolality result?
Hypoosmolality can result from excessive body water retention with subsequent dilution of body solutes or from solute loss in excess of water loss(e.g., diarrhea). Because the kidney excretes large volumes of water daily, persistent water retention resulting in hypoosmolality occurs only in the presence of decreased renal water excretion. In patients with normal renal function, hypoosmolality must therefore be due to solute loss in excess of body water loss.
 
6. How does hypovolemia (i.e., dehydration) increase the circulating volume?Hypovolemia causes an increase in renin secretion. The subsequent increase in angiotensin II causes an increase in blood pressure (as a result of arterial vasoconstriction), as well as renal sodium retention (this is both a direct effect and also the result of increased aldosterone secretion). With sodium retention, water is also retained.
 
7. How do you determine the degree of dehydration in an...