Intravascular fluid volume

Diuretics, typically spironolactone, form the main therapy, combined with restricted salt intake. Sodium restriction is usually unnecessary where fluid retention is mild, and if marked limitation (less than 40 mmol per day intake) is imposed, may lead to impaired nutrition and is poorly accepted. Diuretic treatment often requires reinforcement with loop diuretics. Treatment can be maintained if urinary sodium excretion is at least 30 mmol per day. Removal of ascites through diuresis requires fluid transfer through the intravascular fluid compartment. If diuresis is too intense the intravascular fluid volume is reduced and hypotension causes hepatorenal failure to follow. The aim should be, through monitoring weight loss, to restrict fluid removal to 0.5 kg per day. In this way the risks of hyponatraemia, renal and hepatic impairment should be reduced. 

As many as 10% of patients show signs of salt and fluid retention and edema (7). Increased intravascular fluid volume is responsible for dilution anemia and increasing cardiac load (SED-8, 216). There is still no explanation for the water-retaining effect, but it might reflect increased production of antidiuretic hormone. 

Naproxen increases intravascular fluid volume and blunts the effects of antihypertensive medications. 

Fluid retention with oliguria in the presence of adequate intravascular fluid volume has been observed in children and is presumably related to the toxic effects of prolonged exposure of the kidney to excessive salicylate concentrations. In some reported cases salicylate poisoning had been present unrecognized for several days. 

The body s normal daily sodium requirement is 1.0 to 1.5 mEq/kg (80 to 130 mEq, which is 80 to 130 mmol) to maintain a normal serum sodium concentration of 136 to 145 mEq/L (136 to 145 mmol/L).15 Sodium is the predominant cation of the ECF and largely determines ECF volume. Sodium is also the primary factor in establishing the osmotic pressure relationship between the ICF and ECF. All body fluids are in osmotic equilibrium and changes in serum sodium concentration are associated with shifts of water into and out of body fluid compartments. When sodium is added to the intravascular fluid compartment, fluid is pulled intravascularly from the interstitial fluid and the ICF until osmotic balance is restored. As such, a patient s measured sodium level should not be viewed as an index of sodium need because this parameter reflects the balance between total body sodium content and TBW. Disturbances in the sodium level most often represent disturbances of TBW. Sodium imbalances cannot be properly assessed without first assessing the body fluid status. 

The parameters Vp, Vg and are the plasma and extracellular fluid volumes and the extravascular to intravascular protein (albumin) ratio, respectively. Their values in human, as an example, are 0.0436 and 0.151 L/kg, respectively, with a ratio of 1.4. 

Physiologically, in both normal and hypertensive individuals, blood pressure is maintained by moment-to-moment regulation of cardiac output and peripheral vascular resistance, exerted at three anatomic sites (Figure 11-1) arterioles, postcapillary venules (capacitance vessels), and heart. A fourth anatomic control site, the kidney, contributes to maintenance of blood pressure by regulating the volume of intravascular fluid. Baroreflexes, mediated by autonomic nerves, act in combination with humoral mechanisms, including the renin-angiotensin-aldosterone system, to coordinate function at these four control sites and to maintain normal blood pressure. Finally, local release of vasoactive substances from vascular endothelium may also be involved in the regulation of vascular resistance. For example, endothelin-1 (see Chapter 17) constricts and nitric oxide (see Chapter 19) dilates blood vessels. 

Extensive burn injuries produce a systemic response that pulls fluid from the vascular system into the interstitial space. This is exacerbated in burns greater than 20% TBSA by a significant capillary leak into the microvasculature and generalized edema. Without proper treatment, intravascular fluid loss and hypovolemic burn shock result. This is why immediate initiation of fluid resuscitation is important. A successful fluid resuscitation will maintain intravascular volume and organ perfusion until capillary membrane integrity is restored (approximately 24 to 48 hours postinjury). 

Pulmonary edema and coagulopathy following intrauterine instillation of 700 ml of 32% dextran 70 has been reported (3). The volume exceeded that recommended by the manufacturer (500 ml), and the installation time (2 hours) was in excess of that recommended (45 minutes). The authors pointed out that hyperosmolarity of the agent is such that if it enters the intravascular compartment, volume overload can result, since 100 ml of intravascular dextran 70 will osmotically expand the intravascular volume by 860 ml, by drawing interstitial fluid into the central compartment. This can further aggravate the risks of pulmonary edema and dilutional coagulopathy. 

Figure 46-1 Volume and distribution of total body water. Note that the intracellular and ECF compartments (ICF and ECF, respectively) are separated by cellular plasma membranes, and within the ECF, interstitial and intravascular fluids are separated by the capillary endothelium.The volumes indicated represent water and not total volume.

Renal ischemia. This is due to several factors. First, OKT3 induces a transient decrease in myocardial contractility [139], which also occurs after infusion of IL-2 [140] and TNF-a [141,142]. Second, the same mediators cause extravasation of intravascular fluid, the so-called "vascular leak syndrome" [138, 143, 144]. This reduces circulating blood volume and further compromises renal perfusion. Finally, OKT3 leads to systemic release of the vasoconstrictor molecule endothehn [145], to which the renal vasculature is particularly sensitive [146]. 

The plasma volume expanders are the substances that are transfused to maintain fluid volume of the blood in event of great necessity, supplemental to the use of whole blood and plasma. Some starch derivatives like hydroxyethyl starch and acetyl starch, which are a group of coUoids, are used to provide sustained intravascular volume expansion. Hydroxyethyl starches are high-polymeric compounds obtained via hydrolysis and subsequent hydroxyl ethylation of glucose units substituted at carbon number 2, 3, and 6 of starch. Recently some waxy starches were also evaluated for plasma volume expander, but more research is needed to establish them as a good substitute for the synthetic polymers. 

The volume of colloid administered is primarily confined to the intravascular space, in contrast to isotonic crystalloid solutions that distribute throughout the extracellular fluid space. 

Understanding the effects of colloid administration on circulating blood volume necessitates a review of those physiologic forces that determine fluid movement between capillaries and the interstitial space throughout the circulation (Fig. 10—5).4 Relative hydrostatic pressure between the capillary lumen and the interstitial space is one of the major determinants of net fluid flow into or out of the circulation. The other major determinant is the relative colloid osmotic pressure between the two spaces. Administration of exogenous colloids results in an increase in the intravascular colloid osmotic pressure. In the case of isosomotic colloids (5% albumin, 6% hetastarch, and dextran products), initial expansion of the intravascular space is essentially that of the volume of colloid administered. In the case of hyperoncotic solutions such as 25% albumin, fluid is pulled from the interstitial space into the vasculature... 

As previously discussed, increased portal pressure triggers the release of nitric oxide to directly vasodilate the splanchnic arterial bed and decrease portal pressure. Unfortunately, nitric oxide also dilates the systemic arterial system, causing a decrease in blood pressure and a decrease in renal perfusion by lowering the effective intravascular volume. The kidney reacts by activating the renin-angiotensin-aldosterone system, which increases plasma renin activity, aldosterone production, and sodium retention. This increase in intravascular volume furthers the imbalance of intravascular oncotic pressure, allowing even more fluid to escape to the extravascular spaces. 

The target in treating ascites is to effect a fluid loss of approximately 0.5 L per day.22 Because ascites equilibrates with vascular fluid at a much slower rate than does peripheral edema, aggressive diuresis is associated with intravascular volume depletion and should be avoided unless patients have concomitant peripheral edema. Patients with peripheral edema in addition to ascites may require increasing furosemide doses until euvolemia is achieved intravenous diuretics are often necessary.22 Diuretic therapy in cirrhosis is typically lifelong. 

Therapeutic intravenous (TV) fluids include crystalloid solutions, colloidal solutions, and oxygen-carrying resuscitation solutions. Crystalloids are composed of water and electrolytes, all of which pass freely through semipermeable membranes and remain in the intravascular space for shorter periods of time. As such, these solutions are very useful for correcting electrolyte imbalances but result in smaller hemodynamic changes for a given unit of volume. 

When determining the appropriate fluid to be utilized, it is important to first determine the type of fluid problem (TBW versus ECF depletion), and start therapy accordingly. For patients demonstrating signs of impaired tissue perfusion, the immediate therapeutic goal is to increase the intravascular volume and restore tissue perfusion. The standard therapy is normal saline given at 150 to 500 mL/hour until perfusion is optimized. Although LR is a therapeutic alternative, lactic... 

For peritonitis, early and aggressive intravenous fluid resuscitation and electrolyte replacement therapy are essential. A common cause of early death is hypovolemic shock caused by inadequate intravascular volume expansion and tissue perfusion. 

In the early phase of serious intraabdominal infections, attention should be given to preserving major organ system function. With generalized peritonitis, large volumes of intravenous (IV) fluids are required to maintain intravascular volume, to improve cardiovascular function, and to ensure adequate tissue perfusion and oxygenation. Adequate urine output should be maintained to ensure appropriate fluid resuscitation and to preserve renal function. A common cause of early death is hypovolemic shock caused by inadequate intravascular volume expansion and tissue perfusion. 

In patients with peritonitis, hypovolemia is often accompanied by acidosis, so large volumes of a solution such as lac-tated Ringers may be required initially to restore intravascular volume. Maintenance fluids should be instituted (after intravascular volume is restored) with 0.9% sodium chloride and potassium chloride (20 mEq/L) or 5% dextrose and 0.45% sodium chloride with potassium chloride (20 mEq/L). The administration rate should be based on estimated daily fluid loss through urine and nasogastric suction, including 0.5 to 1.0 L for insensible fluid loss. Potassium would not be included routinely if the patient is hyperkalemic or has renal insufficiency. Aggressive fluid therapy often must be continued in the postoperative period because fluid will continue to sequester in the peritoneal cavity, bowel wall, and lumen. 

The mainstay of treatment for established SOS is supportive care aimed at sodium restriction, increasing intravascular volume, decreasing extracellular fluid accumulation, and minimizing factors that contribute to or exacerbate hepatotoxicity and encephalopathy. Defibrotide has shown promising results in the treatment of SOS.44... 

The answer is c (HardmanT pp 695-697.) Mannitol increases serum osmolarity and therefore pulls water out of cells, cerebrospinal fluid (C5F), and aqueous humor. This effect can be useful in the treatment of elevated intraocular or intracranial pressure. However, by expanding the intravascular volume, mannitol can exacerbate CHF... 

Crystalloids are administered at a rate of 500 to 2,000 mL/hour, depending on the severity of the deficit, degree of ongoing fluid loss, and tolerance to infusion volume. Usually 2 to 4 L of crystalloid normalizes intravascular volume. 

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