Intravascular fluid

Treatment focuses on increasing CO with positive inotropic agents and/or replacing intravascular fluids... 

In PD, prewarmed dialysate is instilled into the peritoneal cavity where it dwells for a specified length of time (usually one to several hours, depending on the type of PD) to adequately clear metabolic waste products. At the end of the dwell time, the dialysate is drained and replaced with fresh dialysate. The continuous nature of PD provides for a more physiologic removal of waste products from the bloodstream, which mimics endogenous renal function by decreasing the fluctuations seen in serum concentrations of the waste products. Similarly, water is removed at a more constant rate, lessening the fluctuations in intravascular fluid balance and providing for more hemodynamic stability. 

The extracellular fluid (ECF) is the fluid outside the cell and is rich in sodium, chloride, and bicarbonate. O The ECF is approximately one-third of TBW (14 L in a 70-kg man or 12 Lin a 70-kg woman) and is subdivided into two compartments the interstitial fluid and the intravascular fluid. The interstitial fluid (also known as lymphatic fluid) represents the fluid occupying the spaces between cells, and is about 25% of TBW (10.5 L in a 70-kg man or 8.8 L in a 70-kg woman). The intravascular fluid (also known as plasma) represents the fluid within the blood vessels and is about 8% of TBW (3.4 L in a 70-kg man or 2.8 L in a 70-kg woman). The ECF is approximately one-third of TBW or 14 L in a 70-kg male. Because the exact percentages are cumbersome to recall, many clinicians accept that the ECF represents roughly 20% of body weight (regardless of gender) with 15% in the interstitial space and 5% in the intravascular space.6 Note that serum electrolytes are routinely measured from the ECF. 

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. 

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. 

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. 

Egress from Intravascular Fluid Compartment into Interstitial... 

Rosenstein M, Ettinghausen SE, Rosenberg SA. Extravasation of intravascular fluid mediated by the systemic administration of recombinant interleukin-2. J Immunol 1986 137 1735-42. 

The aim is to remove the fluid gradually with a maximum weight loss of 0.5 kg/day in the absence of peripheral oedema, or 1.0 kg/day if peripheral oedema is present. Too rapid a diuresis will result in intravascular fluid loss rather than the peripheral oedema. The diuretic should be stopped if the serum sodium falls below 120 mmol/L or if there is a rising serum creatinine. Urinary electrolytes should be monitored to ensure that the spironolactone therapy is effective. The aim is to reverse the sodium/potassium ratio in the urine so that more sodium than potassium is excreted. Most frequent side-effects of spironolactone are those related to its anti-androgenic activity, such as decreased libido, impotence and gynaecomastia in men and menstrual irregularities in women. Other side-effects include hyperkalaemia, uraemia, hyponatraemia and nausea. 

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). 

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. 

Lmge exposures to Lewisite can cause Lewisite shock due to increased capillary membrane permeability and subsequent protein and plasma leakage across the capillary membranes. As a result, patients suffer intravascular fluid loss, hemoconcentration, hypovolemia, and hypotension (8,24). Cutaneous exposures can produce localized edema and pulmonary edema secondary to damage at the alveolm - capillary membrane (8). 

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.

Hypotension Intravascular fluids intravenous sodium bicarbonate consider norepinephrine or dopamine treat hyperthermia, acidosis, seizures, hypokalemia if present... 

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]. 

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