الفهرس 
The Physiology of Fluid CompartmentsOnly 14 pages are availabe for public view
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Abstract
Water makes up 50-75 % of the body mass. The water compartment is divided into intracellular fluid and extracellular fluid. TBW is the solvent for most of the solutes in the body, and it is assumed that water moves freely between the intracellular fluid and extracellular fluid in an effort to equalize the concentration of solutes within each space.
The intracellular compartment contains about two-third of TBW and the remaining is held in the extracellular compartment. The extracellular compartment is further subdivided into the interstitial and the intravascular compartments (blood volume), which contain two-thirds and one-third of the extracellular fluid, respectively.
There are many fluids available for intravenous administration. They are normally categorized as crystalloids or colloids. All fluids cause an initial expansion of the intravascular compartment. The duration of this effect depends on how freely the fluid can move across the vascular endothelium.
Crystalloids freely distribute across the vascular barrier. Only one fifth of the intravenously infused amount remains intravascularly. A fourfold amount of crystalloid infusion is needed to reach comparable volume effects as achieved with colloid administration.
Volume expansion, in an effort to improve CO and augment tissue perfusion, is a common therapeutic goal in the hemodynamically unstable patient. Volume expansion is not without adverse effects, including pulmonary edema, worsening gas exchange, and hyperchloremic acidosis. It has been shown that not all patients in circulatory collapse respond to volume with improved cardiac function. Moreover, patients with capillary leak may have total body volume overload and yet still benefit from augmented intravascular volume. Discriminating between patients who will benefit from volume expansion and those for whom an inotrope or vasopressive agent will better augment perfusion can limit the adverse effects of volume overload.
CVP and PAOP have traditionally been used to estimate preload and intravascular volume status. These pressure-derived preload values, or filling pressures, have been central to the management of fluid resuscitation and titration; however, numerous studies have challenged the notion that these indicators accurately predict volume status. In fact, more than a dozen studies that examined various patient populations (sepsis, perioperative cardiovascular surgery, trauma, and other critical illnesses) all failed to demonstrate a correlation among CVP/PAOP, volume status, and cardiac performance.
The Frank-Starling mechanism means that within physiologic limits the greater the cardiac muscle is stretched during filling, the greater is the force of contraction and the volume of blood pumped into the aorta. The shape of the Frank-Starling relationship is curvilinear. The initial part of the curve is called the steep portion and the second part is called the plateau.
Pressure-derived preload values do not identify a position of or place on the Starling curve and, therefore, poorly predict whether volume will improve hemodynamics. For example, a low CVP might prompt the clinician to give a fluid bolus; however, because of the patient’s position on the curve, volume will not result in an increase in the CO and may even result in pulmonary edema. Conversely, a patient can have “high” filling pressures yet still be on the vertical portion of the curve. Traditionally, an elevated CVP or PAOP would trigger an order to diurese, when, in actuality, the patient’s physiology would benefit from volume enhancement.
CVP and PAOP are also poor indicators of cardiac preload because they fail to reflect cardiac volume in the setting of reduced ventricular compliance. A noncompliant, “stiff” heart may generate high filling pressures even in the setting of underfilled ventricles. The CVP or PAOP may be elevated, yet the patient’s CO would improve with volume infusion. Finally, external forces, including PEEP, abdominal pressures, and vascular compliance, alter the relationship between filling pressures and end diastolic volume.
Additional parameters that have proved to be moderately useful in quantifying intravascular volume status include left ventricular end diastolic volume and area determined by echocardiogram. Although these cardiac dimensions are more direct assessments of intravascular volume, they still have limited ability to predict whether changes in preload will affect hemodynamics. Cardiomyopathy, valvular disease, and echocardiogram variability adversely affect the reliability of these measurements.
In contrast to PAOP, CVP, and cardiac dimensions, the so called “static” markers, “dynamic” markers are those that use variations in either SV or arterial pressure because the physiologic effects of respiratory variation more reliably predict volume responsiveness. In patients who are on positive pressure mechanical ventilation, inspiration causes a reduction in right ventricular preload as a result of compression of the vena cava, whereas right ventricular afterload is increased because of increased alveolar pressures. The result is a reduction in right ventricular ejection during inspiration. Because of the transit time of blood flow from the right to the left side of the heart, a fall in SV and blood pressure is seen during expiration.
Because the hemodynamic effects that are induced by mechanical ventilation are exaggerated in the hypovolemic patient, the greater the variation, the more likely the patient’s hemodynamics will improve with volume. These dynamic markers can be seen at the bedside as variations in arterial pressure (SPV), pulse pressure (PPV), or stroke volume (SVV).
There are some limitations to the use of dynamic markers. For example, dynamic parameters are affected by varying tidal volumes and therefore require a well-sedated, mechanically ventilated patient to ensure accuracy. Arrhythmias, particularly atrial fibrillation, will also affect the precision of SVV analyses. Finally, alterations in myocardial contractility as a result of titration of inotropic or vasopressive agents can affect the accuracy of these dynamic markers.
Because tissue hypoxia is a key trigger for organ dysfunction, adequacy of DO2 to tissue oxygen metabolic demand is essential during the perioperative period. Optimization of DO2, using either or both fluid loading and inotropic support, to prevent tissue hypoxia in relation to increased VO2, could improve outcome. In this context, the use of ScvO2 which reflects important changes in the DO2/VO2 relationship to address adequacy of oxygen utilization, has shown promising results.