Hemodynamic Aspects of Edema Formation

Approximately one-third of the total body water content is confined to the extracellular space. This compartment is composed of the plasma volume, which under normal circumstances comprises 25 percent of the extracellular space, and the remainder is interstitial fluid. Sodium content governs the total fluid volume in both intravascular and interstitial compartments while plasma proteins (mainly albumin) govern the partitioning between these two compartments. The main regulatory hemodynamic mechanism that controls the disposition of fluid between the intravascular and interstitial compartments contains two sets of opposing forces known as Starling forces [2]. The Starling principle provides a framework for analyzing fluid movement across capillaries. Thus, the direction and rate of fluid movement are determined by the balance between the hydraulic and osmotic pressures of the intravascular and interstitial compartments. The Starling equation may be expressed as follows:

where Qf = rate of fluid movement across capillaries; Kf = filtration coefficient; Pc = capillary hydraulic pressure; P; = interstitial hydraulic pressure; pc = plasma osmotic pressure; and pc = interstitial osmotic pressure. Hence, according to the Starling equation, the hydraulic pressure within the vascular system and the colloid osmotic pressure in the interstitial fluid promote the movement of fluid from the circulation toward the extracellular space. In contrast, the hydraulic pressure of the interstitial fluid and the intravas-cular colloid osmotic pressure produced by the plasma proteins tend to drive fluid back into the vascular system. Thus, any change in any one of these driving forces may alter the direction of fluid movement from one compartment to the other [3]. These forces are usually delicately balanced, resulting in a volume steady state between the intravascular and the extravascular compartments. At the arteriolar end of the microcirculation the hydraulic pressure (about 32mmHg) is higher than the colloid oncotic pressure (25mmHg) such that the prevailing balance of Starling forces favors the net filtration of fluid into the interstitium. Net outward movement of fluid along the length of the capillary is associated with an axial decrease in the capillary hydraulic pressure and an increase in the plasma colloid osmotic pressure. Thus, at the venular end of the capillary the intravascular hydraulic pressure (about 12mmHg) is lower than the colloid osmotic pressure, favoring movement of fluid back to the circulation. Nevertheless, in several tissues the local transcapillary hydraulic pressure gradient continues to exceed the opposing colloid osmotic pressure gradient throughout the length of the capillary bed, such that filtration occurs along its entire length. In such capillary beds, a substantial volume of filtered fluid must therefore be returned to the circulation via lymphatics. Given this importance of lymphatic drainage in this situation, the ability of lymphatics to expand and proliferate and the ability of lymphatic flow to increase in response to increased interstitial fluid formation provide protective mechanisms for minimizing edema formation.

Other mechanisms for minimizing edema formation even under normal conditions have also been identified [4]. A rise in the venous pressure causes myogenic arteriolar constriction that will lower capillary pressure and decrease capillary surface area. Precapillary vasoconstriction tends to lower capillary hydrostatic pressure and diminish the filtering surface area in a given capillary bed. Indeed, excessive pre-capillary vasodilatation in the absence of appropriate microcirculatory myogenic reflex regulation appears to account for lower extremity interstitial edema associated with calcium blocker vasodilator therapy. Increased net filtration itself is associated with dissipation of capillary hydraulic pressure, dilution of interstitial fluid protein concentration, and a corresponding rise in intracapillary plasma protein concentration. The resulting change in the profile of Starling forces associated with increased filtration therefore tends to mitigate against further interstitial fluid accumulation. Furthermore, even small increases in interstitial fluid volume tend to augment tissue hydraulic pressure, again opposing further transudation of fluid into the interstitial space. Finally, as tissue pressure increases, the lymphatic network is widely opened, allowing the return of large volumes of fluid to the microcirculation. Therefore, it is evident that maintenance of adequate steady state between fluid volumes of the circulation and the interstitial space depends on the delicate balance among the microcirculatory hydraulic pressure, the level of plasma proteins, and the adequacy of the lymphatic drainage system.

The appearance of generalized edema implies one or more disturbances in the microcirculatory hemodynamics associated with expansion of the extracellular volume. There are multiple factors that may affect hemodynamic stability, such as increased venous pressure transmitted to the capillary bed, unfavorable adjustments in pre- and postcap-illary resistances, reduced plasma colloid osmotic pressure, renal sodium retention, or lymphatic flow inadequate to drain the interstitial compartment and replenish the intravas-cular compartment. All of these factors may shift the Starling forces toward increased movement of fluids to the extracellular space and hence promote the formation of edema (Figure 1A).

Increased Hydraulic Pressure

An increase in the hydraulic pressure at the venular end of the microcirculation raises the capillary filtration pressure resulting in increased movement of transudate to the interstitial compartment. In clinical practice, this mechanism of edema formation is most commonly seen in congestive heart failure. When primarily right ventricular function is affected, the distribution of the edema is systemic, involving all body tissues. In contrast, decreased left ventricular function results in increased venous pressure that primarily affects the lungs. The factors leading to edema in congestive heart failure, however, are far more complex [5]. The decrease in cardiac output results in a decrease in the effective arterial blood volume. This in turn decreases renal blood flow, which triggers the renin-angiotensin-aldosterone axis in a compensatory attempt to increase the effective arterial blood volume through increased sodium and water retention in the kidney. In addition, reduction in the arterial renal blood flow leads to renal vasoconstriction with a marked reduction in the glomerular filtration rate. The direct consequence of the glomerular hemodynamic alterations is an increase in the fractional reabsorption of filtered sodium and water at the level of the proximal tubule. At the same time there is increased secretion of arginine vasopressin (AVP). The stimulus for increased AVP secretion in congestive heart failure appears to involve a nonosmotic drive such as attenuated compliance of the left atrium, hypotension, and activation of the renin-angiotensin system. The net effect at the kidney level is again enhanced water retention, this time at the distal nephron. The resultant increase in plasma volume from all of these compensatory mechanisms increases significantly the venous hydraulic pressure, which in turn imposes a further burden on the

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Essentials of Human Physiology

Essentials of Human Physiology

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