Capillary hydrostatic pressure

Glomerular filtration rate (GFR) is the volume of plasma-like fluid that is filtered per unit time across the glomerular capillary membranes to enter the tubular space. Filtrate formation is driven by the net filtration pressure that is equal to the capillary hydrostatic pressure diminished by the sum of capillary oncotic... 

Note that, except for capillary hydrostatic pressure, the magnitude of these forces remains constant throughout the length of the capillary. The capillary hydrostatic pressure decreases steadily as blood flows from the arteriolar end to the venular end of the capillary. The steady decline in this pressure results in filtration of fluid at one end and reabsorption of fluid at the other end of the capillary. 

At the venular end of the capillary, the sum of the pressures forcing fluid out of the capillary is decreased due to the fall in capillary hydrostatic pressure ... 

Bulk flow plays only a minor role in the exchange of specific solutes between blood and tissue cells. A far more important function of bulk flow is to regulate distribution of extracellular fluid between the vascular compartment (plasma) and the interstitial space. Maintenance of an appropriate circulating volume of blood is an important factor in the maintenance of blood pressure. For example, dehydration and hemorrhage will cause a decrease in blood pressure leading to a decrease in capillary hydrostatic pressure. As a result, net filtration decreases and net reabsorption increases, causing movement, or bulk flow, of extracellular fluid from interstitial space into the vascular compartment. This fluid shift expands the plasma volume and compensates for the fall in blood pressure. 

Increased capillary hydrostatic pressure promotes filtration and inhibits reabsorption. As a result, excess fluid is forced out of the capillary into the interstitial space. An increase in capillary pressure is generally caused by an... 

Draw and label the axes and mark a horizontal line at a pressure of 23 mmHg to represent the constant nc. Next draw a line sloping downwards from left to right from 35 mmHg to 15 mmHg to represent the falling capillary hydrostatic pressure (Pc). Area A represents the fluid filtered out of the capillary on the arteriolar side and area B represents that which is reabsorbed on the venous side. Normally these two areas are equal and there is no net loss or gain of fluid. 

Q3 Tissue fluid is formed by capillaries. At the arterial end of the capillary, hydrostatic pressure filters out fluid, without protein or cells, into the tissues. As the blood reaches the venous end of the capillary, the hydrostatic pressure has fallen and the osmotic pressure that is due to the plasma proteins has... 

Pccap = glomerular-capillary hydrostatic pressure IIbc - oncotic pressure in Bowman s capsule Pbc = hydrostatic pressure in Bowman s capsule Ifccap - oncotic pressure in the glomerular capillary... 

Pc = capillary hydrostatic pressure (indirectly estimated in the clinical setting, e.g., pulmonary artery occlusive pressure)... 

Pulmonary edema may result from the failure of any of a number of homeostatic mechanisms. The most common cause of pulmonary edema is an increase in capillary hydrostatic pressure because of left ventricular failure. Excessive fluid administration in compensated and decompensated heart failure patients is the most frequent cause of iatrogenic pulmonary edema. Besides hydrostatic forces, other homeostatic mechanisms that may be disrupted include the osmotic and oncotic pressures in the vasculature, the integrity of the alveolar epithelium, interstitial pulmonary pressure, and the interstitial lymph flow. The edema fluid in cardiogenic pulmonary edema contains a low amount of protein, whereas noncardiogenic pulmonary edema fluid has a high protein concentration. This indicates that noncardiogenic pulmonary edema results primarily from disruption of the alveolar epithehum. The reader is referred to Chap. 28 for a detailed discussion of this topic. 

Angiotensin-converting enzyme inhibitors and nonsteroidal anti-inflammatory drugs are associated with hemodynamically-mediated renal failure, the pathogenesis of which is a decrease in glomerular capillary hydrostatic pressure. 

FIGURE 46-2. Normal glomerular autoregulation serves to maintain intraglomerular capillary hydrostatic pressure, glomerular filtration rate (GFR), and ultimately, urine output. This is accomplished by modulation of afferent and efferent arterioles. Afferent and efferent arteriolar vasoconstriction are primarily mediated by angiotensin II, whereas afferent vasodilation is primarily mediated by prostaglandins. 

The glomerular capillary wall is particularly susceptible to immune-mediated injury. Antigen and antibody tend to localize in the glomerulus, probably because of its high blood flow and capillary hydrostatic pressure. Parenchymal damage can be induced as a result of humoral- and cell-mediated immune reactions (Table 47-1). Antibodies and sensitized T lymphocytes are the primary mediators of glomerular injury. ... 

Edema is clinically detectable in adults when the interstitial volume increases by approximately 2.5 to 3 L, which correlates with a 4- to 4.5-L increase in ECF volume, and a 500 to 600 mEq increase in ECF sodium. Edema develops when excess sodium is retained either as a primary defect in renal sodium excretion, or as a response to a decrease in the EABV despite an already expanded or normal ECF volume. An increase in the capillary hydrostatic pressure because of... 

Blood is returned to the heart via series of veins connecting to the renal vein and then to vena cava. Renal perfusion with nutrients and oxygen is essentially for normal renal functions and this is dependent on adequate renal blood flow. This balance is controlled by several factors, including systemic blood pressure, glomerular capillary hydrostatic pressure, afferent/efferent arteriolar vasoconstriction, edema, plasma total protein and albumin concentration, glomerular ultraflltration rates, and permeability—all of which also will affect the glomerular filtration rate. 

The mechanism of action and the injury potential of lipid mediators are still a matter of debate (Figure 4.3). Malik and co-workers recently reviewed the role of cellular and humoral mediators in pulmonary oedema and concluded that few humoral factors act independently to increase capillary permeability and that these mediators might cause pulmonary venoconstriction and raise pulmonary capillary hydrostatic pressure. This concept is in agreement with results of Shasby et al which demonstrated that leukotriene C4 applied directly to an endothelium monolayer did not accelerate albumin transfer across the monolayer. However, because the culture medium was rich in serum proteins (which avidly bind leukotrienes ), one cannot rule out a direct damaging effect to endothelial cells given access of the molecule to the endothelial cell. 

Edema results from the abnormal accumulation of fluid in the interstitial tissue. Edema may be localized, resulting from local changes in vascular permeability or hydrostatic pressure. Systemic edema is associated with changes in protein or electrolyte content of the body fluids. (The causes of allergic and inflammatory edema are discussed in separate sections.) Obstruction of the lumina of the veins or lymphatics induces changes in capillary hydrostatic pressure or prevents lymphatic drainage [52]. 

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