Robbins Basic Pathology / Основи на Патологията на Робинс: 4. Hemodynamic Disorders, Thromboembolism, and Shock

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The health of cells and tissues depends on the circulation of blood, which delivers oxygen and nutrients and removes wastes generated by cellular metabolism. Under normal conditions, as blood passes through capillary beds, proteins in the plasma are retained within the vasculature and there is little net movement of water and electrolytes into the tissues. This balance is often disturbed by patho- logic conditions that alter endothelial function, increase vascular hydrostatic pressure, or decrease plasma protein content, all of which promote edema—the accumulation of fluid in tissues resulting from a net movement of water into extravascular spaces. Depending on its severity and location, edema may have minimal or profound effects. In the lower extremities, it may only make one’s shoes feel snugger after a long sedentary day; in the lungs, however, edema fluid can fill alveoli, causing life-threatening hypoxia.


The structural integrity of blood vessels is frequently compromised by trauma. Hemostasis is the process of blood clotting that prevents excessive bleeding after blood-vessel damage. Inadequate hemostasis may result in hemorrhage, which can compromise regional tissue perfusion and, if massive and rapid, may lead to hypotension, shock, and death. Conversely, inappropriate clotting (thrombosis) or migration of clots (embolism) can obstruct blood vessels, potentially causing ischemic cell death (infarction). Indeed, thromboembolism lies at the heart of three major causes of morbidity and death in developed countries: myocardial infarction, pulmonary embolism (PE), and cerebrovascular accident (stroke).


With this as a preface, we begin our discussion of hemodynamic disorders with conditions that increase tissue blood volumes.




Hyperemia and congestion both refer to an increase in blood volume within a tissue, but have different underly- ing mechanisms. Hyperemia is an active process resulting from arteriolar dilation and increased blood inflow, as occurs at sites of inflammation or in exercising skeletal muscle. Hyperemic tissues are redder than normal because of engorgement with oxygenated blood. Congestion is a passive process resulting from impaired outflow of venous blood from a tissue. It can occur systemically, as in cardiac failure, or locally as a consequence of an isolated venous obstruction. Congested tissues have an abnormal blue-red color (cyanosis) that stems from the accumulation of deoxy- genated hemoglobin in the affected area. In long-standing chronic congestion, inadequate tissue perfusion and per- sistent hypoxia may lead to parenchymal cell death and secondary tissue fibrosis, and the elevated intravascular pressures may cause edema or sometimes rupture capillar- ies, producing focal hemorrhages.




Cut  surfaces  of  hyperemic  or  congested  tissues  feel  wet  and 


typically ooze blood. On microscopic examination, acute pul- monary congestion  is  marked  by  blood-engorged  alveolar  capillaries  and  variable  degrees  of  alveolar  septal  edema  and  intraalveolar hemorrhage. In chronic pulmonary congestion,  the septa become thickened and fibrotic, and the alveolar spaces  contain numerous macrophages laden with hemosiderin (“heart  failure  cells”)  derived  from  phagocytosed  red  cells.  In  acute hepatic congestion,  the  central  vein  and  sinusoids  are  dis- tended with blood, and there may even be necrosis of centrally  located hepatocytes. The periportal hepatocytes, better oxygen- ated because of their proximity to hepatic arterioles, experience  less severe hypoxia and may develop only reversible fatty change.  In  chronic passive congestion of the liver,  the  central  regions of the hepatic lobules, viewed on gross examination, are  red-brown and slightly depressed (owing to cell loss) and are  accentuated against the surrounding zones of uncongested tan,  sometimes fatty, liver (nutmeg liver) (Fig. 4.1A). Microscopic  findings include centrilobular hepatocyte necrosis, hemorrhage,  and hemosiderin-laden macrophages (Fig. 4.1B).


Fig. 4.1  Liver with chronic passive congestion and hemorrhagic necrosis.  (A) In this autopsy specimen, central areas are red and slightly depressed  compared  with  the  surrounding  tan  viable  parenchyma,  creating “nutmeg  liver”  (so  called  because  it  resembles  the  cut  surface  of  a  nutmeg).  (B)  Microscopic preparation shows centrilobular hepatic necrosis with hemor- rhage and scattered inflammatory cells. (Courtesy of Dr. James Crawford.)




Approximately 60% of lean body weight is water, two- thirds of which is intracellular. Most of the remaining water is found in extracellular compartments in the form of interstitial fluid; only 5% of the body’s water is in blood plasma. As noted earlier, edema is an accumulation of interstitial fluid within tissues. Extravascular fluid can also collect in body cavities and such accumulations are often referred to collectively as effusions. Examples include effu- sions in the pleural cavity (hydrothorax), the pericardial cavity (hydropericardium), or the peritoneal cavity (hydro- peritoneum, or ascites). Anasarca is severe, generalized edema marked by profound swelling of subcutaneous


tissues and accumulation of fluid in body cavities.


Table 4.1 lists the major causes of edema. The mecha- nisms of inflammatory edema are largely related to increased vascular permeability and are discussed in Chapter 3; the noninflammatory causes are described in the following discussion.


Fluid movement between the vascular and interstitial spaces is governed mainly by two opposing forces—the vascular hydrostatic pressure and the colloid osmotic pres- sure produced by plasma proteins. Normally, the outflow of fluid produced by hydrostatic pressure at the arteriolar end of the microcirculation is nearly balanced by inflow at the venular end owing to slightly elevated osmotic pres- sure; hence there is only a small net outflow of fluid into the interstitial space, which is drained by lymphatic vessels. Either increased hydrostatic pressure or diminished colloid osmotic pressure causes increased movement of water into the interstitium (Fig. 4.2). This in turn increases the tissue’s hydrostatic pressure, and eventually a new equilibrium is achieved. Excess edema fluid is removed by lymphatic drainage and is returned to the bloodstream by way of the thoracic duct (Fig. 4.2).


The edema fluid that accumulates in the setting of increased hydrostatic pressure or reduced intravascular colloid typically is a protein-poor transudate; by contrast, because of increased vascular permeability, inflammatory edema fluid is a protein-rich exudate with a high specific gravity. The usual cutoffs for specific gravity (<1.012 for transudates and >1.020 for exudates) illustrate the point but are not clinically useful. We will now discuss the various causes of edema.


Table 4.1 Causes of Edema


Increased Hydrostatic Pressure


Impaired Venous Return


Congestive heart failure


Constrictive pericarditis


Ascites (liver cirrhosis)


Venous obstruction or compression




External pressure (e.g., mass)


Lower extremity inactivity with prolonged dependency


Arteriolar Dilation




Neurohumoral dysregulation


Reduced Plasma Osmotic Pressure (Hypoproteinemia)


Protein-losing glomerulopathies (nephrotic syndrome)


Liver cirrhosis (ascites)




Protein-losing gastroenteropathy


Lymphatic Obstruction










Sodium Retention


Excessive salt intake with renal insufficiency


Increased tubular reabsorption of sodium


Renal hypoperfusion


Increased renin-angiotensin-aldosterone secretion




Acute inflammation


Chronic inflammation




Data from Leaf A, Cotran RS: Renal pathophysiology, ed 3, New York, 1985, Oxford 


University Press, p 146.


Fig. 4.2  Factors influencing fluid movement across capillary walls. Capillary 


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