1. Edema, Hyperemia and Congestion

2. Cardiovascular disease
Most important cause of morbidity and mortality in developed nations
In US, 81 million affected in 2005, causing 35 to 40% of deaths
Components of cardiovascular system include
Heart
Vessels
Blood
Water, salts, proteins, clotting factors, cells

3. Blood Hemodynamics Edema Hyperemia Congestion Shock
Water build-up in interstitial spaces and cavities
Hydrodynamic transudate is dilute, protein-poor
Inflammatory exudate is concentrated, protein rich
Hyperemia
Acute, actively increased blood flow—arteriole dilation, increased heart rate
Tissues look red (erythema)
Congestion
Chronic, passively reduced outflow—venule dilation
Tissues look pale or blue (cyanosis)
Shock
Circulatory failure

4. Fluids—water
This unit addresses factors affecting the distribution between intravascular and interstitial spaces

5. Factors affecting intravascular and interstitial water movement
Concentration of solutes
Albumin and other proteins (huge difference)
Sodium and other ions (small difference)
Hydrostatic pressure
Higher on arteriolar side
Lower on venular side
Lowest in interstitium
Blood volume  decreased b.p.
Water intake/deprivation
Water loss from skin or gut
Perspiration, vomiting, diarrhea
Blood loss; acute hemorrhage

6. Fluid transit
FIGURE 4-1 Factors influencing fluid transit across capillary walls. Capillary hydrostatic and osmotic forces are normally balanced so that there is no net loss or gain of fluid across the capillary bed. However, increased hydrostatic pressure or diminished plasma osmotic pressure will cause extravascular fluid to accumulate. Tissue lymphatics remove much of the excess volume, eventually returning it to the circulation via the thoracic duct; however, if the capacity for lymphatic drainage is exceeded, tissue edema results

7. Edema
Localized or generalized accumulation of fluid in interstitial spaces
Anasarca: severe, generalized edema
ana = throughout, sark = flesh
Most commonly used to describe fetal or neonatal whole-body, subcutaneous swelling
Effusions into body cavities
Hydrothorax: within thorax, around lungs; also pleural effusion
Hydropericardium: Fluid in the pericardial sac
Hydroperitoneum or ascites: Fluid in the peritoneal cavity
Extravasate: (v.) to move out of the vasculature

8. Responses to edema Skin: swells according to elasticity
dependent edema: distribution affected by gravity (ankles, sacrum)
dependent = hanging down in this context
Brain: compresses without room to swell
Lung: alveoli fill preventing gas exchange

9. Appearance of edema
Swollen tissues (not cells—fluid is outside the cells)
Heavy tissues
Wet tissues
Widening of fascial planes or interlobular septa
Filled cavities

10. Causes of edema Increased hydrostatic pressure
Focal impairment—deep vein thrombosis
Generalized impairment—right heart failure
Decreased plasma osmotic pressure
Hypoproteinemia
Decreased protein synthesis—serum albumin
Increased protein loss to nephrotic syndrome
Sodium (and water) retention
Increased capillary permeability
inflammation or injury (burns)
Lymphatic obstruction
Filariasis, breast carcinoma

11. Appearance and causes of hyperemia
Increased flow of blood into tissue
Local process of arteriole dilation greater than venule dilation
Appearance of blood flow is RED
Normal physiological examples:
Exercise
Blushing
Erection
Inflammatory response (rubor)
Small contribution to edema

12. Congestion Impaired venous outflow from tissue
Local increases in venous pressure
Central congestive heart disease increases diastolic (venous) b.p.
Right-side failure congests portal drainage, liver, generalized edema
Left-side failure congests pulmonary drainage, lungs, hypoxemia

13. FIGURE 4-2 Pathways leading to systemic edema from primary heart failure, primary renal failure, or reduced plasma osmotic pressure (e.g., from malnutrition, diminished hepatic synthesis, or protein loss from nephrotic syndrome).

14. Congestive heart failure
Right side failure—volume backs up behind pulmonary circulation
Generalized edema
Portal edema—nutmeg liver
Left side failure—volume backs up behind systemic circulation
Pulmonary edema and pleural effusion
Distension of alveolar capillaries leading to capillary rupture and red cells in alveoli
Intra-alveolar macrophages phagocytose red cells and accumulate hemosiderin
Fibrosis of the interstitium with hemosiderin deposition
Serous or serosanguinous effusions surrounding lungs

15. Congestive heart failure
Reduced cardiac output
Renal hypoperfusion
Activation of renin-angiotensin-aldosterone axis
Early response is beneficial
sodium and water retention increased vascular toneelevated antidiuretic hormone (ADH) improved cardiac outputrestored renal perfusion
Ongoing response increases edema
Volume of blood exceeds volume of vasculature
Fluids build up in tissues

16. Anasarca

17. Hyperemia, injury

18. Trivial and life-threatening edema
This example of a fluid collection, a friction blister of the skin, is an almost trivial example of edema.
This example of edema with inflammation is not trivial at all: there is marked laryngeal edema such that the airway is narrowed. This is life-threatening. Thus, fluid collections can be serious depending upon their location

19. Pitting edema From GRIPE

20. Elephantiasis--lymphedema
From GRIPE
Left: elephantiasis; Right: elephantiasis secondary to carcinoma

21. Peau d’orange and post-mastectomy lymphedema

22. Ascites due to portal congestion
American Gastroenterological Association, AGA Teaching Project, 1975 UI Medical Library call # WI, 720, P8423, 1975
Ascites with "caput madusae" (medusa head), also known as "Cruveilhier-Baumgarten Syndrome". Cirrhosis and portal hypertension sometimes create anastomoses of portal drainage with the umbilical vein. Also note protrusion of the naval from abdominal pressure.

23. Nutmeg liver
Here is an example of a "nutmeg" liver seen with chronic passive congestion of the liver. Note the dark red congested regions that represent accumulation of RBC's in centrilobular regions. Microscopically, the nutmeg pattern results from congestion around the central veins, as seen here. This is usually due to a "right sided" heart failure.

24. Hepatic congestion
If chronic hepatic passive congestion continues for a long time, a condition called "cardiac cirrhosis" may develop in which there is fibrosis bridging between central zonal regions, as shown below, so that the portal tracts appear to be in the center of the reorganized lobule. This process is best termed "cardiac sclerosis" because, unlike a true cirrhosis, there is minimal nodular regeneration.
If the passive congestion is pronounced, then there can be centrilobular necrosis, because the oxygenation in zone 3 of the hepatic lobule is not great. The light brown pigment seen here in the necrotic hepatocytes around the central vein is lipochrome.

25. Effusions
Extravascular fluid collections can be classified as follows:
Exudate: extravascular fluid collection that is rich in protein and/or cells. Fluid appears grossly cloudy.
Transudate: extravascular fluid collection that is basically an ultrafiltrate of plasma with little protein and few or no cells. Fluid appears grossly clear.
Effusions into body cavities can be further described as follows:
Serous: a transudate with mainly edema fluid and few cells.
Serosanguinous: an effusion with red blood cells.
Fibrinous (serofibrinous): fibrin strands are derived from a protein-rich exudate.
Purulent: numerous PMN's are present. Also called "empyema" in the pleural space.

26. Pleural effusions and edema
This is a right pleural effusion (in a baby). Note the clear, pale yellow appearance of the fluid. This is a serous effusion.
Here is an example of bilateral pleural effusions. Note that the fluid appears reddish, because there has been hemorrhage into the effusion. This is a serosanguinous effusion.

27. Fibrinous exudate Fibrinous exudate of pericardium

28. Pleural effusion

29. Pleural effusion

30. Pulmonary edema http://peir.path.uab.edu:3555/images/med/00011603.jpg

31. Dilated lymphatic vessels