Principles Of Fluid Balance

Front 1

Anasarca

Back 1

An accumulation of serous fluid in various tissues and cavities of the body. (a generalized massive edema)

Front 2

Ascites

Back 2

The accumulation of fluid in the peritoneal cavity, causing abdominal swelling.

Front 3

Brown Induration

Back 3

Brown induration is fibrosis and hemosiderin pigmentation of the lungs due to long standing pulmonary congestion (chronic passive congestion)

Front 4

Congestion

Back 4

excessive accumulation of blood or other fluid in a body part

Front 5

Cyanosis

Back 5

A bluish discoloration of the skin resulting from poor circulation or inadequate oxygenation of the blood

Front 6

Diapedesis

Back 6

The passage of blood cells through the intact walls of the capillaries, typically accompanying inflammation

Front 7

Dyspnea

Back 7

Difficult or labored breathing

Front 8

Edema

Back 8

A condition characterized by an excess of watery fluid collecting in the cavities or tissues of the body

Front 9

Effusion

Back 9

An escape of fluid into a body cavity

Front 10

Erythema

Back 10

Superficial reddening of the skin, usually in patches, as a result of injury or irritation causing dilatation of the blood capillaries

Front 11

Exudate

Back 11

A mass of cells and fluid that has seeped out of blood vessels or an organ, esp. in inflammation (protein rich)

Front 12

Heart failure cells

Back 12

Heart failure cells are hemosiderin-containing macrophages in the alveoli. The main causes are left heart failure and chronic pulmonary edema.

Front 13

Hydrostatic pressure

Back 13

The pressure equivalent to that exerted on a surface by a column of water of a given height

Front 14

Hyperemia

Back 14

An excess of blood in the vessels supplying an organ or other part of the body

Front 15

Nutmeg liver

Back 15

In hepatology, congestive hepatopathy, also known as nutmeg liver and chronic passive congestion of the liver, is liver dysfunction due to venous congestion, usually cardiac dysfunction, i.e. right heart failure or (less specifically) congestive heart failure.

Front 16

Oncotic pressure

Back 16

Oncotic pressure, or colloid osmotic pressure, is a form of osmotic pressure exerted by proteins in blood plasma that usually tends to pull water into the circulatory system.

Front 17

Orthopnea

Back 17

form of dyspnea in which the person can breathe comfortably only when standing or sitting erect; associated with asthma and emphysema and angina pectoris

Front 18

Osmotic pressure

Back 18

The pressure that would have to be applied to a pure solvent to prevent it from passing into a given solution by osmosis, often used to express the concentration of the solution

Front 19

Rales/crackles

Back 19

An abnormal rattling sound heard when examining unhealthy lungs with a stethoscope

Front 20

Transudate

Back 20

Transudate is extravascular fluid with low protein content and a low specific gravity (< 1.012). It has low nucleated cell counts (less than 500 to 1000 /microlit) and the primary cell types are mononuclear cells: macrophages, lymphocytes and mesothelia cells. For instance, an ultrafiltrate of blood plasma is transudate. It results from increased fluid pressures or diminished colloid oncotic forces in the plasma .

Front 21

Describe the physiologic processes responsible for maintaining normal fluid balance.

Back 21

The normal exchange of fluid b/t plasma and interstitial tissues is dependent on opposing forces which are fairly well balanced. The hydrostatic pressure of the intravascular space in combination w/ the osmotic pressure of the interstitial space (primarily influenced by the sodium content) causes fluid to leave the vasculature and enter the interstitial space. The opposing force is the oncotic pressure of the intravascular fluid (primarily influenced by the albumin content of the plasma) which draws water back into the vasculature. Under normal conditions, on the arterial side of the vascular bed, the hydrostatic pressure is greater than the oncotic pressure and fluid is transferred from the vasculature to the interstitial space. As fluid leaves the vasculature, however, the hydrostatic pressure falls while the oncotic pressure rises due to the increasing concentration of plasma albumin. On the venous side of the vascular bed, oncotic pressure becomes greater than the hydrostatic pressure and fluid is therefore drawn back into the vasculature. Any excess fluid remaining in the interstitial tissue is borne off by the lymphatic channels and ultimately returned to the intravascular space via the thoracic duct. Any alteration of the factors that control this equilibrium can lead to interstitial edema.

Front 22

Describe the mechanisms by which the physiologic processes that maintain normal fluid balance may be altered, and discuss the clinical consequences of altering those processes.

Back 22

1. Increased Osmotic pressure of the Interstitial Fluid – An increase in total body sodium due to excessive salt intake, increased renal tubular sodium absorption, decreased renal tubular sodium excretion, or reduced renal perfusion can lead to a generalized edema.

2. Decreased Oncotic Pressure of the Plasma Portio – A decrease in serum albumin may also produce a generalized edema. This may be due to a failure of albumin synthesis or excessive albumin loss.

3. Increased Hydrostatic Pressure of the Intravascular Fluid – This leads to a localized edema and usually involves increased hydrostatic pressure on the venous side of the vascular bed resulting from interference w/ or obstruction to venous blood flow.

4. Obstruction of Lymphatic Drainage (Lymphedema) – This also produces a localized edema and is usually the result of lymphatic obstruction by cancer, scarring, parasite disease, or lymphadenectomy.

5. Increased Endothelial Permeability – This produces a localized edema and is the result of inflammation, immunologic reactions, or other tissue injury.

Front 23

Compare and contrast intracellular and interstitial edema, and discuss the clinical significance of each

Back 23

Intracellular edema is generally a reflection of cellular injury and altered cell membrane permeability, interstitial edema reflects either a disturbance in the normal hemodynamic forces that control fluid transfer b/t the vascular and intravascular space, or it indicates endothelial injury and increased vascular permeability. Interstitial edema may be confined to a localized area or it may be a diffuse process involving all tissues of the body (anasarca).

Front 24

Given a clinical situation, be able to discuss possible mechanisms underlying the development of interstitial edema.

Back 24

pulmonary edema diffuse extravascular accumulation of fluid in the tissues and air spaces of the lung due to changes in hydrostatic forces in the capillaries or to increased capillary permeability. It is most often symptomatic of left ventricular heart failure, but can also be a complication of mitral stenosis, aortic stenosis, altitude sickness, acute hypertension, volume overload during intravenous therapy, or reduced serum oncotic pressure, as in patients who have nephrosis, cirrhosis, or hypoalbuminemia.

Front 25

Compare and contrast transudate and exudates in terms of etiology, key features, and clinical significance.

Back 25

Transudate is a protein-poor fluid which has a specific gravity. It develops from imbalances in the normal hemodynamic forces and is frequently seen w/ congestive heart failure, liver disease, renal disease, and GI disorders. Exudate is a protein-rich fluid which has a specific gravity. It is generally the result of endothelial damage and alteration of vascular permeability and is seen with inflammatory/immunologic disorders.

Front 26

Compare and contrast vascular congestion and hyperemia in terms of mechanisms of development and clinical significance.

Back 26

Vascular congestion is a decreased blood flow in veins, venules, and capillaries usually due to impaired venous drainage. Clinically, it results in a bluish discoloration of tissue (cyanosis) due to accumulation of reduced hemoglobin. Since impaired venous drainage also leads to increased hydrostatic pressure, edema is a common accompaniment of congestion. While acute congestion does not produce any permanent tissue changes, chronic congestion may lead to sufficient impaired tissue oxygenation that there is tissue necrosis and subsequent fibrosis. The effects of chronic congestion are most often seen in the liver, lungs, and spleen. Vascular hyperemia refers to increased blood flow through dilated arteries, arterioles, and capillary beds. Clinically, this results in increased warmth and redness in affected tissue. Basically, hyperemia is an active, reflexive mechanism designed to allow greater flow to areas of inflammation, to tissues needing more oxygen, or as a mechanism of heat dissipation. When associated w/ inflammation, hyperemia is followed by localized edema resulting from increased vascular permeability.

Hyperemia is increased blood flow to an organ, resulting in increased blood content. This happens when the arterioles have dilated more than its venules have dilated. Examples are blushing, erections, reddening of skin to disperse heat, and "rubor" of acute inflammation. Congestion is decreased blood flow from an organ, resulting in increased blood content. This happens when something is interfering with the organ's venous drainage.

Front 27

Discuss the physiologic effects and resultant clinical signs and symptoms of left-sided heart failure

Back 27

Failure of the left side of the heart to pump sufficient blood.
The common causes of left-sided failure
Ischemia (old or recent myocardial infarct, ischemic muscle disease)
Aortic or mitral valve disease
Systemic hypertension
Myocardial disease
The common effects of left-sided failure
• Dyspnea (from pulmonary edema and total-body hypoxia)
First, on exertion
Later, paroxysmal nocturnal dyspnea ("cardiac dyspnea"); on lying down for a while, fluid redistributes itself in the body, resulting in pulmonary edema. I think that the reason that it's paroxysmal (i.e., comes on all of a sudden) is that as the lungs become heavier (i.e., congestion, maybe edema) their weight presses on the pulmonary veins which in turn makes them more congested. Patients may throw the windows open at night, or learn to sleep on various numbers of pillows; you the physician will hear rales; the pathologist may see "brown induration" and hemosiderin-laden "heart failure" macrophages; remember these?
• Cough ("from the left atrium pushing on the bronchus"; this is common in mitral valve disease even in the absence of failure; why?)
• Prerenal azotemia
• Hypoxic encephalopathy
• Sodium overload and systemic dependent edema (from hypoperfused kidneys; these patients may also have nocturia; why do you think?)

Front 28

Discuss the physiologic effects and resultant clinical signs and symptoms of right-sided heart failure

Back 28

Failure of the right side of the heart to pump enough blood. As you'd expect, the right ventricle and atrium will usually be hypertrophied and dilated.
The common causes of right-sided failure
Pulmonary emboli (acute or chronic)
Any disease interfering with lung ventilation
Emphysema
Cystic fibrosis
Most others
NOTE: The mechanism, of course, is increased pulmonary vascular resistance (due to fibrosis and/or the hypoxic vascular response)
Left-sided heart failure!
Cardiac defects with left-to-right shunts
The effects of right-sided failure
Splanchnic congestion
Jugular venous distention (look carefully)
Total-body dependent edema (from increased venous hydrostatic pressure, etc.)
Effusions (transudates, of course; notably pleural, notably more on the right side than on the left; why?)
NOTE: "Cardiac cirrhosis" of the liver, often discussed in textbooks as the result of right-sided failure, almost never happens. The one time you might see it is in longstanding, severe tricuspid insufficiency, with or without right-sided failure

Front 29

Describe the effects of primary pulmonary hypertension on the pulmonary vasculature

Back 29

Primary pulmonary hypertension causes an increase in vascular resistance resulting from vascular obstruction or obliteration, vasoconstriction, or increased flow.

Front 30

Compare and contrast primary pulmonary hypertension and secondary pulmonary hypertension in terms of etiology, clinical signs and symptoms, and clinical course

Back 30

Primary pulmonary hypertension is mostly a disease of young women. Prolonged vasoconstriction of the pulmonary vessels, induced by hypersensitivity to neurohormonal regulators, produces marked thickening of the small arteries and arterioles w/ smooth muscle hypertrophy of the media, reduplication of the elastic lamina, and intimal thickening and fibrosis. Intralumenal webs (plexiform lesions) in small arterioles are considered diagnostic hallmarks.

Secondary pulmonary hypertension is far more common and occurs in patients w/ known underlying conditions that increase pulmonary vascular pressures or resistance (congestive heart failure, primary pulmonary disease, recurrent emboli, left-to-right shunts, etc.)

Front 31

Compare and contrast acute and chronic congestion of the lungs and describe its effect on involved tissue and clinical significance

Back 31

Acute congestion is reflected by engorgement of hepatic central veins and sinusoids. Chronic congestion of the central veins and sinusoids, however, results in hypoxia and atrophy of centrilobular hepatocytes and fatty change of peripheral periportal hepatocytes. This imparts a mottled red-brown and yellow-tan gross appearance known as “nutmeg liver”. Long standing chronic congestion may induce a centrilobular fibrosis known as cardiac sclerosis.

Front 32

List the major causes of chronic passive congestion of the lungs and describe its effects in terms of morphologic changes and clinical signs and symptoms

Back 32

Etiology of passive congestion of the lung : chronic left heart (ventricular) failure.
Alveolar walls are thickened due to dilated capillaries. Alveolar lumens are filled with transudate (amorphous, eosinophilic and homogenous) which replaced the air, red blood cells (microhemorrhages) and hemosiderin-laden macrophages (also called "heart failure cells"). (H&E, ob. x20)
With progression, interstitial fibrosis may appear and, together with hemosiderin pigmentation, generates the aspect of "brown induration". Extensive fibrosis leads to intrapulmonary hypertension.

Front 33

List the major causes of chronic congestion of the liver and describe its effects in terms of morphologic changes and clinical signs and symptoms

Back 33

Hepatic injury may result in decreased synthesis of plasma protein, increased hydrostatic pressure and pooling of blood in portal venous circulation, hepatic lymphatic obstruction. (cirrhosis, hepatocellular damage)