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Chapter 4Hemodynamic Disorders, Thrombosis, and Shock

Edema- Approximately 60% of lean body weight is water. Of that water about 60% of that is in theintracellular "compartment" and about 30% is in the extracellular compartment. Only about 7% is inthe vascular compartment (blood and lymphatic fluid). The intravascular compartment is the mostfluid (no pun intended) and is influenced by several factors. Intracellular water is the least fluid. A

migration of water from the vascular compartment into the extracellular compartment (interstitialspace) creates the clinic sign of edema (swelling of affected body part or parts).

Edema results if the primary hydrostatic pressure is increased (hypertension), if albumins leak out ofthe vessel because of disruption of the semipermeable capillary membrane (resulting in an increase inthe tissue osmotic pressure and decreases the intravscular osmotic pressure), and/or there is aprimary lack of albumin (causing a decreased blood osmotic pressure). Review the vascular events inchapter 2 (you may also find Figures 2-2and 2-3helpful reminders). Table 4-1is a good summaryof the more common causes of edema.

Anasarca: a term used to describe extensive, body-wide, edema.Ascitesis used to describe theretention of fluid within the abdominal cavity.

Subcutaneous edema- somewhat dependent on gravity in its manifestatio n.(Also known asdependent edema) Seen in hypertension and in heart failure (decreased ability of the heart topump causing an increase in the venous blood pressure). May also occur in severe liver disease(where albumins are synthesized) and in renal disease where excess water isn't excreted. Pittingedemais a common sign.Pulmonary edema- major cause is left ventricular heart failure.Cerebral edema- most common causes are infection, trauma, and obstruction of the

ventricular syste m of the brain.

Morphology of edema (Table 4-1) 1. Increase in hydrostatic pressure

Acute pulmonary e demais most common in infections and in high altitude situations("mountain sickness"). Chronic pulmonary edemais usually the result of heart failure (left

ventricular). A cha racteristic finding is the presence of "heart failure cells."These arehemosiderin laden macrophages (hemosiderin from lysis of RBCs that leak out).

2. Reduction of osmotic pressure-causes:Reduced protein synthesis

Mainly in liver disease such as cirrhosis or in protein nutritional deficiencies such

as kwashiorkor .- edema in belly (ascites) due to not able to form albumin!osmotic pressure unbalanced

Increased protein lossRenal diseases such as nephrotic syndromewhere albumin leaks out.

- peeing out albumin even though body makes it

-elephantiasis: edema in legs due to a parasite

3. Lymphatic obstructionLymphedema seen predominantly from infections (filariasis), post surgical

scarring, and other fibroactive reactions (radiation therapy).

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4.Sodium and water retention. Mostly seen in renal diseaseand increased salt intake.

Hyperemia and Congestion- Hyperemia is a active process (certain vascular events take placeto create the edema. Congestion is a passive process, primarily pump (heart) failure or someobstruction reducing return of fluid. Chronic passive congestionseems like a redundantterm; but, it is used to signify a long standing process.Acute hepatic congestion is more

common in infections of the liver (hepatitis). Chronic passive congestion of the liverusuallyresults from fibrosis (cirrhosis) of the liver. The liver has a gross appearance of the cut surface of anutmet and referred to as "nutmeg liver."

- Hyperemia= !in blood flow- An obstruction leads to s luggish blood ak a stasis- Blood stasis!s intervascular pressure which ultimately causes the edema

HEMORRHAGE Hemorrhage is the extravasation of blood from its vessels. Different terms are used to define the extent ofthe extravasation. Hematomais used to describe the accumulation of blood in a tissue or organ. A bruiseis he simplest form of a hematoma (literal translation a "swelling of blood"). This is a generic term.Petechiae is used to describe small, usually multiple, hemorrhages. While there is no magiccut off point, usually they are commonly only a millimeter or two in diameter. Purpurais used todescribe larger hematomas, which can be up to a centimeter or more is size. Ecchymosis describes large

bleeds, usual ly over a couple of centim eters in size.

The coloration of a hematoma changes over time, starting off as a dark red to bluish color. Over the nextfew days, the color changes toward green hues (degradation of bilirubin to biliverdin) and finally to

yellows and browns as a s biliverdin is converte d to hemosiderin.

Bleeds into specific body cavities have specific names. A hemothorax is a chest bleed. A hemarthrosis is a joint bleed. A bleed into the pericardial sac is a hemopericardium .

HEMOSTASIS & THROMBOSISFigure 4-6illustrates the primary steps in hemostasis, a small vascular bleed. Once thrombin isdeposited, you now have a clot ( thrombosis). There are a few key elements in this process, a) injury tothe endothelial lining of the vessel, b) exposure to collagen, activation one or both arms of the coagulationcascade, c) formation of fibrin, and d) lysis of the thrombus.

Endothelium -

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Platelets-

Coagulation Cascade

Fibrinolytic System-

THROMBOSIS Pathogenesis: Virchow's triad(Figure 4-13) illustrates the three components that can lead tothrombosis: a) endothelial injury, b) hypercoagulability) and c) abnormal blood flow(slowing oreddies).

Morphology of ThrombiAntemortem vrs.post-mortem thrombi. Clots before death usually are somewhat uniform in color or

may exhibit accretion lines (like rings in a tree) called lines of Zahn. Clots that form after deathexhibit what is referred to as "chicken fat" thrombi. These are clots that form afterthe red cells havesettled out of "solution" which leaves a thick top layer of clotted serum over a clotted mass of RBCs

which resemb les the color of ch icken fat.Mural thrombi- These are clots that form on the wall of the heart or larger vessels (wall painting -

mural). Common in heart failure where the ventricles have dilated and blood flow is reduced.

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Arterial thrombi - usually occlusive (as in a myocardial infarction).Venous thrombi - phlebothrombosis - usually occlusive. Most frequent site of formation is in the

deep leg veins (above the knee). As a result, they are often long and can cause significant harm. Theseare commonly referred to as "red" thrombi. Fortunately, most emboli are small and frequently gounnoticed (60-80%). The most dangerous are "saddle"thrombi in the lungs. These can produceinstant death (accounts for about 10% of all in hospital deaths).

FATE OF THROMBIPropagation - form more clotsEmbolism- break away and float to some distant site. If large, they can result in death.Organization/recanalization - the clot is replaced by granulation tissue (organization) which may

grow new (albeit smaller) canals through the clot (recanalization).

DIC(disseminated intravascular coagulation).This is a widespread, multi-organ system processusually associated with sepsis or massive necrosis. The net result is a shower of thrombotic events whichconsume the host reserves of coagulation components. This leads to more bleeding and eventual death ifnor treated aggressively. DIC is not a primary disease but combination of processes that lead to the sameresult.

Embolism.A detached intravas cular substance that is insoluble and tr aveling in the blood str eam. 99%come from thrombi (thromboembolism).

Pulmonary Thromboembolism.Most develop in the deep veins of the leg. May cause rightventricular failur e.

Systemic thromboembolism- Arterial emboli. Mostly caused by "seeding" from cardiac muralthrombi or thrombi associated with atherosclerosis.

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Fat embolism- usually associated with trauma (bone breaks - although rarely fatal).Air embolism - usually seen in decompression events (scuba diving - the "bends" or caisson disease-

chronic decompression disease - long term workers in highly pressurized environments).Amniotic fluid - 1:50,000 live births. 80% fatality.

INFARCTION Ischemic necrosis following an occlusive events. 99% arise from thrombi or emboli

TYPESred- lung is classic location (lots of hemorrhage), in organs with dual circulation, and fromre-perfusion.

white- occlusive event in a solid organ - ischemic event.

RESULTScoagulative necrosis - typical ischemic infarction necrosisliquefactive necrosis- commonly seen in the brain (little connective tissue).abscess- bacterial infections in ischemic areas often lead to liquefactive necrosis

FACTORSnature of vascular supply- dual or richly vascularizedrate of occlusion- the slower the better the prognosis - collateral abilitiessusceptibility to hypoxia- neural tissue last only a few minutes in hypoxia. Muscle can last

formany minutes before irreversible damage has occurred.oxygen content of blood- anemia or heart failure

SHOCK

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Table 4-3outlines the three basic types of shock, symptoms and mechanisms of the process. Two othersto be added are neurogenic (brain damage associated) shock and anaphylactic shock. The cascade ofcytokines in septic shock are illustrated in Figure 4-21(which is very similar to the section on cytokinesin chapter 2). Shock is a sudden cardiovascular collapse. (systolic BP less than 50 mm Hg)

hypovolemic shock- in acute situations, it usually requires > 20% blood loss. In chronicbleeds, much more can be lost b efore shock occur s. Most curable of th e forms of shock, es peciallyin the young.cardiogenic shock- heart attack or what ever may throw the heart into ventricular fibrillationseptic shock- common in terminal cancer patients (with large quantities of necrotic tissue) andin mothers with fetal death. Septic and cardiogenic shock have about a 70% mortality each.(about 200,000 cases/year.)

Systems involved- about all. Brain, lungs (usually associated with sepsis), heart, kidney, adrenals, GItract and liver are the primary targets.