fluid and hemodynamics review manual

8/11/2019 Fluid and Hemodynamics Review Manual

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FLUID AND HEMODYNAMICS DERANGEMENTS

TERMINAL OBJECTIVES

Once this section is completed, each student should be able to perform the

following tasks.

1. Give the identifying feature and distinguish between active hyperemia,congestion and hemorrhage on the basis of causative mechanisms, grosslesions, microscopic findings and prognosis.

2. Briefly outline the manner in which heart lesions may lead to passivecongestion of the lungs, passive congestion of the liver, lung infarction, kidneyinfarction, ischemia or the myocardium, generalized edema and shock.

. !iscuss the causes, types, significance and fate of hemorrhage.

". !iscuss the interrelationship between thrombi, emboli and ischemia in theformation of renal infarction, beginning with a lesion in the left atrium of theheart.

#. !iscuss the role of platelets, components of the blood vessel wall and theclotting se$uence in normal hemostasis.

%. &ist and describe the factor which predisposes to thrombosis. !ifferentiatebetween a thrombus and a postmortem clot on the basis of gross andmicroscopic findings.

'. Give the identifying feature of "disseminated intraas!#ar !$a%#ati$n"and e(plain why bleeding tendencies are induced by this condition.

). Briefly discuss the causes and effects of pulmonary and systemicembolism.

*. Briefly outline the manner in which red and pale infarcts develop in variousorgans and+or tissues.

1. !iscuss the causative mechanisms of generalized and localized edema.

11. !iscuss the manner by which a loss of blood volume and the pooling ofblood in capillary beds may induce shock

12. -rovide appropriate answers for the postinstructional selfe(amination$uestions outlined at the end of this section.

AN OVERVIE&


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/t this point, the student understands the ways in which normal and abnormalcells accumulate a variety of products.

Remember,the gamut of cellular changes discussed in thepreceding sections will be encountered over and over again

throughout all subsequent considerations of disease states.

0n this section, lesions related to circulatory disturbances are considered. ostlesions that develop in the body are influenced directly or indirectly by the bloodand+or blood vessels. hose circulatory disturbances common to many types oflesions include hemorrhage, hyperemia, congestion, ischemia, thrombosis,embolism, infarction, edema, shock and disseminated intravascular coagulation.

TERMINAL OBJECTIVES

Once this section is completed, each student should be able to perform the

following tasks.

1. Give the identifying feature and distinguish between active hyperemia,

congestion and hemorrhage on the basis of causative mechanisms, grosslesions, microscopic findings and prognosis.

2. Briefly outline the manner in which heart lesions may lead to passive

congestion of the lungs, passive congestion of the liver, lung infarction,kidney infarction, ischemia or the myocardium, generalized edema andshock.

. !iscuss the causes, types, significance and fate of hemorrhage.

". !iscuss the interrelationship between thrombi, emboli and ischemia in

the formation of renal infarction, beginning with a lesion in the left atrium ofthe heart.

#. !iscuss the role of platelets, components of the blood vessel wall and

the clotting se$uence in normal hemostasis. %. &ist and describe the factor which predisposes an animal to thrombosis.

!ifferentiate between a thrombus and a postmortem clot on the basis ofgross and microscopic findings.

'. Give the identifying feature of 3disseminated intravascular coagulation3

and e(plain why bleeding tendencies are induced by this condition. ). Briefly discuss the causes and effects of pulmonary and systemic

embolism. *. Briefly outline the manner in which red and pale infarcts develop in

various organs and+or tissues. 1. !iscuss the causative mechanisms of generalized and localized

edema. 11. !iscuss the manner by which a loss of blood volume and the pooling

of blood in capillary beds may induce shock in an animal. 12. -rovide appropriate answers for the postinstructional selfe(amination

$uestions outlined at the end of this section.


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'EY &ORDS

he student should attempt to define, spell and use the following terms prior toand after embarking on a study of circulatory disturbances.

/ctive hyperemia !iapedesis

-assive congestion 4emostasis 5enous congestion 4ypostatic congestion

Generalized passive congestion 6ludged blood

7yanosis 4emorrhage

Brown induration of the lungs -etechiae

4eart failure cells 8cchymoses

7ardiac compensation -urpura

7ongestive heart failure /gonal

7ardiac decompensation 8(travasation

&eftsided heart failure 4emothora(

9ightsided heart failure 4emoperitoneum

-hagocytosis 4emopericardium

/no(ia 8pista(is

0schemia 4emoptysis

4ypo(ia 4ematemesis 4emorrhage by rhe(is 4ypercoagulability

4emorrhage by diapedesis /rterial thrombi

4ematuria ural thrombi

etorrhagia 5enous thrombi

8nterorrhagia 5alvular thrombi

&inear hemorrhages /septic thrombi

-aintbrush hemorrhages 6eptic thrombi

/gonal hemorrhages 7analized thrombi

0ntercellular spaces 6addle thrombi

0nterstitial spaces Occluding thrombi

Bruise 7hicken fat clots

4ematocyst 7urrent :elly clots

4emorrhagic shock -ostmortem clots

elena !isseminated intravascular 6uffusion coagulation

38nd artery3 -arado(ical embolism

7ollateral circulation 9ed infarct

/nemia 4emorrhagic infarct

hrombosis /nasarca

hrombi 4ydropericardium

hrombus /scites

8mbolism 4ydrothrora(

8mboli 8(udate

8mbolus ransudate


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0nfarction 0nflammatory edema

0nfarct ;oninflammatory edema hromboembolism 4ydrostatic pressure

hrombocytes Osmotic pressure

-latelets 4ypoproteinemia

8ndothelial cells 4ypovolemic shock

7oagulation system 6eptic shock

results from impaired venousdrainage. 9emember, in both hyperemia and congestion, blood is retained withinthe vascular system? whereas in hemorrhage, blood is found outside of thevascular system.

ACTIVE HY(EREMIA

Occurs when too much arterial blood is brought to an organ or tissue by dilatedarterioles and capillaries. he arteriolar dilatation is brought about by sympathetic

neurogenic mechanisms or by the release of vasoactive substances. 0n mostinstances, active hyperemia occurs subse$uent to an inflammatory reaction = it ist)e -irst sta%e $- in-#ammati$n>. Other situations characterized by activehyperemia include@

=1> heat applied locally to a part and

=2> increased physiological activity.

icroscopically, the capillaries are dilated and filled with blood. Grossly, theinvolved organ+part takes on the bright red color of arterial blood = de+endin% $nt)e $ri%ina# !$#$r.. 7linically, the organ+part is warmer than normal.

Remember,active hyperemia is usually localized (if it wasgeneralized, there would be insufficient blood in majorvessels to maintain systemic blood pressure and shockwould occur).

(ASSIVE CONGESTION


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,C$n%esti$n> occurs when the flow of blood leaving an organ or part is impeded=impaired venous drainage>. icroscopically, congestion is similar to hyperemia=!a+i##aries and eins are di#ated and -i##ed /it) 0#$$d>. Grossly, the involvedtissues appear bluishred because of the poorly o(ygenated venous blood.

Remember,congestion of capillary beds is closely related to thedevelopment of edema thus, passive congestion and edemacommonly occur together.

&ocalized -assive 7ongestion is usually caused by pressure placed on veinsleaving an organ or part ,ia 0anda%e1 r00er 0and1 t$rsi$n1 et!2>. Oftentimes,the compression on vessels is such that blood still gets in through thickwalled,muscular arteries but pressure on thinnerwalled veins restrict the outflow andvenous blood accumulates.

Generalized -assive 7ongestion is associated with impediment of blood flow in

the central circulation =)eart1 #n%s1 ma3$r esse#s1 et!2>. 0t may be acute orchronic. /cute generalized passive congestion is usually associated with a failingheart. 7hronic generalized passive congestion is most obviously manifested inthe lungs, liver and spleen.

7hronic Generalized -assive 7ongestion of the &ungs is encountered in all formsof cardiac decompensation that occurs subse$uent to reduced left ventricularoutput =#e-t4sided )eart -ai#re.. /n accumulation of blood and increasedhydrostatic pressure occurs in the lungs. 6ome of the distended lung capillariesmay rupture or hemorrhage per diapedesis may occur. 8ventually, thebreakdown and phagocytosis of erythrocyte debris leads to the appearance of

hemosiderinladen macrophages =)eart4-ai#re !e##s> in the alveolar spaces. 0ntime, the alveolar walls become fibrotic. hus, the fibrosis and hemosiderinpigmentation constitute the basis for the designation"0r$/n indrati$n $- t)e#n%2"

7hronic -assive 7ongestion of the &iver results from rightsided heart failure=rare#* -r$m $0str!ti$n $- t)e +$steri$r ena !aa..

HEMORRHAGE

4emorrhage refers to the presence of erythrocytes outside the blood vessels.

he vessel may be physically damaged so that erythrocytes flow out through abreak in the wall or the erythrocytes may pass through an intact vascular wall bya process called diapedesis. he various etiologic agents that play a role in thedevelopment of hemorrhage are discussed in your te(tbook =pages !""#!"!>.he following are some of the terms used to denote hemorrhage.

-etechiae5 re-erto very tiny hemorrhages which occur as "tin* +in

+$ints3 up to 12 mm in diameter. 6uch hemorrhages occur in the skin,


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mucous membranes and serosal surfaces. -etechiae are commonlyobserved in septicemia where the endothelium is damaged or destroyed.

8cchymoses@ re-erto larger hemorrhagic areas up to 2 cm in size

=#ar%e 0rises are e!!)*m$ses>. -urpura@re-erto hemorrhages which are slightly larger than petechiae.

6uch hemorrhages are associated most commonly with disturbances ofthe clotting mechanism. /gonal hemorrhages@re-er to small hemorrhages the size of petechiae

and ecchymoses that arise :ust prior to death ,ass$!iated /it) t)e deat)str%%#e..

&inear hemorrhages@re-erto hemorrhages which appear as lines.

-aintbrush hemorrhages@re-ers to e(tensive streaking with

hemorrhages =seera# #inear )em$rr)a%es /)i!) a++ear side 0* side.2 8(travasation@re-ersto hemorrhages in tissues spread over

considerable areas. 6uffusions are diffuse, flat, often irregularshapedareas of bleeding. 4ematocyst re-ersto more or less spherical shaped

collection of blood in tissues =si6e /i## ar*.2

4emothora(@ re-ersto hemorrhage into the thoracic cavity.

4emopericardium@re-ersto hemorrhage into the pericardial sac.

8pista(is@ re-ers to hemorrhage from the nostrils.

4emoptysis@re-ers to the e(pectoration of blood that originates from the

respiratory tract. 8nterorrhagia@ re-ersto intestinal bleeding.

etorrhagia@re-ersto uterine bleeding.

4ematuria@re-ersto blood in the urine.

4emorrhage by rhe(is@ re-ersto hemorrhage that occurs subse$uent toa break in the wall of a vessel ,a## !$nstitents $- t)e 0#$$d es!a+es.2

4emorrhage by diapedesis@re-ersto hemorrhage that occurs whenerythrocytes escape through an apparently intact vessel wall.

he significance of hemorrhage depends on@

=1> the volume of blood loss,

=2> the rate of blood loss and

=> the site of hemorrhage.

/bout A of the total blood volume is the ma(imum which can be lost and theanimal still recover. 0f more is lost, death is likely to occur subse$uent to

hypovolemic shock. 4owever, the amount of blood which can be lost dependsupon the rapidity with which it leaves the vascular system. $or e%ample, whenthe rate of hemorrhage is slow ,st$ma!) /$rm in-e!ti$ns>, fluid can be addedto the blood rapid enough to maintain near normal blood pressure? thus, the lossof large amounts may have little clinical significance. /lso, the site of hemorrhagewill influence its effect on the host. / hemorrhage which would be trivial in thesubcutaneous tissues may cause death when located in the brain stem.


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9epeated or chronic e(ternal hemorrhages ,i2e21 /)en 0#$$d is s)ed -r$m t)es7in1 G2I2 tra!t1 et!2.represent losses not only of blood volume but also ofvaluable iron. sually, the small but repeated volume losses are rapidly correctedby movement of water from the interstitial spaces into the vascular compartment,but the chronic losses or iron may lead to iron deficiency anemia. 0n contrast,

when erythrocytes are retained, as occurs with hemorrhages into the bodycavities, :oints or tissues, the iron can be recaptured for synthesis of hemoglobin.

he fate of an area of hemorrhage depends upon the amount of blood that hasescaped from the vascular system. 0f the hemorrhage is relatively small, the fluidportion of the blood is absorbed, the leukocytes move back into the vascularsystem and the erythrocytes are phagocytized. 0n a larger hemorrhage, there isdisintegration and breakdown of erythrocytes with the formation of hematoidinand hemosiderin. 7holesterol may also be seen in the tissues. he escapedblood also clots with the formation of fibrin and this fibrin and the remainingleukocytes may eventually be phagocytized. 0n still larger areas of hemorrhage,

fibroblasts and new capillaries may proliferate into the area of clotted blood. hisprocess is known as organization of the area of hemorrhage.

SLUDGED BLOOD

6ludged blood refers to the conglutination or sticking together of erythrocyteswithin blood vessels and should be distinguished from simple rouleau( formationin which erythrocytes merely stack one on top of another. 0n the formation ofsludged blood, large masses of erythrocytes adhere to each other and may settleto the lower portion of large vessels or even block smaller vessels. he etiologicmechanism is uncertain, but for some reason the erythrocytes lose their ability to

repel each other and conglutinate. his condition has been studied e(tensively inman by microscopic e(amination of vessels in the con:uctiva during life and hasalso been reported in swine infected with hog cholera virus. 0t is postulated thatsludged blood flows more slowly, may give rise to blood clots within the vesseland may cause hypo(ia of the tissues involved.

ISCHEMIA

0schemia refers to local anemia or a deficiency of arterial blood to a portion of anorgan or part. he chief causes of ischemia are

=1> e(ternal pressure upon an artery, =2> narrowing of the lumen of an artery and

=> a thrombus or embolus.

4owever, ischemia may be caused by vasoconstriction as observed in ergotpoisoning. he effects of ischemia are dependent on the organ involved, the sizeof the vessel, the degree of occlusion and the degree of collateral circulation. 0fischemia occurs in an "end arter*1"as in the kidneys, the result is likely to be


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acute necrosis of tissue supplied by the vessel. 0f the obstruction to blood flow isgradual, atrophy may occur.

THROMBOSIS

hrombosis refers to the formation of a clot from elements of the circulating bloodwithin the vascular system during life. his clot is known as a thrombus ,+#ra#1t)r$m0i.2he development of a clot is lifesaving when a large vessel rupturesor is severed. 4owever, when a thrombus develops within the vascular system, itmay be lifethreatening because@

0t may decrease of obstruct vascular flow causing ischemic+hypo(icin:ury to cells, tissues and organs.

0t may become dislodged or fragmented to create emboli =an em0$#s

is an intraas!#ar mass !arried in t)e 0#$$dstream t$ s$me siterem$ed -r$m its $ri%in..

he ischemic necrosis created by a thrombus ,em0$#s.is referred to as aninfarct ,t)r$m0$sis and em0$#ism are s$ !#$se#* interre#ated as t$ %ie riset$ t)e term t)r$m0$em0$#ism.. o a considerable e(tent, thrombosis is theconse$uence of inappropriate activation of the processes of normal hemostasis.herefore, the student should review normal hemostasis as outlined in thete(tbook before considering the pathogenesis of thrombosis.

"N$rma# Hem$stasis"is influenced by components of the blood vessel wall,platelets and the clotting se$uence. he integrity of the blood vessel wall iscrucial in normal hemostasis as well as in thrombosis. he lining endothelium

provides a nonreactive interface between the underlying reactive element of thevessel wall and the fluid blood. 0n addition, the endothelial cells serve to protectagainst thrombi formation by@

=1> releasing plasminogen activator which initiates fibrinolysis and

=2> degrading plateletaggregating agents such as adenosine phosphate

and certain forms of prostaglandins. nderlying the endothelial layer is thesubendothelial connective tissue which contains collagen fibrils. hesecollagen fibrils are potent activators of clotting factors, and they promoteplatelet adhesion. 0n summary, the endothelial cells of the vessel wall arecrucial in the maintenance of normal blood flow. 0f the endothelial layer is

damaged, the subendothelial collagen fibrils will release 3tissue factors3that activate the coagulation system.

-latelets are assigned a central role in normal hemostasis and thrombosis. heyadhere to sites of endothelial in:ury, aggregate to form platelet masses, releasegranules rich in a variety of secretory products and synthesize several types ofprostaglandins. 0n normal hemostasis, platelets adhere to the severed margins ofa vessel within seconds to a few minutes. he most important stimulus to such


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adherence is the e(posure of collagen fibrils. Once adhered, platelets releasetwo types of granules@

=1> alpha granules which contain fibrinogen, beta thromboglobulin, cationic

protein and platelet factor " =a )e+arin netra#i6in% +r$tein> and

=2> dense bodies, which are rich in serotonin, /!-, /- and ionizedcalcium.

he release of platelet granules is triggered by a number of substances,including collagen fibrils, thrombin, plasmin, trypsin, endoto(in and antigenantibody comple(es. 0t is believed that these stimuli to platelet activation inhibitmembranebound adenyl cyclase ,de!reased am$nts $- !*!#i! AM( are-$nd in a%%re%ated +#ate#ets.. Cithin aggregated platelets, there is increasedconcentration of calcium ,t)is !ati$n is a +$tent stim#s t$ +#ate#eta!tiati$n.20n addition, platelet factor , which participates in the intrinsicpathway of the clotting se$uence, becomes activated. 0nitially, the platelet

aggregation forms a temporary hemostatic plug which is friable and easilydislocated in rapidly flowing bloodstreams ,)$/eer1 at t)is time1 t)e !#$ttin%se8en!e #eads t$ t)e -$rmati$n $- t)r$m0in /)i!) is t)e m$st +$/er-#+#ate#et a%%re%at$r *et identi-ied.. 0n summary, platelets@

=1> provide a temporary plug capable of controlling blood flow in small

vessels in low pressure systems, =2> initiate the development of a permanent plug composed of aggregated

platelets and fibrin, => release serotonin which augments vasoconstriction and ="> contributes to the coagulation mechanism.

he coagulation system plays a ma:or role in normal hemostasis. aintenance ofnormal fluidity of blood involves the interplay between procoagulants andanticoagulants. Chen the procoagulants dominate and clotting is triggeredinappropriately in the intact cardiovascular system, thrombi result. 7oncurrentwith the formation of the platelet plug, the coagulation system is activated =theclotting factors involved are listed on page 1# of your te(tbook>. he criticalevents in blood clotting are the conversion of prothrombin to thrombin and thesubse$uent conversion of soluble fibrinogen into the stable fibrin polymer ,t)ese8en!e $- intera!ti$ns am$n% t)e !#$ttin% -a!t$rs is +resent in *$rte9t0$$7.29emember, clotting may be initiated by the intrinsic pathway when

blood is e(posed to a negatively charged surface, such as collagen. he e(trinsicpathway initiates clotting when in:ury e(poses the blood to factors derived fromin:ured cells and tissues. hus, the evolution of a thrombus begins with theadherence of platelets at sites of vascular in:ury followed by the buildup, first of atemporary aggregation of platelets, and then the formation of a more permanentplatelet mass which in turn leads to the standard clotting se$uence, possiblyinvolving both the intrinsic and e(trinsic pathways.


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hrombosis is influenced by three ma:or factors@

=1> in:ury to vascular endothelium,

=2> alterations in normal blood flow and

=> alterations in the blood =)*+er!$a%#a0i#it*>.

8ndothelial in:ury plays a dominant role in the formation of thrombi in arteries andin the heart. Once the endothelium is damaged, subendothelial collagen may bee(posed and tissue thromboplastic, etc., is released and the se$uence of plateletadherence and activation of the clotting se$uence follows.

/lterations in ;ormal


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Occluding thrombi are attached to the entire circumference of the

vessel. 5alvular thrombi are attached to the heart valves.

7analized thrombi occur when new blood channels form in an

organized thrombus.

6addle thrombi straddle the bifurcation of blood vessels.

6eptic thrombi are those which contain bacteria.

/septic thrombi are those that do not contain bacteria, etc.

icroscopically, thrombi are eosinophilic masses in which leukocytes anderythrocytes may be seen. increase in size and, by its enlargement, eventually cause obstructionof some critical vessel,

=2> give rise to emboli =t$ 0e dis!ssed.,

=> be removed by fibrinolytic action or ="> become organized.

(OSTMORTEM CLOTS5

/ thrombus must not be confused with postmortem clotting of blood within the

vascular system. he two types of postmortem clots are@

=1> red or current :elly clots and

=2> yellow or chicken fat clots.

9ed or 7urrent Delly 7lots occur when the components of the blood are evenlydistributed throughout the clot. his type develops when there is rapid clotting ofblood.

Eellow or 7hicken


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DISSEMINATED INTRAVASCULAR COAGULATION

!isseminated intravascular coagulation ,DIC.refers to widespread microthrombiformation in capillaries, arterioles and venules. he thrombi are composedlargely of fibrin and aggregated platelets. he disorder may be a complication ofa diverse group of clinical diseases in which there is activation of the intrinsicpathway of blood clotting. !uring the widespread intravascular coagulation, fibrinis deposited throughout the vascular tree resulting in microthrombi. /lthough thefibrinolytic system is activated, it cannot effectively deal with the large deposits of

fibrin. /s a result, there is rapid consumption and eventually a deficiency ofclotting factors, including fibrinogen, platelets, prothrombin and factor 5, 500, andF =a de-i!ien!* $- -i0rin$%en1 +#ate#ets and +r$t)r$m0in is re8ired -$r t)edia%n$sis $- DIC.2herefore, animals with !07 have bleeding tendencies onhemorrhagic diathesis. /lso the widespread occlusion of the microcirculation mayinduce signs of shock, acute respiratory distress, central nervous systemdepression, heart failure or renal failure. 9emember, affected tissues may notnecessarily disclose the microthrombi because of prompt activation of thefibrinolytic system.

EMBOLISM

8mbolism refers to the process of a foreign body moving through the circulatorysystem and becoming lodged in a vessel causing obstruction. /n embolus,+#ra#4 em0$#i.is a detached intravascular solid, li$uid or gaseous mass that iscarried by the blood to a site distant from its point of origin. 0nevitably, embolilodge in vessels too small to permit their further passage resulting in partial orcomplete occlusion of the vessel. he ma:ority of all emboli arise from thrombi,t)r$m0$em0$#ism.. hese are pieces of thrombi which have been broken


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loose by the force of the bloodstream. &ess common forms of emboli include fatemboli, gas emboli, bacterial emboli, tumor emboli and parasitic emboli (seeyour te%tbook).

!epending on their site of origin, emboli may come to rest anywhere within the

cardiovascular system. ,Un#ess $t)er/ise 8a#i-ied1 t)e term "em0$#s"im+#ies t)r$m0$em0$#ism t)r$%)$t t)is dis!ssi$n.2

(ULMONARY EMBOLISM5

-ulmonary emboli usually originate from thrombi in veins or in theright heart. !islodgement of venous thrombi, in part or whole,produces an embolus which flows with the venous drainagethrough progressively larger vessels to the right heart. nless theembolus is very large, it passes through the spacious chambersand valve openings of the right heart and enters the pulmonary

arterial circulation. &odgement of emboli in ma:or pulmonaryvessels is commonly fatal, resulting in sudden death. Chenpulmonary emboli occlude smaller vessels, they usually cause lunghemorrhage or infarcts. 4owever, in animals without cardiac orcirculatory insufficiency, the bronchial circulation suffices tosubstain the vitality of lung tissue. 9emember, pulmonary infarctionresults only when the bronchial circulation is inade$uate tocompensate, which is common in animals with impairedcardiovascular function.

SYSTEMIC EMBOLISM5

6ystemic embolism re-ersto emboli which travel through thearterial circulation. 6uch emboli usually arise from thrombi withinthe left heart. 0n contrast to venous embolism, arterial emboli travelthrough vessels of progressively diminishing caliber. hemyocardium, spleen, kidneys, brain and lower e(tremities arecommonly the victims of arterial embolism.

-arado(ical embolism refers to emboli which enters the right side ofthe heart and pass through interatrial or interventricular septaldefects to gain access to the arterial side of the circulation.

INFARCTION

/n infarct is a localized area of ischemic necrosis in an organ or tissue resultingfrom occlusion of either its arterial supply or venous drainage. he vascularocclusion is usually caused by thrombosis and+or embolism of the arterial bloodsupply. ore rarely, e(ternal compression of vessels by e(panding tumors, etc.,may result in infarction.


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0nfarcts are classified on the basis of their color =red $r +a#e in-ar!ts> and on thepresence or absence of bacterial contamination ,se+ti! $r ase+ti! in-ar!ts.2-ale or anemic infarcts are encountered with arterial occlusion and in solidtissue. Chen a solid tissue is deprived of its arterial circulation, the infarct may betransiently hemorrhagic, but most become pale in a very short time. he reasons

for the development of pale infarcts are as follows@

"T)e arteria# !ir!#ati$n t$ an area is $!!#ded2 Vesse#s1 +arti!#ar#*!a+i##aries1 as /e## as +aren!)*ma# !e##s are destr$*ed2 At t)e m$ment $-as!#ar $!!#si$n1 0#$$d -r$m anast$m$ti! +eri+)era# esse#s -#$/s int$t)e -$!s $- in3r*1 +r$d!in% t)e initia# )em$rr)a%i! a++earan!e2 I- t)ea--e!ted tisse is s$#id1 see+a%e $- 0#$$d -r$m t)e anast$m$ti! esse#s isminima#2 S$$n a-ter t)e initia# 0#$$d see+a%e1 t)e er*t)r$!*tes are #*sedand t)e re#eased )em$%#$0in +i%ment eit)er di--ses $t $r is !$nerted t$)em$siderin2 T)ere-$re1 in s$#id $r%ans1 t)e arteria# in-ar!t /i## s$$n ,;< t$ in tissues previously congested.

9ed or hemorrhagic infarcts develops in loose tissue subse$uent to arterial

obstruction in the following manner.

he arterial circulation to an area is obstructed. 0f the tissue is loose ,#n%1 et!2>,large amounts of blood collect in the spongy, loose tissue at the moment ofvascular occlusion. his blood remains for long periods? thus, the arterial infarctremains red. he lungs and intestine are sites where red infarcts tend to occur.

Remember,red infarcts may occasionally be encountered in solidtissue or white infarcts in loose tissue.


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2./natomic -attern of /rterial Blood 6upply@ he various tissues and

organs of the body receive their arterial supply through one of severalpatterns@

o =1> a dual arterial blood supply,

o =2> a "sin%#e" arterial blood supply with few anastomoses

,ins--i!ient t$ +r$ide ade8ate 0*+ass !)anne#s., socalled3end arteries,3

o => a "sin%#e"arterial blood supply with rich interarterial

anastomoses ando ="> parallel arterial systems.

/ dual blood supply is received by the lungs and liver. 0n animals with normalcardiac and cardiovascular status, the bronchial circulation is capable ofpreventing ischemic necrosis of the lungs when a branch of the pulmonary arteryis obstructed. 6imilarly, infarction is uncommon in the liver because the portalsupply of blood may be ade$uate, even when the hepatic arterial supply is

compromised. 4owever, in the presence of cardiac failure, severe anemia, orreduced o(ygenation of the blood, occlusion of one system may precipitateischemic necrosis.

/n arterial blood supply with rich interarterial anastomoses is found in the smallintestine. 4ere, blood is able to bypass focal areas of occlusion.

/n arterial blood supply with socalled "end arteries" is found in the kidneys, fore(ample. he ma:or branches of the renal artery supply welldefined segments ofthe kidneys. Occlusion of one of the ma:or branches, or of the main renal artery,is invariably followed by ischemic necrosis. 4owever, if the occlusion occurs at

the terminal ramification and involves subcapsular parenchyma, there may besufficient blood flow from capsular vessels to prevent tissue damage.

-arallel arterial system is encountered in the forelimbs. 8ither the radial or theulnar artery is sufficient to sustain the vitality of the tissues when one or the otheris occluded.

.9ate of !evelopment of Occlusion@ 6lowly developing occlusions are

better tolerated than those occurring suddenly since they provide anopportunity for alternative pathways and collateral circulation to becomeactivated.

icroscopically, all areas of infarction undergo coagulative necrosis andresorption as discussed in 6ection

(Remember, central nervous tissue undergoes liquefactive ratherthan coagulative type necrosis).


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he typical coagulative appearance may be modified by e(tensive hemorrhage inred infarcts and by bacterial suppuration in septic infarcts. Cithin a few days afteran infarct is initiated, an inflammatory reaction becomes welldefined. &ater, areparative process begins.

Grossly, both red and pale infarcts tend to be wedgedshaped, with the ape( ofthe wedge pointing toward the focus of vascular occlusion.

EDEMA

8dema refers to an abnormal accumulation of fluid ,/ater.in the intercellulartissue spaces or body cavities. 0t may occur as a localized ,e2%2 $0str!ti$n $-en$s $t-#$/ -r$m t)e #e%., or it may be generalized in distribution ,e2%21 in!)r$ni! !$n%estie )eart -ai#re.. he following terms are used to describe

edema@

/nasarca@ re-ers to generalized edema in which fluid in subcutaneous

tissues is especially prominent. /scites@ re-ersto a collection of edematous fluid in the peritoneal cavity.

4ydrothora(@ re-ers to a collection of edematous fluid in the thoracic

cavity. 4ydropericardium or -ericardial 8ffusion@ re-ersto a collection of

edematous fluid in the pericardial sac.

8dematous fluid may be inflammatory or noninflammatory. 0nflammatory edema

is referred to as an e(udate and it is associated with an inflammatory reaction.;oninflammatory edema is referred to as a transudate.

he term "edema" refers to noninflammatory edema throughout this discussion,unless otherwise $ualified.

;oninflammatory edema =transdate.can be distinguished from aninflammatory edema ,e9date.on the basis of the following features.


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Me!)anisms $- Edema F$rmati$n5

Before embarking on a study of the pathogenic mechanisms of edema, thenormal control and relationships of tissue fluid must be clearly understood.

nder normal physiologic conditions, the main filtration force that e(pels fluidfrom the vessel is the hydrostatic pressure at the arterial end of the capillaryminus the osmotic pressure of the blood. he main absorption force that drawsfluid into the vessel is the osmotic pressure of the blood minus the hydrostaticpressure at the venous end of the capillary. 0n the normal animal, there is acontinuous circulation of fluid from the arterial end of the capillary through thetissues and back into the venous end of the capillary.

-hysiologically, blood enters the arterial end of a capillary with a hydrostaticpressure =0#$$d +ressre.of about "# millimeters of mercury, which e(pels fluidand smaller dissolved molecules into the intercellular spaces. 4owever, thishydrostatic pressure ,e9+#sie -$r!e.is opposed by the osmotic pressure of

blood e(erted by such molecules as albumin and globulin. he osmotic pressureis about mm of mercury. herefore, at the arterial end of the capillary,hydrostatic pressure at "# mm of mercury is overcoming the mm osmoticpressure of the blood plasma, and fluid is forced into the intercellular spaces atthe rate of 1# mm of mercury. /s blood travels through capillaries, its hydrostaticpressure decreases rapidly to about 1# mm of mercury. herefore, at the venousend of the capillary, hydrostatic pressure at 1# mm of mercury cannot overcome mm osmotic pressure of the blood, and fluid flows from the intercellular


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spaces into the bloodstream at the rate of 1# mm of mercury. 6ince fluid enterstissues at about the same rate as it leaves, there is no accumulation of fluid inthe intercellular spaces in the normal animal. 4owever, edema occurs if there isany interference with this normal flow.

Basi!a##*1 edema is !ased 0*5

=1> decreased plasma osmotic pressure,

=2> increased hydrostatic pressure,

=> increased permeability of vascular endothelium and ="> lymphatic obstruction.

DECREASED (LASMA OSMOTIC (RESSURE5

Occurs when there is a deficiency of blood proteins ,)*+$+r$teinemia.2hus, hypoproteinemia may result from decreased formation or e(cessive

loss from the blood. /lbumin is most important in maintaining osmoticpressure and it e(erts four times the osmotic pressure of globulin. / lowosmotic pressure in the blood increases the pressure differential at thearterial end of the capillary so that more fluid is pushed into theintercellular spaces. /lso, the force available to pull fluid into thebloodstream at the venous end of the capillary is reduced. hus, there isan accumulation of fluid in intercellular spaces and+or body cavities.

/ failure to form blood proteins results from malnutrition ,starati$n1ema!iati$n> in which the "0i#din% 0#$!7s" for blood protein formationare not available. 6evere or advanced liver diseases ,!irr)$sis1 et!.> may

lead to hypoproteinemia since this is the site in which blood proteins=a#0min and %#$0#in> are synthesized. he loss of plasma proteinsfrom the blood occurs through the intestine and kidneys. 0n the intestine,blood protein loss is usually the result of hemorrhage over a long period oftime ,st$ma!) /$rms in s)ee+ and !att#e1 s#$/#* 0#eedin% st$ma!)#!ers in +i%s and d$%s1 et!2>. 0n the kidneys, renal amyloidosis is theonly fre$uently encountered condition in animals in which large volumes ofblood protein are lost through the urine.

Remember, decreased plasma osmotic pressure alwaysleads to generalized edema.

INCREASED HYDROSTATIC (RESSURE5

0s influenced mainly at the venous end of the capillary and it usuallyresults from venous stasis =severe passive congestion that results inincreased back pressure in the venous circulation>. he increasedhydrostatic pressure at the venous end of the capillary which pushed fluidout of the bloodstream counterbalances the osmotic pressure which pulls


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fluids into the bloodstream. herefore, fluid fails to return to the vesselfrom the intercellular tissue. 6ubse$uent to venous stasis, the capillariesbecome more permeable to large molecules ,a#0min and %#$0#in.,since they are deprived of their normal supply of o(ygen and othernutrients.

Remember,the usual causes of venous stasis andsubsequent increased hydrostatic pressure are impairedheart function or a lesion in which the venous flow isobstructed.

INCREASED (ERMEABILITY OF CA(ILLARY ENDOTHELIUM5

Occurs subse$uent to venous stasis,res#tin% in in!reased )*dr$stati!+ressre.1as well as from direct damage, as in inflammation. 0ncreasedvascular permeability is the most important mechanism in the formation of

inflammatory edema ,e9date.2

LYM(HATIC OBSTRUCTION5

Occurs when any lesion impedes normal lymphatic drainage by pressureor obstruction. nder normal conditions, the lymphatics constantly drainsmall amounts of fluid from the intercellular spaces. hus, in the absenceof lymphatic drainage from a area, fluid accumulates.

0n summary, decreased plasma osmotic pressure produces generalizededema, whereas increased hydrostatic pressure may induce eitherlocalized or generalized edema. 0ncreased permeability of capillaryendothelium and lymphatic obstruction almost always lead to localizededema.

icroscopically, when welldefined, edema appears as a granular,eosinophilic interstitial precipitate that separates the cellular and fibrillarelements of tissue ,t)e +in74stainin% a++earan!e is de +rimari#* t$t)e +resen!e $- a#0min in t)e edemat$s -#id.. 0n the absence ofalbuminous precipitate, edema is represented by empty spaces in theinterstitial areas.

Grossly, edematous tissues are swollen, firm, doughy and pit on pressure.here is no redness and not sign of pain. 0f the edematous part is e(ternal,it is cool to the touch.

8dema of the brain and lungs is the most lifethreatening form of abnormalfluid retention. 0n animals, edema is almost always parasitic, nutritional,cardiac or renal in origin. 0f the cause is removed, edematous fluid


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disappears $uickly, leaving no permanent defect in the area. 4owever, ifedematous fluid persists, it acts as a tissue irritant.

SHOC'

6hock is a clinical term which refers to peripheral circulatory failure with poolingof the blood in the terminal circulatory beds =sma## !a+i##aries>. he fundamentaldisturbance is that blood volume is too small to fill the vascular system, resultingin a fall of blood pressure and cell damage due to ano(ia.

&'*+f all capillary beds in the body were to open up, there wouldnot be enough blood to fill the major vessels andor heartthus, blood pressure falls and the flow of blood is decreased.

-lso, the loss of massive amounts of blood via hemorrhage,etc., would have a similar effect. ubsequently, o%ygen andnutrient delivery to cells and removal of waste products aredecreased. herefore, depending on the severity andduration of the shock state, the cells of many vital organssuffer injury and even death.

he clinical signs of shock are inconsistent and vary with the precipitating cause.4owever, animals with shock are usually inactive and unresponsive to e(ternalstimuli. uscle weakness is prominent and there is pallor and coolness of theskin. Body temperature is subnormal and the heart rate is increased in mosttypes of shock ,0t it ma* 0e s#$/ and irre%#ar.. !epression of renal functionand urine production often occur.

he causes of shock may be classified as hypovolemic, septic, cardiogenic andneurogenic.

HY(OVOLEMIC SHOC'5

0s due to loss of blood volume =)em$rr)a%e1 trama1 #$ss $--#ids in 0rns1 et!2.which directly induces inade$uate perfusionof organs and tissues.

Remember, e%tensive blood loss is required before

animals develop hypovolemic shock. he followingsequence of changes is associated with hypovolemicshock (as well as other forms).

6evere blood loss occurs. he arterial blood pressure drops andvenous return to the heart decreases. he heart rate may increasebut stroke volume and cardiac output are decreased. /rterial


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vasoconstriction occurs rapidly with the drop in blood pressure andincreased peripheral resistance is produced which shunts bloodfrom the skin and viscera to the heart and brain. 0n the kidneys,vasoconstriction reduces perfusion and causes activation of the

:u(taglomerular apparatus with the release of the enzyme renin into

the plasma. 9enin acts on an unidentified plasma protein substrateconverting it to a polypeptide angiotensin 0. /ngiotensin 0 isconverted to the potent vasoactive polypeptide angiotensin 00 byanother converting enzyme. /lso, the pituitary gland is stimulated torelease the antidiuretic hormone ,as$+ressin> which acts toconserve water normally lost from the lower nephrons. /ldosteronesecretion by the adrenal corte( is augmented which leads toincreased resorption of salt and water by the renal tubules. /ll ofthe above mechanisms conserve fluid and support blood volume.

Remember,progressive deterioration of the circulatory

system may occur despite the above compensatorymechanisms. he term /irreversible shock/implies therefractory state of circulatory failure with inability toclinically control the condition.

SE(TIC SHOC'5

0mplies septicemia or an overwhelming infection with gramnegative,end$t$9i! s)$!7> or grampositive =e9$t$9i! s)$!7.organisms.0n to(ic and septicemic conditions, there is oftentimes peripheraldilatation of the capillary beds which subse$uently lead to shock.Chen capillary beds are fully dilated ,as$di#ati$n>, they have thecapacity to accommodate nearly the total blood volume. 0f thisoccurred, blood pressure would drop to zero =n$rma##*1 !$ntina#as$!$nstri!ti$n $- t)e termina# arteri$#es +reents t)is -r$m)a++enin%.2

CARDIOGENIC ,CARDIAC. SHOC'5

7an be viewed as"+m+ -ai#re23 0t occurs subse$uent to thesudden decrease in cardiac output which accompanies suddene(tensive damage to the heart. 4owever, most animals succumbdirectly to the myocardial failure. 0n those animals that do not,shock may ensue because of the pooling of the blood.

NEUROGENIC SHOC'5


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0mplies a shock state mediated by the nervous system whichinduces peripheral dilatation ,di#atati$n $- t)e !a+i##ar* 0ed.. 0toccurs in animals with severe fright, pain and trauma =/it)$t)em$rr)a%e.2

he manifestations of shock involve many vital organs =de+endin%$n t)e seerit* and drati$n $- t)e s)$!7 state>. he se$uenceof changes at the cellular and subcellular levels are thosedescribed for hypo(ic in:ury ,re-er t$ se!ti$n > $- t)is s*##a0s. .0n general, the brain and heart are highly susceptible to hypo(iagenerated by the shock state.

(OST4INSTRUCTIONAL SELF4E?AMINATION

/fter completing this section, each student should be in a positionto provide appropriate answers for the following $uestions.

-lease complete the following statements@

@esti$ns

is t)e t*+e $- s)$!7 !ased 0* massie )em$rr)a%e -r$ma %ns)$t /$nd2

is t)e t*+e $- s)$!7 t)at ma* dee#$+ -r$m massie%an%rene $- t)e #$/er e9tremities 2

is t)e t*+e $- s)$!7 e9+e!ted in a +9 /it) -$rt) de%ree0rns2

is t)e t*+e $- s)$!7 mediated 0* t)e ner$s s*stem2

is t)e -ndamenta# !ase $- edema in a 4*ear4$#d +9 /it)seere ne+)riti! s*ndr$me 2

is t)e -ndamenta# !ase $- edema in a *r $#d +9 /it)!$n%estie )eart -ai#re 2

is t)e -ndamenta# !ase $- edema in a *ear4$#d ma#e/it) a#!$)$#i! !irr)$sis 2

re-ers t$ an a0n$rma# a!!m#ati$n $- -#id in tisse t)atis ass$!iated /it) an in-#ammat$r* rea!ti$n2

re-ers t$ an a!!m#ati$n $- a transdate in t)e s!r$ta#


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sa!2

is t)e +r$tein /)i!) e9erts a++r$9imate#* = $- t)e$sm$ti! +ressre in t)e 0#$$dstream2

re-ers t$ a !$##e!ti$n $- -#id in t)e t)$ra!i! !ait*2

re-ers t$ #$!a# anemia in an $r%an $r +art2

re-ers t$ a #$!a#i6ed area $- is!)emi! ne!r$sis in an $r%ant)at dee#$+s s0se8ent t$ $!!#si$n $- its arteria# 0#$$d s++#* 0* at)r$m0s2

re-ers t$ t)e +r$!ess $- a -$rei%n 0$d* m$in% in t)e0#$$dstream and s0se8ent#* 0e!$min% #$d%ed in a esse# !asin%

is!)emia and in-ar!ti$n2

re-ers t$ !#$ttin% /)i!) is tri%%ered ina++r$+riate#* in t)einta!t !ardi$as!#ar s*stem $- a #iin% +atient 2

re-ers t$ t)e !$n%#tinati$n $- er*t)r$!*tes /it)in 0#$$desse#s $- a #iin% anima#2

re-ers t$ )em$siderin #aden ma!r$+)a%es -$nd in t)e#n% $- a 4*ear4$#d -ema#e /it) CHF 2

re-ers t$ )em$rr)a%e t)at $!!rs s0se8ent t$ a 0rea7in t)e /a## $- a 0#$$d esse#2

;2H$/ /$#d *$ distin%is) a!tie )*+eremia -r$m +assie !$n%esti$n

>2Distin%is) )em$rr)a%e -r$m )*+eremia and !$n%esti$n $n t)e 0asis $-%r$ss -indin%s2


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t$ dee#$+ in a 4*ear4$#d C$$n)$nd

=2Brie-#* $t#ine t)e eents t)at #ead t$ "0r$/n indrati$n $- t)e #n%" t)atdee#$+s s0se8ent t$ a$rti! sten$sis2

2&)* /$#d #n% edema $!!r in a d$% /it) seere a$rti! sten$sis

2Brie-#* $t#ine t)e +at)$%enesis $- !)r$ni! +assie !$n%esti$n $- t)e#ier t)at dee#$+s s0se8ent t$ sten$sis $- t)e +#m$nar* a#e2

2Distin%is) )em$rr)a%e 0* r)e9is -r$m )em$rr)a%e 0* dia+edesis $n t)e0asis $- !asatie me!)anisms2

;2On t)e 0asis $- %r$ss -indin%s1 )$/ /$#d *$ distin%is) +ete!)ia# -r$me!!)*m$ti! )em$rr)a%es

>2Distin%is) s--si$n )em$rr)a%e -r$m a )emat$!*st2


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;. -a!t$rs e9ert t)e ma3$r in-#en!e $n n$rma# )em$stasis

;2&)* is t)e inta!t end$t)e#im t)at #ines t)e 0#$$d esse#s im+$rtant in+reentin% t)r$m0$sis

;2&)* /$#d *$ e9+e!t t)r$m0$sis t$ dee#$+ s0se8ent t$ in3r* t$as!#ar end$t)e#im

;2&)* is t)e r$te $- s0end$t)e#ia# !$nne!tie tisse in t)r$m0s-$rmati$n

;=2Brie-#* $t#ine t)e r$#e $- +#ate#ets in t)r$m0s -$rmati$n2

;2Ot#ine t)e se8en!e $- eents t)at $!!r in t)e dee#$+ment $- atem+$rar* )em$stati! +#%2 &)at is a +ermanent )em$stati! +#%

>2List t)e t)irteen ,>. 0#$$d !#$ttin% -a!t$rs 0* t)eir R$man Nmera#termin$#$%* as /e## as 0* a!!e+ta0#e s*n$n*ms2

>2Ot#ine t)e se8en!e $- eents t)at $!!r in t)e intrinsi! !#$ttin%+at)/a*1 0e%innin% /it) a!tiati$n $- Ha%eman -a!t$r and endin% /it) t)e-$rmati$n $- ins$#0#e -i0rin +$#*mers2

>;2Ot#ine t)e se8en!e $- eents t)at $!!r in t)e e9trinsi! !#$ttin%+at)/a*1 0e%innin% /it) e9+$sre $- -#$/in% 0#$$d t$ s0end$t)e#ia#!$nne!tie tisse and endin% /it) t)e -$rmati$n $- ins$#0#e -i0rin

+$#*mers2

>>2&)at t)ree ,>. -a!t$rs e9ert t)e ma3$r in-#en!e $n t)r$m0s -$rmati$n int)e -#$/in% 0#$$dstream

>2&)at is +r$0a0#* t)e m$st im+$rtant +redis+$sin% -a!t$r t)at #eads t$t)r$m0$sis in eins

>2&)at is t)e distri0ti$n $- !e###ar e#ements in t)e n$rma# -#$/in%0#$$dstream

>2&)at is )*+er!$a%#a0i#it* &)* /$#d *$ e9+e!t )*+er!$a%#a0i#it* t$#ead t$ t)r$m0i -$rmati$n

>=2On t)e 0asis $- %r$ss a++earan!e1 )$/ /$#d *$ distin%is) an arteria#


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t)r$m0s -r$m a en$s t)r$m0s

>2Distin%is) a !)i!7en -at !#$t -r$m a !rrent 3e##* !#$t $n t)e 0asis $-!asatie me!)anisms and %r$ss a++earan!e2


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>H$/ /$#d *$ distin%is) a +a#e in-ar!t -r$m a red in-ar!t


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