Chapter ThreeChapter ThreeHemodynamic DisordersHemodynamic Disorders

Chapter ThreeChapter ThreeHemodynamic DisordersHemodynamic Disorders

Normal fluid homeostasis

• vessel wall integrity hemorrhage• Intravascular pressure or vascular volume ischemia hyperemia edema• Maintenance of blood as a liquid thrombosis embolism infarction

Hyperemia:Hyperemia:Arterial hyperemiaArterial hyperemiaVenous hyperemiaVenous hyperemia

• a local increased volume of blood in a particular tissue.

Normal blood fluid

Hyperemia

Congestion

HyperemiaHyperemia

Physiological: exercisePathological : Inflammatory

Post-ischemic

Arterial hyperemia:Arterial hyperemia:•Hyperemia is a local increased volume of blood in a particular tissue resulting from augmented blood flow due to arteriolar dilation.

• Gross: Larger; redder; increased temperature; cut

surface is hemorrhage and wet.• LM: Dilatation of arteriole and capillary.

Morphology of hyperemia

Congestion

• Congestion is a local increased volume of blood in capillaries and veinules resulting from impaired venous return from a tissue.

Systemic —cardiac failure•Etiology

-L. heart failure

-R. heart failure

Pulmonary cong.

Systemic cong.

1. External pressure1. External pressure2. Internal occlusion 2. Internal occlusion LocalLocal

EdemaEdemaHemorrhageHemorrhageHeart failure cellsHeart failure cellsBrown indurationBrown induration

Pulmonary congestionPulmonary congestion

• Gross:

Increased volume and weight of organs; blue-red color (cyanosis); reduced temp.; wetness and excessive blood on the cut surface.

Morphology

Acute pulmonary congestion

Chronic pulmonary congestion

Liver congestion

AtrophyAtrophyFatty changeFatty changeNutmeg liverNutmeg liverCentrilobular necrosisCentrilobular necrosisliver cirrhosisliver cirrhosis

•Hepatic congestion

Central veins and hepatic sinuses of the centrilobular regions are distended with blood.

• Microscopically: nutmeg liver ：

1) Degeneration, atrophy and/or necrosis of the liver cells in the centrilobular regions

2) Fatty degeneration of the liver cells in the peripheral part of the lobules

The central regions of the lobules become red-blue surrounded by a yellow-brown zone of uncongested liver substance.

“ Nutmeg liver”

Cardiac cirrhosis of the liver in the longstanding cases

ThrombosisThrombus

ThrombosisThrombus

• Thrombosis is the process of formation of a clotted mass of blood within blood vessels or the heart in living body.

• The resultant mass is called a thrombus.

Normal hemostatic process

• Endothelium

• Platelets

• Coagulation cascade

• Fig 5-6

Pro- and anticoagulant activities of endothelial cells

Platelet adhesion and aggregation

• Fig 5-8

The coagulation cascade

Fibrinolytic system

THREE INFLUENCES OF THROMBOSISTHREE INFLUENCES OF THROMBOSIS

• Endothelial injury (most important). Endothelial injury (most important).

Alone can induce thrombosis.Alone can induce thrombosis.• Alterations in normal flow.Alterations in normal flow.• Hypercoagulability.Hypercoagulability.

When the last two are both present, When the last two are both present,

endothelial injury is not requisite.endothelial injury is not requisite.

• Fig 5-6

Pro- and anticoagulant activities of endothelial cells

Endothelial injuryEndothelial injury

• Ulcerative atherosclerosis• Transmural myocardial infarction• Vasculitis• Trauma• Radiation• Bacterial toxins

Alterations in normal blood flowAlterations in normal blood flow

• Platelets activated by contact with Platelets activated by contact with endothelium.endothelium.• Slowed flow retards dilution of activated Slowed flow retards dilution of activated clotting factors and hepatic clearance.clotting factors and hepatic clearance.• Stasis or turbulence retards the inflow of Stasis or turbulence retards the inflow of inhibitors.inhibitors.• Turbulence may induce endothelial Turbulence may induce endothelial

injuryinjury

Hypercoagulable statesHypercoagulable states

Primary (genetic):Primary (genetic):

Antithrombin III deficiencyAntithrombin III deficiency

Protein C deficiencyProtein C deficiency

Protein S deficiencyProtein S deficiency

Other combined deficiencyOther combined deficiency

Hypercoagulable statesHypercoagulable states

Secondary (acquired):Secondary (acquired):High risk:High risk:Prolonged bed rest or immobilization.Prolonged bed rest or immobilization.Myocardial infarction. Tissue damage Myocardial infarction. Tissue damage (surgery, fractures, burns). Cardiac failure. (surgery, fractures, burns). Cardiac failure. Cancer. Acute leukemia. DIC. Cancer. Acute leukemia. DIC. Thrombotic thrombocytopenia.Thrombotic thrombocytopenia.

Hypercoagulable statesHypercoagulable states

Secondary (acquired):Secondary (acquired):Low risk:Low risk:Atrial fibrillation. Cardiomyopathy. Atrial fibrillation. Cardiomyopathy. Nephrotic syndrome. Hyperlipidemia. Nephrotic syndrome. Hyperlipidemia. Late pregnancy/postdelivery. Late pregnancy/postdelivery. Oral contraceptives. Lupus anticoagulant. Oral contraceptives. Lupus anticoagulant. Sickle cell anemia. Smoking. Sickle cell anemia. Smoking. Thrombocytosis.Thrombocytosis.

White thrombusWhite thrombus

Red thrombusRed thrombus

Mixed thrombusMixed thrombus

Fibrin thrombusFibrin thrombus

Types of thrombusTypes of thrombus

White thrombusWhite thrombusSite: heart valve , arterySite: heart valve , artery

Component: Platelet, fibrinComponent: Platelet, fibrin

Mixed thrombus Site: heart chamber, veinSite: heart chamber, veinComponent: Platelet, fibrin,RBCComponent: Platelet, fibrin,RBC

Mural thrombosis

Mural thrombosis

RED THROMBUS

Fibrinous thrombi are visible within parts of capi. of the glomerulus

hyaline thrombi in a glomerulus

AbsorptionAbsorption

OrganizationOrganization

CalcificationCalcification

DetachmentDetachment

Fate of thrombusFate of thrombus

Organization and recanalization of thrombus

During organization, the thrombus dissolved and blood could flow again.

IschemiaIschemiaCongestionCongestionHeart valve diseaseHeart valve diseaseDICDICEmbolismEmbolism

Effects of thrombosisEffects of thrombosis

Embolism

EmbolusEmbolus

Embolism

EmbolusEmbolus

• Embolism is a partial or complete obstruction of some part of the vascular system by any mass carried there in the circulation.

• The transported material is called an embolus.

• 99% thromboembolism.

Types of embolus

• ThromboembolismThromboembolism

• Fat embolism

• Air embolism

• Amniotic fluid embolism

• Other types

Etiology:Etiology:

Fractures of long bonesFractures of long bones

Soft tissue traumaSoft tissue trauma

BurnsBurns

Fat embolismFat embolism

90% of individuals with severe skeletal 90% of individuals with severe skeletal

injuriesinjuries

10% with clinical findings(1-3 days)10% with clinical findings(1-3 days)

Pulmonary insufficiencyPulmonary insufficiency

Neurologic symptoms Neurologic symptoms

Fat embolismFat embolism

• Fig 5-17

Etiology:Etiology:

Intravenous therapeutic proceduresIntravenous therapeutic procedures

Obstetric proceduresObstetric procedures

Chest wall injuryChest wall injury

Decompression sickness (nitrogen)Decompression sickness (nitrogen)

Air embolismAir embolism•Gas bubbles within the circulation can obstruct vascular flow.

•A particular form of gas embolism called decompression sickness occurs when individuals are exposed to sudden changes in atmospheric pressure.

AMNIOTIC FLUID EMBOLISMAMNIOTIC FLUID EMBOLISM

Incidence:Incidence: 1/50 000 deliveries 1/50 000 deliveries

Mortality rate:Mortality rate: 80% 80%

Clinical onset:Clinical onset: Sudden severe dyspnea, Sudden severe dyspnea,

cyanosis, hypotensive shock, DICcyanosis, hypotensive shock, DIC

• Embolus from left heart cavity or Embolus from left heart cavity or arterial systemarterial system• Embolus from right heart cavity or Embolus from right heart cavity or venous systemvenous system• Embolus from portal veinsEmbolus from portal veins• Paradoxical embolismParadoxical embolism• Retrograde embolismRetrograde embolism

Motional pathway of embolus:Motional pathway of embolus:

• Fig 5-16

THROMBOEMBOLISMTHROMBOEMBOLISM

•Instantaneous death (>60%).Instantaneous death (>60%).•Cardiovascular collapse.Cardiovascular collapse.•Right heart failureRight heart failure

PulmonaryPulmonary1.Large emboli (5%):1.Large emboli (5%):

2.Small emboli (60-80%):2.Small emboli (60-80%):

•Clinical silent in patients without Clinical silent in patients without cardiovascular failure.cardiovascular failure.• blood flow from bronchial arteriesblood flow from bronchial arteries(collateral vascular supply)(collateral vascular supply)

3. Between the extremes of large and 3. Between the extremes of large and

small emboli (10-15%):small emboli (10-15%):

Pulmonary hemorrhage.Pulmonary hemorrhage.

4. Multiple small emboli:4. Multiple small emboli:

Pulmonary hypertension and vascularPulmonary hypertension and vascular

sclerosis.sclerosis.

Systemic embolismSystemic embolism

II.. 80-85% from heart, secondary to myocardial infarction. 80-85% from heart, secondary to myocardial infarction.

IIII.. 5-10% from auricular thrombi associated with rheumatic 5-10% from auricular thrombi associated with rheumatic

heart disease and atrial fibrillation.heart disease and atrial fibrillation.

IIIIII.. 5% from the dilated cardiac chamber of myocarditis / 5% from the dilated cardiac chamber of myocarditis /

cardiomyopathy.cardiomyopathy.

VIVI.. Less common sources: Debris from ulcerative atheromata, Less common sources: Debris from ulcerative atheromata,

or thrombi in aneurysms, infectious endocarditis, or thrombi in aneurysms, infectious endocarditis,

prosthetic valves, paradoxical emboli.prosthetic valves, paradoxical emboli.

VV.. Unknown. Unknown.

INFARCTION(INFARCT)

INFARCTION(INFARCT)

infarct/infarction

• An infarct is a localized area of ischemic necrosis in a tissue or organ produced by occlusion of either its arterial supply or its venous drainage.

• The process whereby the infarct is developed is known as infarction.

Intrinsic occlusionIntrinsic occlusion for example, thrombosis, for example, thrombosis, embolismembolism expansion of atheromaexpansion of atheromaVasospasmVasospasm

Extrinsic compressionExtrinsic compression for example, twisting of the vesselsfor example, twisting of the vessels

EtiologyEtiology

INFARCTIONINFARCTION

• Shape: Wedge-shapedShape: Wedge-shaped SegmentalSegmental IrregularIrregular• Nature of necrosisNature of necrosis• Types: Red and white infarctsTypes: Red and white infarcts

Morphology of infarctMorphology of infarct

• LM:

1) Ischemic coagulative necrosis

2) Anemic infarct with few RBC

3) Hemorrhagic infarct has engorgement and hemorrhage

4) The pathology changes secondary to infarct such as hyperemia, hemorrhage, infla., organization and so on.

•Myocardial infarct

The myocardial cells shows coagulative necrosis with the outline of the myocardium. In the margin of the infarct there are numerous inflammatory exudation and connective tissue.

white infarct/anemic infarctwhite infarct/anemic infarct

• arterial occlusionsarterial occlusions

• firm tissuesfirm tissues

Venous occlusionsVenous occlusionsLoose tissuesLoose tissuesTissues with dual circulationsTissues with dual circulationsTissues previously congestedTissues previously congestedBlood flow reestablishedBlood flow reestablished

Red infarct/hemorrhagic infarctRed infarct/hemorrhagic infarct

The alteration of blood in pulmonary embolism

•Hemorrhagic infarct of the lung

Hemorrhage

• Hemorrhage denotes an escape of blood from the cardiovascular system, usually is the result of the rupture of a blood vessel or the heart.