6 hemodynamic disorders

HEMODYNAMIC DISORDERS

1. Hemodynamic
Disorders

2. •Normalfluidhomeostasisismaintainedbyvessel
wallintegrity,intravascularpressureandosmolarity
withincertainphysiologicranges.
•Changesinintravascularvolume,pressure,or
proteincontent,oralterationsinendothelial
functionwillaffectthemovementofwateracross
thevascularwall.

3. 1-Edema
Increased fluid in the interstitial tissue spaces.

4. Patho-physiologic Causes of Edema
-IncreasedHydrostaticPressure:Impairedvenousreturn
-Reducedplasmaosmoticpressure(Hypo-proteinemia):Liver
cirrhosis,nephroticsyndrome
-LymphaticObstruction:Neoplastic,orpostsurgical
-SodiumRetention: Excessivesaltintakewithrenalinsufficiency
-Inflammation :Acuteinflammation,Chronicinflammation

5. Types of edema
•Anasarca:Generalizededema
•Dependentedema:Prominentfeatureofcongestive
heartfailure,particularlyoftherightventricle.
•Renaledema:Edemaasaresultofrenaldysfunctionor
nephroticsyndromeisgenerallymoreseverethan
cardiacedemaandaffectsallpartsofthebodyequally.

6. •Peri-orbitaledema:isacharacteristicfindingin
severerenaldisease.
•Pittingedema:fingerpressureoversubstantially
edematoussubcutaneoustissuedisplacestheinterstitial
fluidandleavesafinger-shapeddepression
•Pulmonaryedema:mosttypicallyseeninthesetting
ofleftventricularfailure

7. Fetal Anasarca

8. EDEMA

9. Effusion

10. 2-Hyperemia and Congestion
•Bothindicatealocalincreasedvolumeofbloodin
aparticulartissue.

11. Hyperemia versus congestion.
Inbothcasesthereisanincreasedvolumeandpressureof
bloodinagiventissuewithassociatedcapillarydilatation
andapotentialforfluidextravasation.

12. Inhyperemia,increasedinflow
leadstoengorgementwith
oxygenatedblood,resultingin
erythema.
Incongestion,diminished
outflowleadstoacapillarybed
swollenwithdeoxygenated
venousbloodandresultingin
cyanosis.

13. Hyperemia

14. Varicose Veins
Congestion

15. 3-Hemorrhage
Extravasation of blood due to vessel rupture

16. Types
•Hematoma:accumulationofbloodwithintissue.
•Petechiae:minute1to2mmhemorrhagesintoskin,
mucousmembranes,orserosalsurfaces.
•Purpura:slightlylarger(≥3mm)hemorrhages.

17. •Ecchymoses:larger(>1to2cm)subcutaneous
hematomas(i.e.,bruises)
•Hemothorax,hemopericardium,hemoperitoneum,or
hemarthrosis(injoints):Largeaccumulationsofbloodin
oneofthebodycavities

18. Petechialhemorrhagesof
thecolonicmucosa
Intracerebralbleeding

19. Subarachnoid Haemorrhage:

20. Petechiae &
Ecchymoses

21. Conjunctival Petechiae

22. Hemorrhage: Epidural hematoma

23. Hemothorax

24. 4-Thrombosis

25. Hemostasisand Thrombosis
Normalhemostasisresultofasetofwell-regulated
processesthataccomplishtwoimportantfunctions:
(1)Theymaintainbloodinafluid,clot-freestatein
normalvessels.
(2)Theyareaimedtoinducearapidandlocalized
hemostaticplugatasiteofvascularinjury.

26. •Thrombosis:aninappropriateactivationof
normalhemostaticprocesses,suchasthe
formationofabloodclot(thrombus)in
uninjuredvasculatureorthromboticocclusionof
avesselafterrelativelyminorinjury.

27. Bothhemostasisandthrombosisareregulatedby
threegeneralcomponents:-
–thevascularwall
–platelets
–thecoagulationfactors.

29. •Threeprimarycausesforthrombusformation,
theso-calledVirchowtriad:
(1)Endothelialinjury
(2)Stasisorslowingofbloodflow
(3)Bloodhyper-coagulability

30. •Virchowtriadinthrombosis.Endothelialintegrityisthesinglemostimportant
factor.Notethatinjurytoendothelialcellscanaffectlocalbloodflowand/or
coagulability;abnormalbloodflow(stasisorturbulence)can,inturn,cause
endothelialinjury.Theelementsofthetriadmayactindependentlyormay
combinetocausethrombusformation.

31. •Thrombimaydevelopanywhereinthe
cardiovascularsystem,butstasisisamajorfactor
inthedevelopmentofvenousthrombi
•Anareaofattachmenttotheunderlyingvessel
orheartwall,frequentlyfirmestatthepointof
origin,ischaracteristicofallthromboses.

32. •Thepropagatingtailmaynotbewellattachedand,
particularlyinveins,ispronetofragmentation,
creatinganembolus.
•Muralthrombi-arterialthrombithatariseinheart
chambersorintheaorticlumen,thatusuallyadhere
tothewalloftheunderlyingstructure

33. •Muralthrombi.Thrombusintheleftandrightventricular
apices,overlyingawhitefibrousscar.

34. Thrombosis

35. •Fate of the Thrombus.
1. Propagation.
2. Embolization.
3. Dissolution.
4. Organization and recanalization.

36. •Potential outcomes of venous thrombosis.

37. Laminated thrombus in a dilated abdominal aortic
aneurysm.
Mural thrombi.

39. Lines of Zahn: alternating
layers of platelets and
fibrin in the thrombus

40. 5-Embolism

41. •Anembolusisadetachedintravascularsolid,
liquid,orgaseousmassthatiscarriedbythe
bloodtoasitedistantfromitspointoforigin.
•Embolilodgeinvesselstoosmalltopermit
furtherpassage,resultinginpartialorcomplete
vascularocclusion

42. Pulmonary Thrombo-embolism
•95% of venous emboli originate from deep
leg vein thrombi

43. •Largeembolusderived
fromalowerextremitydeep
venousthrombosisandnow
impactedinapulmonary
arterybranch.

44. Systemic Thromboembolism
•Emboli traveling within the arterial circulation.
•Most (80%) arise from intra-cardiac mural thrombi,
•Two thirds of which are associated with left ventricular
wall infarcts
•The major sites for arteriolar embolizationare:
1. Lower extremities (75%)
2. Brain (10%)

45. A-Fat Embolism
•Microscopicfatglobulesmaybefoundinthe
circulationafterfracturesoflongbones(which
havefattymarrow)or,rarely,inthesettingofsoft
tissuetraumaandburns.

46. •Bonemarrowembolusinthepulmonarycirculation.The
clearedvacuolesrepresentmarrowfatthatisnow
impactedinadistalvesselalongwiththecellular
hematopoieticprecursors.

47. Fat embolus in a glomerulus (kidney)

48. B-Air Embolism
•Gasbubbleswithinthecirculationcanobstructvascularflow.
•Enterthecirculationduringobstetricproceduresorasa
consequenceofchestwallinjury.
•Inexcessof100ccisrequiredtohaveaclinicaleffect

49. C-Amniotic Fluid Embolism
•Underlyingcauseistheinfusionofamnioticfluidorfetal
tissueintothematernalcirculationviaatearintheplacental
membranesorruptureofuterineveins.
•Characterizedbysuddenseveredyspnea,cyanosis,and
hypotensiveshock,followedbyseizuresandcoma.

50. 6-Infarction

51. •Aninfarctisanareaofischemicnecrosiscausedby
occlusionofeitherthearterialsupplyorthevenous
drainageinaparticulartissue.
•Nearly99%ofallinfarctsresultfromthromboticor
embolicevents,andalmostallresultfromarterial
occlusion.

52. •Infarctsareclassifiedonthebasisoftheircolor
(reflectingtheamountofhemorrhage)andthe
presenceorabsenceofmicrobialinfection

53. •Red(hemorrhagic)infarctsoccur
(1)withvenousocclusions(suchasinovariantorsion);
(2)inloosetissues(suchaslung)
(3)intissueswithdualcirculations(e.g.,lungandsmall
intestine).

54. •White(anemic)infarctsoccur
1.witharterialocclusionsinsolidorganswithend-
arterialcirculation(suchasheart,spleen,andkidney)
2.Solidtissues

55. Examples of infarcts. (A) Hemorrhagic, roughly wedge-shaped
pulmonary infarct. (B) Sharply demarcated white infarct in
the spleen.

56. •Thedominanthistologiccharacteristicofinfarctionis
ischemiccoagulativenecrosis
•mostinfarctsareultimatelyreplacedbyscartissue.
•Thebrainisanexceptiontothesegeneralizations;
ischemicinjuryinthecentralnervoussystemresults
inliquefactivenecrosis

57. •Remotekidneyinfarct,
nowreplacedbyalarge
fibroticcorticalscar.

58. •Septicinfarctionsmaydevelopwhenembolization
occursbyfragmentationofabacterialvegetation
fromaheartvalveorwhenmicrobesseedanarea
ofnecrotictissue.

60. 7-Shock

61. •Shock,orcardiovascularcollapse,isthefinal
commonpathwayforanumberofpotentially
lethalclinicalevents,includingseverehemorrhage,
extensivetraumaorburns,largemyocardial
infarction,massivepulmonaryembolism,and
microbialsepsis.

62. •givesrisetosystemichypo-perfusioncausedby
reductionin:
1.cardiacoutput
2.theeffectivecirculatingbloodvolume.
•Theendresultsarehypotension,followedby
impairedtissueperfusionandcellularhypoxia.

63. Principal MechanismClinical ExamplesType of Shock
Failureofmyocardial
pump owingtointrinsic
myocardial damage,
extrinsicpressure,
orobstructiontooutflow
-Ventricularrupture
-Arrhythmia
-Cardiactamponade
-Pulmonaryembolism
-Myocardialinfarction
Cardiogenic
Inadequatebloodorplasma
volume
-Hemorrhage
-Fluidloss,e.g.,vomiting,
diarrhea,burns,ortrauma
Hypo-volemic
Peripheralvasodilationand
poolingof blood;
endothelial
activation/injury;
leukocyte-induced
damage; disseminated
intravascularcoagulation;
activationofcytokine
cascades
-Overwhelming microbial infections
-Endotoxic shock
-Gram-positive septicemia
-Fungal sepsis
Septic

64. Lesscommonly:
1.Neurogenicshock-inthesettingofanesthetic
accidentorspinalcordinjury,owingtolossof
vasculartoneandperipheralpoolingofblood.
2.Anaphylacticshock,initiatedbyageneralized
IgE-mediatedhypersensitivityresponse,is
associatedwithsystemicvasodilatationand
increasedvascularpermeability

65. Clinical Course
•Theclinicalmanifestationsdependontheprecipitating
insult.
•Inhypovolemicandcardiogenicshock,thepatient
presentswithhypotension;aweak,rapidpulse;
tachypnea;andcool,clammy,cyanoticskin.
•Insepticshock,theskinmayinitiallybewarmand
flushedbecauseofperipheralvasodilation.

66. END