The document covers hemodynamic disorders, focusing on the pathological mechanisms related to bleeding, hyperemia, and thrombosis. It discusses various types of hemorrhage, their causes, and the physiological and pathological implications of increased blood volume and flow, including conditions related to thrombus formation and embolism. Additionally, it details infarction, its processes, morphology, and outcomes within different tissues and organs.

1. Hemodynamic Disorders
Nasuhi Engin AYDIN, M.D.
Department of Pathology

2. Aims and scope of the lecture
•Basic mechanisms and clinical relevance
with pathological aspects

3. Pathological aspects of normal
• Loss of vessel wall integrity : bleeding (hemorrhage)
•Changes in intravascular pressure or vascular
volüme : hyperemia, edema, ischemia
• Disorders in maintence of blood as a liquid :
thrombosis, embolism, infarction

4. 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.

5. Hemorrhage
1-2 mm petechiae
3-5 mm purpura
1-2 cm ecchymose
Nomenculature according to site:
Hemothorax, hemopericardium,
hemoperitoneum, hemarthrosis
5

6. 6
Petechial hemorrhages seen on the epicardium of the heart.
Petechiae are classically found when a coagulopathy is due
to a low platelet count. They can also appear following sudden hypoxia.

7. 7
Petechial hemorrhages on the conjunctiva

8. 8
The blotchy areas of hemorrhage in the skin are called ecchymoses , or also as areas of
purpura. Ecchymoses are larger than petechiae. They can appear with coagulation disorders.

9. 9
Localized collection of blood outside the vascular system within tissues is known as a
hematoma. Here is a small hematoma under the toenail following trauma, which has a bluish
appearance from the deoxygenated blood within it.

10. 10
This is hemopericardium as demonstrated by the dark blood in the pericardial sac opened
at autopsy. Massive blunt force trauma to the chest (often from the steering wheel) causes
a rupture of the myocardium and/or coronary arteries with bleeding into the pericardial
cavity. This leads to cardiac tamponade

11. 11
A blood clot is seen over the external surface of the dura. Thus, this is an epidural
hematoma. Such a location for hemorrhage is virtually always the result of trauma
that causes a tear in the middle meningeal artery

12. 12
This cerebral hemorrhage occurred in conjunction with an overdose of cocaine.
Such acute hemorrhages can occasionally be seen with cocaine use.

13. Hyperemia
•a local increase of blood volume and flow in
a particular tissue.
Normal blood flow
Hyperemia

14. Physiological : Exercise
Pathological : Inflammation
•Hyperemia is a increase of blood flow and volume
in a particular tissue due to arteriolar dilation

15. • Gross or macroscopic ( i.e., naked eye examination):
Larger, red, increased temperature, cut surface is full rich
in blood and wet
• Light microscopic: Dilation of arterioles and capillaries
Morphology of hyperemia

16. •Congestion is a local increase of blood volüme in
capillaries and venules resulting from impaired venous
return from a tissue.
Congestion
Normal blood fluid
Hyperemia
Congestion

17. Local increase of blood volume
Hyperemia : active process arteriolar dilatation
Congestion : passive process venous stagnation
Cyanosis: accumulation of deoxygenated hemoglobin
giving the tissue a blue-red color
17

18. 18

19.  Congestion
Systemic due to heart failure
•Etiology
-Left heart failure
-Right heart failure
Pulmonary cong.
Systemic cong.
1. External pressure
2. Internal occlusion
Local

20. Edema
Hemorrhage
Heart failure cells
Brown induration
Consequences of pulmonary congestion

21. Gross (macroscopic) :
Increased volume and
weight of the organ; blue-
red color (cyanosis),
wetness and excessive
blood on the cut surface.
Morphology

22. 22
The lung has a red, hyperemic cut surface, reflecting congestion,
due to increased hydrostatic pressure, as seen in cases of left
heart failure. The transudate, mixed with air in the alveoli, gives
the cut surface a frothy appearance

23. Acute pulmonary congestion
Chronic pulmonary congestion

24. Consequences of liver congestion
Atrophy
Fatty change
Centrilobular necrosis
Fibrosis ‘cardiac cirrhosis’

25. 25
A "nutmeg" liver seen with chronic congestion of the liver. The dark red congested regions
represent accumulation of erythrocytes in centrilobular regions.

26.  The central regions of the lobules become dark red
surrounded by a lighter zone of uncongested liver substance.
“ Nutmeg liver”

27. •Liver congestion
Central veins and hepatic sinuses of the
centrilobular regions are distended with
blood.

28. 28
Microscopically, the nutmeg pattern results from congestion around
the central veins, as seen here. This is usually due to a "right sided" heart failure.

29. • Microscopic changes in ‘nutmeg’ liver：
1) Atrophy and/or necrosis of the liver cells in the
mainly in centrilobular regions
2) Fatty change of the liver cells in the peripheral
part of the lobules

30. ‘Cardiac cirrhosis’ of the liver in the longstanding cases
F
F
F

31. Thrombosis and thrombus

32. Thrombosis and thrombus
• Thrombosis is the process of formation of
a solid mass of blood within blood vessels
or the heart in living body.
• The resultant mass is called a thrombus.

33. Normal hemostatic process
when a vessell is severed
normal hemostatic process
stops bleeding

34. VIRCHOW’S TRIAD,
i.e., factors effective in thrombus formation
• Endothelial injury (most important).
can induce thrombosis alone !
• Alterations in blood flow (stasis, turbulence)
• Hypercoagulability states

35. Antithrombotic activities of endothelial cells

36. Endothelial injury
• Trauma
• Radiation
• Vasculitis
• ‘cigarette smoke’ , Atherosclerosis
• Bacterial toxins
• Heart infarction

37. Alterations in normal blood flow
• Platelets are activated endothelial contact
• Slowed flow retards dilution of activated
clotting factors and also hepatic clearance
• Turbulence may also induce endothelial injury

38. Hypercoagulable states
Primary (genetic):
Factor V Leiden mutation
Antithrombin III deficiency
Protein C deficiency
Protein S deficiency

39. Hypercoagulable states
Secondary (acquired): High risk
Prolonged bed rest or immobilization.
Heart infarction,
Tissue damage
(surgery, fractures, burns),
Cardiac failure.
Cancer, leukemia

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

41. Initiation and propagation of thrombus

43. White thrombus
Red thrombus
Mixed thrombus
Fibrin thrombus
Types of thrombus

44. Mural thrombus
in heart chamber

45. RED THROMBUS IN A VEIN

46. White thrombus
Site: heart valves , arteries
Components: Platelet, fibrin
F F
F

47. Mixed thrombus
Site: heart chambers, veins
Components: Platelet, fibrin, erythrocytes
E
E
F
P
F

48. Fibrin thrombi
are visible
within
capillaries
 Fibrin thrombi in a glomerulus

49. Organization and recanalization
Detachment, ‘embolism’
Fate of thrombus formation

50. Organization and recanalization of thrombus
Thrombus is dissolved and
blood could flow again.

51. Recanalization
Arterial thrombus

52. Congestion, ischemia
Occlusion of a distal vessel by emboli
(i.e., detached thrombi)
Effects of thrombus formation

53. Embolism and embolus

54. • Embolism is a partial or complete obstruction of some
part of the vascular system by any mass (solid, liquid
or even gas !) carried in the circulation.
• The transported material is called an embolus
• The etiology of embolism > 95 % is detached thrombi

55. Types of embolus
•Thrombi >95 %, i.e., thromboemboli
•Foreign body
•Fat embolism
•Air embolism
•Fluid (amniotic) embolism

56. Sources:
Fractures of long bones
Soft tissue trauma
Fat embolism

57. 90% of individuals with severe skeletal injuries
10% with clinical findings(1-3 days)
Pulmonary insufficiency, neurologic symptoms
Fat embolism

58. Fat embolism

60. Etiology:
Intravenous therapeutic procedures
Obstetric procedures
Chest wall injury
Decompression sickness (nitrogen)
Air 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.

61. AMNIOTIC FLUID EMBOLISM
Incidence: 1/50 000 deliveries
Mortality rate: 80%
Clinical onset: Sudden severe dyspnea,
cyanosis, hypotensive shock, DIC

63. • Embolus from left heart cavity or arterial system
• Embolus from right heart cavity or venous system
• Embolus from portal veins
• Paradoxical embolism
• Retrograde embolism
Pathway of an embolus depends
on the part of the circulation:

65. PULMONARY THROMBOEMBOLISM
•Instantaneous death (>60%).
•Cardiovascular collapse.
•Right heart failure
1.Large emboli (5%):

67. 2. Small emboli (60-80%):
•Clinical silent in patients without
cardiovascular failure.
• blood flow from bronchial arteries
(collateral vascular supply)

68. 3. Between the extremes of large and small
emboli (10-15%): Pulmonary hemorrhage.
4. Multiple small emboli: Pulmonary
hypertension and vascular sclerosis.

69. Systemic (arteriel) embolism
I. 80-85% from heart, secondary to myocardial infarction.
II. 5-10% from auricular thrombi associated with rheumatic
heart disease and atrial fibrillation.
III. 5% from the dilated cardiac chamber of myocarditis /
cardiomyopathy.
VI. Less common sources: Debris from ulcerative
atheromata, or thrombi in aneurysms, infectious
endocarditis, prosthetic valves, paradoxical emboli.

70. INFARCTION
(INFARCT)

71. 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.

72. Intrinsic occlusion
for example, thrombosis,
embolism
expansion of atheroma
Vasospasm
Extrinsic compression
for example, twisting of the vessels
Etiology

73. INFARCTION
• Shape: Wedge-shaped
Segmental
Irregular
• Nature of necrosis
• Types: Red and white infarcts
Morphology of infarct

77. • 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.

78. •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.

79. white infarct/anemic infarct
•arterial occlusions
•firm tissues

83. Venous occlusions
Loose tissues
Tissues with dual circulations
Tissues previously congested
Blood flow reestablished
Red infarct/hemorrhagic infarct

84. The alteration of blood in pulmonary embolism

85. •Hemorrhagic infarct of the lung