The document discusses various hemodynamic disorders including edema, hemorrhage, thrombosis, embolism, and shock. It defines each condition and describes their mechanisms and presentations. Edema is an accumulation of fluid in tissues and can be caused by increased hydrostatic pressure, decreased oncotic pressure, lymphatic obstruction, or sodium retention. Hemorrhage is the leakage of blood from vessels, while thrombosis is the formation of a clot within vessels. Embolism occurs when a clot or other material travels through the bloodstream and blocks a vessel in another part of the body.

1. Haemodynamic disorders
By
Chapima F.
Lecturer/ Special Research Fellow

2. Introduction
 Hemodynamics is the study of blood flow
 The circulatory system is controlled by homeostatic
mechanisms
 The best known homeostatic mechanisms are regulators
that keep the composition of the extracellular fluid constant,
especially with regard to temperature, pH, osmolality, and
the concentrations of sodium, potassium, glucose, carbon
dioxide, and oxygen

3. Introduction …………
 Normal fluid homeostasis is maintained by blood vessel
wall integrity, intravascular pressure and osmolarity
with in certain physiologic ranges
 Therefore, changes in intravascular volume, pressure,
protein content, or alterations in endothelial function affects
the movement of water across the vascular wall

4. Lecture outline
This lecture reviews the following major disturbances
involving the hemodynamic system;
 Edema
 Hemorrhage
 Thrombosis
 Embolism
 Infarction
 Hyperemia and Congestion
 Shock

5. Oedema

6. Definition
 Accumulation of fluid in
the interstitial spaces
(Localized or Generalized)
 Approximately 60% of the
lean body weight is water
 40% is intracellular
 15% interstitial
 5% plasma

7. Types
1. Anasarca: (ana =
throughout, sark = flesh) it is
a severe and generalized form
of edema with widespread
subcutaneous tissue swelling
usually caused by renal
failure, liver failure, heart
failure

8. Types ……..
Effusions into body cavities
2. Hydrothorax – in the pleural cavity
3. Hydropericardium – in the pericardial cavity
4. hydroperitoneum (ascites) – in the peritoneal cavity.
Note: (extravagate: to move out of the vasculature)

9. Mechanism of oedema formation
 Edema formation is determined by the following factors:
◼ Hydrostatic pressure – force fluid out of its
compartment
◼ Oncotic pressure – pulls water into its compartment
◼ Lymphatic channels – obstruction
◼ Sodium levels and water retention
◼ Vascular permeability

10. Mechanism of oedema formation……
 Fluid movement between the vascular and interstitial
spaces is governed mainly by two opposing forces
◼ The hydrostatic pressure and
◼ The colloid osmotic pressure
 Based on this, there are four primary forces that can
determine fluid movement between two spaces (Starling
forces)

11. Mechanism of oedema formation……
1. The Capillary Hydrostatic Pressure - forces fluid out of
the intravascular space into the interstitium
2. The Interstitial Fluid Hydrostatic Pressure forces fluid
out of the interstitial space into the intravascular space
3. The Plasma Colloid Osmotic (Oncotic) Pressure -
causes osmosis of fluid into the intravascular space from
the interstitium space due to the presence of plasma
proteins

12. Mechanism of oedema formation……
4. The Interstitial Fluid Colloid Osmotic (Oncotic)
Pressure - tends to cause osmosis of fluid into the
interstitium from the intravascular space

13. Mechanism of oedema formation……
 Normally, the outflow of fluid (due
to increased hydrostatic
pressure) at the arteriolar end of
the microcirculation is nearly
balanced by the inflow of fluid at
the venular end (due to slightly
elevated osmotic pressure)
 The small net outflow of fluid in the
interstitial space, then drained by
the lymphatic vessels

14. Mechanism of oedema formation……
 Edema results when the
movement of fluid from
the vasculature into the
interstitial spaces and vice
versa is not well balanced
and tends to accumulates
in the interstitial space
 May be transudate or
exudate

15. Types of oedema ……..
1. Edema due to increased capillary hydrostatic pressure;
◼ Deep venous thrombosis due to impaired venous return
◼ Congestive heart failure
◼ Pulmonary oedema
◼ Cerebral oedema

16. Types of oedema
2. Edema due to decreased plasma oncotic pressure as a
result of decreased plasma proteins;
◼ Protein loosing glomerulopathies such as nephrotic
syndrome
◼ Decreased protein synthesis as in liver cirrhosis due to
liver damaged
◼ Malnutrition

17. Categories of oedema ……
3. Lymphatic obstruction
 Obstruction of the lymphatic channels
leads to the accumulation of fluid in the
interstitial space
 Such kind of edema is called lymphatic
edema
Seen in;
 Parasitic infection. e.g. filariasis
 Lymphatic obstruction secondary to
neoplastic infiltration e.g. breast cancer
 Post surgical resection or post
irradiation

18. Categories of oedema ……
4. Sodium and water retention
 Sodium & subsequently water retention occurs in various
clinical conditions such as congestive heart failure & renal
failure.
 In these conditions, the retained sodium & water result in
increased capillary hydrostatic pressure which leads to the
edema

19. Clinical presentation of edema
Localized
 Deep venous thrombosis
 Pulmonary edema
 Lymphatic edema
 Brain edema
Generalized
 Nephrotic syndrome
 Liver cirrhosis
 Heart failure
 Renal failure
 Malnutrition

20. Morphology of edema
 Microscopically, manifests as subtle cell swelling where
there is clearing and separation of extracellular matrix

21. Haemorrhage

22. Definition
 Haemorrhage is the extravasation of blood outside the
blood vessel
 Can be capillary or venous haemorrhage
 External or internal
Causes
 Can be due to damaged blood vessel or defective clot
formation.
◼ Trauma
◼ Atherosclerosis
◼ Inflammatory or neoplastic erosion of a blood vessel wall

23. Types
 Hematoma: accumulation of blood with in tissue.
 Petechiae: minute 1 to 2mm hemorrhages into skin,
mucous membranes, or serosal surfaces
 Purpura: slightly larger (≥3mm) hemorrhages
 Ecchymoses: larger (>1 to 2cm) subcutaneous
hematomas (such as bruises)
 Haemothorax, hemopericardium, hemoperitoneum, or
hemarthrosis (in joints): Large accumulations of blood in
respective body cavities

24. Types of haemorrhage …….

25. Types of haemorrhage …….

26. Complications of haemorrhage
 Depends on the volume of blood loss and the rate of
bleeding.
◼ Rapid loss of up to 20%, or slow losses of even larger
amounts, may have little impact in healthy adults
◼ Greater losses may cause hypovolemic shock
 The site of hemorrhage is also important; bleeding that
would be trivial in the subcutaneous tissues can cause
death if located in the brain

27. Complications of haemorrhage ………
 Chronic or recurrent external blood loss (e.g., due to peptic
ulcer or menstrual bleeding may cause iron deficiency
anaemia
 By contrast, internal bleeding does not lead to iron
deficiency as iron is recycled from phagocytosed red cells
(e.g., a hematoma)

28. Thrombosis

29. Thrombosis
 Clotting of blood (thrombus) in the cardiovascular system
of a living body
Normal hemostasis
 Is achieved by well-regulated processes that accomplish
two important functions:
◼ Maintenance of blood in a clot-free state in blood
vessels
◼ Localize haemostatic plug at a site of vascular injury

30. Pathogenesis
 There are three factors that
influence thrombus formation
referred to as a Virchow’s triad:
◼ Endothelial injury
◼ Stasis or turbulence of blood flow
◼ Blood hypercoagulability

31. 1. Endothelial injury
 Is the most important factor in thrombus formation and by
itself can lead to thrombosis.
 Endothelial injury is particularly important in heart and
arterial thrombus formation
 Endothelial injury trigger fibrin formation, as well as platelet
adhesion and aggregation.

32. Endothelial injury …………
Causes;
 Myocardial infarction
 Hemodynamic stress such as hypertension directly
damaging the endothelium
 Bacterial toxins, hypercholesterolemia, radiation and
cigarette smoking
 Eosinophilia - eosinophils release granules called Charcot
– Leyden damaging the endocardial endothelium

33. 2. Alterations in normal blood flow
 Under normal conditions, blood flow is laminar, that is,
cellular elements flow centrally and separated from the
endothelium by the plasma.
Stasis & turbulence therefore:
1. Disrupt the laminar flow and bring platelets into contact
with the endothelium there by triggering platelet adhesion
and aggregation
2. Also prevent dilution of activated clotting factors by freshly
flowing blood

34. Alterations in normal blood flow ……..
3. Retard the inflow of clotting factor inhibitors and permit
the build up of thrombi.
 Stasis is a major factor in the development of venous
thrombi while turbulence contributes to arterial &
cardiac thrombosis

35. 3. Hypercoagulability
 Hypercoagulability is any alteration in the coagulation
pathway
 It is a less common cause of thrombosis
 It can be divided into primary and secondary factors
Primary (Genetic)
 Mutations in factor V (Lieden factor)
 Increased levels of factor VIII, IX, or XI or fibrinogen
 Anti thrombin III deficiency
 Protein C or S deficiency

36. Hypercoagulability …………
 Secondary (Acquired)
◼ Myocardial infarction
◼ Tissue damage (surgery, fracture, burns)
◼ Prolonged bed rest
◼ Smoking, Sickle cell anaemia
◼ Cancers - cancers release procoagulant tissue products
causing thrombosis
◼ Oral contraceptives
◼ Hyper estrogenic state e.g. pregnancy

37. Morphology of Thrombi
 Thrombi may develop any where in the cardiovascular
system and can be divided into venous or arterial thrombi.
Arterial thrombi
 Arise at the site of endothelial injury
 Grow in a retrograde fashion, against site of attachment.
 Flow towards the heart
 Has firm attachment
 They usually occlude the blood flow

38. Most common site of arterial thrombi
 Coronary arteries
 Cerebral arteries
 Temporal arteries
Venous thrombi
 Arise at the area of stasis
 Grow in the direction of blood flow
 Has loose attachment, hence, propagating flow tail may
undergo fragmentation
 On every occasion occlude the blood flow

39. Fate of a thrombus
 Dissolution
 Propagation and obstruction
 Organization and
 Recanalization
 Embolization

40. Embolism

41. Definition
 An embolus is a detached intravascular solid, liquid or
gaseous mass that is carried by blood to distant sites from
its point of origin.
 After traveling via the blood, an embolus can obstruct any
small blood vessel.
Causes of embolism
 Thrombus (99% of emboli arise from a thrombus. Such
embolus is called thromboembolus)

42. Causes …………
 Fat globules - usually follows fracture of bones
 Bubbles of air
 Amniotic fluid - amniotic fluid or foetal tissue enters
maternal circulation via the placental bed or ruptured
uterine veins
◼ Characterized by sudden severe dyspnoea, cyanosis
and hypotensive shock, followed by seizures and coma.

43. Causes …………
 Infected foreign material
 Bits of bone marrow
 Fragment of material from ulcerating atheromatous plaque
 Fragments of a tumour

44. 1. Thromboembolism
 Unless otherwise specified, the term embolism should be
considered to mean thromboembolism.
 This is because thromboembolism is the commonest form
of embolism (99%).
Classifications
 Based on its sites of origin & impaction, thromboembolism
can be divided into:
◼ Pulmonary embolism
◼ Systemic embolism
◼ Crossed embolism (Paradoxical embolism)

45. a. Pulmonary thromboembolism (PTE)
 PTE refers to the impaction of an embolus in the
pulmonary arteries & their branches.
Thrombi origin
 95% is derived from a thrombi in deep vein thrombosis
 Also from the right side of the heart
b. Crossed embolism (Paradoxical embolism)
 This occurs in the presence of patent foremen ovale
where an emboli is transferred from the right side of the
heart to left side, then into the systemic circulation

46. c. Systemic thromboembolism
 Emboli traveling within the arterial circulation
 80% arise from intracardiac mural thrombi which is
associated with left ventricular wall infarcts
 The major sites for arteriolar embolization are:
◼ Lower extremities (75%)
◼ Brain (10%)

47. Infarction

48. Definition
 An infarct is an area of ischemic necrosis caused by
occlusion of either the arterial blood supply or venous
blood drainage in a particular tissue
 Nearly 99% of all infarcts are thrombotic or embolic in
nature and almost all are due to arterial occlusion.
Classifications
 Based on their colour (Red or white infarct)

49. 1. Red (hemorrhagic) infarcts
 Red (hemorrhagic) infarcts occur in venous occlusions
(such as in ovarian or testicular torsion)
 Also in loose tissues (such as the lungs)
 And in tissues with dual circulations such as the lungs and
the small intestine)
2. White (anaemic) infarcts
 White (anaemic) infarcts occur in arterial occlusions and
in solid organs with end-arterial circulation (such as the
heart, the spleen, and the kidneys)

50. Morphological features
 Red (hemorrhagic) infarcts;
Hemorrhagic (red) roughly wedge-
shaped pulmonary infarct.
 White (anaemic) infarcts; Sharply
demarcated white infarct in the
spleen.

51. Morphological features………
 Some infarcts are replaced by scar
tissue e.g. renal fibrotic cortical scar
 However, ischemic injury in the central
nervous system results in liquefactive
necrosis (brain)
 The dominant histologic
characteristic of infarction is ischemic
coagulative necrosis

52. Hyperaemia and Congestion

53. Introduction
 Both indicate a local increase in blood volume in a
particular issue with associated capillary dilatation and a
potential fluid extravasation

54. Hyperaemia
 Hyperaemia is an active process, where there is
increased in flow of blood that leads to engorgement of the
tissue with oxygenated blood, resulting in erythema.

55. Hyperaemia

56. Congestion
 Congestion is a passive process, where there is
diminished outflow of blood which leads to swollen capillary
bed with deoxygenated venous blood resulting in cyanosis

57. Congestion

58. Shock

59. Introduction
 Shock, or cardiovascular collapse, is the final common
pathway for a number of potentially lethal clinical events
such as;
◼ Severe hemorrhage
◼ Extensive trauma or burns
◼ Large myocardial infarction
◼ Massive pulmonary embolism and microbial sepsis.

60. Introduction ……….
 Shock arise due to systemic hypo-perfusion caused by
reduction in:
◼ Cardiac out put and
◼ Effective circulating blood volume
 The end results are hypotension, followed by impaired
tissue perfusion and cellular hypoxia.

61. Types of shock

62. Less common types
 Neurogenic shock - in the setting of anaesthetic accident
or spinal cord injury, owing to loss of vascular tone and
peripheral pooling of blood.
 Anaphylactic shock - initiated by a generalized IgE
mediated hypersensitivity response associated with
systemic vasodilatation and increased vascular
permeability

63. Clinical features
 Depend on the precipitating insult.
 In hypovolemic and cardiogenic shock, the patient presents
with;
◼ Hypotension
◼ Weak and rapid pulse
◼ Tachypnoea
◼ Cool, clammy and cyanotic skin
 In septic shock, the skin may initially be warm and flushed
because of peripheral vasodilation.

64. END OF LECTURE

65. References
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Philadelphia, J.B. Saunders Company. 6th edition 1999
 F.B. Walter and M.S Israel; General Pathology, Churchill Livingston
Edinburgh and London, 4th edition, 1974
 Harsh Mohan. (2015). Textbook of Pathology. 7th Edition. Jaypee
Brothers Medical Publishers (P) Ltd. ISBN: 978-93-5152-369-7
 Macfarlane, Reid, Callander, Illustrated Pathology, Churchill Livingstone,
5th edition, 2000.
 Vinay Kumar, Ramzi S. Cotran and Stanley L. Robbins. (2018). Robin’s
Basic Pathology. 10th Edition. Saunders Elsevier, Philadelphia, USA.
ISBN 978-0-323-48054-3