1. Hemodynamic disturbance
DR. USHA.M

2. HEMODYNAMICS
Literally means “Blood movement” is the study of blood flow.

3. Hemodynamic disturbance
Edema
Hyperemia & congestion
Hemorrhage
Thrombosis
Infarction
Shock

4. Edema Normal body water distribution:- Two compartments:
Intracellular – comprising of two- thirds of total body fluid.
Extracellular – comprising of one- third of total body fluid.
1. Interstitial compartment- 75%
2. Intra vascular compartment – 25%

5. Normal fluid exchange There are two ends for a capillary
1. Arteriolar end
2. Venous end
The pressure is high in the arteriolar end then the venous end.Normally the fluid moves out from the vessel in arteriolar end into interstitial tissue. From interstitial tissue same fluid moves back into vessel at venous end.The small amount of fluid which is left in interstitial space is cleared by lymphatics.

7. Starling forces

9. Normal fluid pressures
1. Osmotic pressure
Is exerted by the chemical constituents of the body fluids
Eg. Electrolytes – crystalloid osmotic pressure
proteins (albumin)- oncotic osmotic pressure.
2. Hydrostatic pressure
Pressure within the blood vessel.

10. Edema
Is accumulation of excessive fluid in the interstitial spaces.

11. Classification of edema according to distribution of fluid
Localized edema
involving one organ or part of the body.
eg-pleural effusion,ascitis,pericardial effusion ,etc.
2. Generalized edema
Involving the entire body- ANSARCA

12. Pathogenesis of edema:-
Increased hydrostatic pressure
Increased permeability of the vessel wall
Decreased oncotic pressure
Sodium retention in the kidneys
Obstruction of lymph flow

13. 1. Hydrostatic edema
Results from increased intra vascular pressure (hydrostatic pressure).

14. Causes :- Impaired venous return congestive cardiac failure
constrictive pericarditis,
ascitis (liver disease)
Venous obstruction
thrombi, tumor
Arteriolar dilatation
heat, inflammation

15. 2. Increased vascular permeability
Commonest cause is inflammation.Release of inflammatory mediators like histamine, bradykinin, PAF & others leads to increased permeability.
Other causes: Injury,

16. 3.Decreased plasma oncotic pressure
1.Decresed synthesis in the liver – end stage liver disease.
2.Incresed loss in urine(nephrotic syndrome) or stool (protein losing enteropathy)
3.Inadequte intake-kwashiokar

18. Lymphatic obstruction
Elephantiasis
Edema of the arm following surgical resection of axillary lymph nodes
Edema of hand following post irradiation fibrosis.

19. Ultra filtrate of plasma Edema of inflamed tissue
TRANSUDATE & EXUDATE
Feature
Transudate
Exudate
Definition
Ultra filtrate of plasma
Edema of inflamed tissue
Endothelial changes
No changes
 endothelial permeability
Character
Non inflammatory edema
Inflammatory edema

20. Feature
Transudate
Exudate
Protein
Low(<1g/dl)
High (>2.5g/dl)
Glucose
Same as plasma
Low(,60mg/dl)
Specific gravity
Low(1.015)
High(>1.018) PH
>7.3
<7.3
LDH
low
High
Cells
Few
Many
Example
CCF
Infections

22. Renal edema Causes:- 1. Nephorotic syndrome 2. Glomerulonephritis
3. Acute tubular injury

23. Nephorotic edema Heavy proteinuria hypoproteinemia
Activation of renin decreased plasma
Angiotensin oncotic pressure
Mechanism
Retention of Na &water
edema

24. Nephritic edema Glomerulonephritis glomerular lesion
I decreased filtration followed by increased absoption of Na & water by tubules
Na & water retention
edema

25. Acute tubular injury Toxins , drugs ATN Fails to excrete Na & water
edema

26. Cardiac edema activation of renin angiotensin
congestive cardiac failure
↓ cardiac output
↑ central venous renal hypoperfusion
Pressure
activation of renin angiotensin
↑ capillary hydrostatic aldosterone mechanism
pressure
Na & water retention
edema

27. Pulmonary edema causes :- Left heart failure ARDS Shock
Infections - pneumonia

28. left ventricular failure
↑ hydroastatic pressure
↑ pressure in pulmonary veins
↑ pressure in pulmonary capillaries
interstitial edema
pressure on alveolar wall &breaks alveolar
linning
alveolar edema

29. Hepatic Oedema hepatic pathology (e.g. cirrhosis) ↓
obstruction of portal venous system
increased hydrostatic pressure
&
↓albumin synthesis d.t. hepatocyte damge
hypoproteinaemia
transudate oedema (ascitis).

30. Ascites

31. Cerebral edema Causes:- 1. Infection - encephalitis,meningitis
2. Brain infarct, hemorrhage
3. Trauma
4. Tumors

32. Localised Oedema: acute inflammatory oedema
↑ vascular permeability exudate
↑ hydrostatic pressure of capillaries  hyperaemia
↑ osmotic pressure of interstitial fluid
↑ fluidity of ground substance
allergic (hypersensitivity) oedema
histamine release  ↑ vascular permeability  exudate (e.g. allergic rhinitis)

33. Pitting & non pitting edema
is clinical terms for subcutaneous edema of leg.

34. Pitting Oedema

37. Clinical Features of Oedema
Considerable quantities must accumulate before clinically apparent (oedema can be assessed by weighing the patient
approx. 5 litres)
Generalised
Cardiac Oedema
gravitational distribution
pitting oedema  holds depression for a few minutes
Renal Oedema
fluid retention
generally distributed in C.T.  puffy face/eyelids
Serous Cavities
e.g. hydrothorax/ascites
Brain Oedema
swollen; narrow sulci & flattened gyri
Pulmonary Oedema
exudate
prone to infection  e.g. bronchopneumonia
rales

38. thank you

39. Hemorrhage
Indicates extravasation of blood due to rupture of vessel.

40. Classification based on origin
1. Cardiac- penetrating wound
rupture of ventricles in MI
2. Arterial – trauma
rupture of aneurysm
3. Capillary – trauma, surgery
4. Venous – trauma, surgery

41. Petechiae, Pupura, Ecchymoses
Refers to the hemorrhage into the skin & mucosae.
Petechiae- pinpoint hemorrhage ( < 1mm)
Purpura- 1mm- 1cm in diameter
Echymoses- >1cm

42. Petechiae
Caused by abnormalities in number or function of platelets or abnormalities in capillary wall (e.g. scurvy)

43. Purpura
The palpable purpura on the foot of this nearly 3-year-old boy are associated with the disease Henoch-Schönlein Purpura.
Henoch-Schönlein Purpura involves small vessels, not capillaries. Another common cause of purpura is vasculitis induced by an allergic reaction to drugs.

44. Ecchymosis
The purpura and ecchymosis on the skin of this 12-year-old boy were the presenting symptoms of his acute myelogenous leukemia.
The hemoglobin is converted to bilirubin (greenish) and hemosiderin (brown)

45. Hematoma
Is grossly visible accumulation of extravasted blood in tissue.
First it is red, then as the blood is deoxygenated it becomes dusky & bluish red.

46. Body cavity hemorrhage
Hemothorax – accumulation of blood in pleural cavity
Hemopericardium – in pericardial cavity
Hemoperitonium – in peritonial cavity
Hemoarthrosis – in intra – articular space
Hematocephalus – in ventricles of brain

47. Hematuria Is appearance of blood in urine.
Microscopic – detectable by microscopic examination of urine.
Macroscopic – visible to naked eye
Hematuria signifies disease of kidney or urinary tract

48. Hematemesis Is vomiting of blood.
Sign of esophageal & gastric hemorrhage like rupture of esophageal varices & peptic ulcer bleeding.

49. Hematochezia Bleeding through rectem.
Sign of diseases in large intestine.

50. Melena Black colored blood in stools. Indicates bleeding in upper GIT.
Blood is partialy digested by HCLof gastric juice & transformed into a black pigment called hematein.This pigmentis not digested in the intestines & is passed in the feces.

51. Epistaxis & Hemoptysis
Epistaxis is bleeding from the nose.
Hemoptysis is bleeding from lungs.

52. Menorrhagia & Metrorrahagia
Menorrhagia is heavy menstrual bleeding.
Metrorrhagia occurs at any time & is not related to menstrual cycle.

53. Effects of Hemorrhage Site of hemorrhage Rate of blood loss
brain, pericardium, pleural spac
Rate of blood loss
acute
loss of > 20% of blood volume may cause hypotension or hypovolemic shock
hemoglobin concentration not altered
non-acute
volume loss compensated by shift of fluid from extravascular to intravascular compartment
hemoglobin concentration decreased

54. HYPEREMIA & CONGESTION
Is increase in volume of blood in a particular tissue.
Hyperemia is an “active process” , the increased blood influx results from arteriolar dilatation.
Congestion, also known as “passive hyperemia”, results due to stagnation of blood because of venous obstruction.

55. Normal
Figure 4-3 Hyperemia versus congestion. In both cases there is an increased volume and pressure of blood in a given tissue with associated capillary dilation and a potential for fluid extravasation.
Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 27 June :26 PM)
© 2005 Elsevier

56. Hyperemia
In hyperemia, increased inflow leads to engorgement with oxygenated blood, resulting in erythema.
Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 27 June :26 PM)
© 2005 Elsevier

57. Congestion
In congestion, diminished outflow leads to a capillary bed swollen with deoxygenated venous blood and resulting in cyanosis.
Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 27 June :26 PM)
© 2005 Elsevier

58. Examples:- Hyperemia:- Inflammation Blushing – adrenergic stimulation
Exercise – incresed blood flow to the muscle.
Congestion:-
Obstruction of veins due to thrombi or backward pressure due to heart failure.

59. Color of hyperemic & congested tissue:-
Hyperemic tissue contains increased amounts of oxygenated blood & therefore the tissue appears bright red.
Congested tissue contains increased amounts of deoxygenated blood & appears blue.
Hyperemic tissue is warm, while congested blood is cold & clammy.

60. Chronic venous congestion (CVC):-
In CVC there is long standing there is accumulation of deoxygenated blood & hence there is damage to the tissue.

61. Mechanism heart failure left heart failure right heart failure
Pressure into pressure into the
Pulmonary vein systemic venous system
CVC LUNGS CVC LIVER SPLEEN KIDNEY

62. CVC Lung Causes:- Left heart failure Gross :-
The lungs are heavy. Lungs appear brown- BROWN INDURATION OF LUNGS.

63. CVC Lungs
Micro:-
Rupture of congested vessel results in edema & hemorrhage. Lysis of RBC’s releases hemosiderin pigment which is taken up by macrophages – HEART FAILURE CELLS.

64. View of pulmonary congestion and edema
View of pulmonary congestion and edema. Often caused by an increase in hydrostatic pressure, a protein poor transudate seeps into interstitial and alveolar spaces. Note the engorged alveolar wall capillaries. If capillaries rupture, RBCs will escape into the alveolar space

65. Heart failure cells are hemosiderin laden macrophages
Heart failure cells are hemosiderin laden macrophages. Blood escapes into the alveolar space because chronic congestion causes the thin walled alveolar capillaries to burst. Note the thickening of the alveolar septae. This is caused by chronic pulmonary congestion and edema.
Note the thickening of the alveolar septae. This is caused by chronic pulmonary congestion and edema.

66. CVC Liver Causes:- Right heart failure
Occlusion of inferior vena cava or portal vein.
GROSS APPEARANCE:-
NUTMEG APPEARANCE – Alternate areas of red & yellow .

67. CVC Liver
Micro:-
Periportal zone
midzonal
Centrilobular

68. CVC Liver (MICRO)
Blood fills up the central vein & sinusoids around it. Followed by centrilobular hepatocytes necrosis.
In the long standing cases the necrotic area is replaced by fibrous tissue.
The areas with blood appears red & areas with fibrosis appears whitish yellow- NUTMEG APPEARANCE.

69. Nutmeg liver compared with actual nutmeg.
Courtesy of Dr. Ed Friedlander

70. This view shows a close up of hemorrhagic central necrosis
This view shows a close up of hemorrhagic central necrosis. Necrotic cells in the central area have been removed (cell dropout) and been replaced by cellular debris and hemorrhge. There is evidence that the passive congestion and hemorrhage is chronic, as many of the RBCs have been degraded into hemosiderin.

72. CVC Spleen Causes:- Right heart failure Portal hypertension GROSS:-
Spleen is enlarged & congested.

73. CVC Spleen (micro) Red pulp appears congested.
GAMMA GANDY BODIES OR SIDEROFIBROTIC NODULES:-
Deposits of hemosiderin & calcium salts on fibrous tissue.

74. Gamma gandy bodies

75. CVC Kidney Cause:- Right heart failure Obstruction of renal vein
Gross:-
Kidney is congested.

76. CVC Kidney (micro) Glomeruli – shows mesangial proliferation.
Tubules – shows degenerative changes (cloudy swelling).

77. Thank you