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Hemodynamic

 Disorders
• Normal fluid homeostasis is maintained by vessel
  wall integrity, intravascular pressure and osmolarity
  within certain physiologic ranges.



• Changes in intravascular volume, pressure, or
  protein content, or alterations in endothelial
  function will affect the movement of water across
  the vascular wall.
1- Edema

Increased fluid in the interstitial tissue spaces.
Patho-physiologic Causes of Edema

- Increased Hydrostatic Pressure: Impaired venous return

- Reduced plasma osmotic pressure (Hypo-proteinemia): Liver

  cirrhosis, nephrotic syndrome

- Lymphatic Obstruction: Neoplastic, or postsurgical

- Sodium Retention: Excessive salt intake with renal insufficiency

- Inflammation: Acute inflammation, Chronic inflammation
Types of edema

• Anasarca: Generalized edema

• Dependent edema: Prominent feature of congestive

  heart failure, particularly of the right ventricle.

• Renal edema: Edema as a result of renal dysfunction or

  nephrotic syndrome is generally more severe than

  cardiac edema and affects all parts of the body equally.
• Peri-orbital edema: is a characteristic finding in
  severe renal disease.

• Pitting edema: finger pressure over substantially
  edematous subcutaneous tissue displaces the interstitial
  fluid and leaves a finger-shaped depression

• Pulmonary edema: most typically seen in the setting
  of left ventricular failure
Fetal Anasarca
EDEMA
Effusion
2- Hyperemia and Congestion


• Both indicate a local increased volume of blood in

  a particular tissue.
Hyperemia versus congestion.

In both cases there is an increased volume and pressure of
blood in a given tissue with associated capillary dilatation
and a potential for fluid extravasation.
In   hyperemia, increased inflow
leads to    engorgement with
oxygenated blood, resulting in

erythema.



In     congestion,     diminished
outflow leads to a capillary bed
swollen     with     deoxygenated
venous blood and resulting in

cyanosis.
Hyperemia
Congestion




Varicose Veins
3- Hemorrhage

Extravasation of blood due to vessel rupture
Types

• Hematoma: accumulation of blood within tissue.


• Petechiae: minute 1 to 2mm hemorrhages into skin,


  mucous membranes, or serosal surfaces.


• Purpura: slightly larger (≥3 mm) hemorrhages.
• Ecchymoses: larger (>1      to   2   cm) subcutaneous

 hematomas (i.e., bruises)

• Hemothorax, hemopericardium, hemoperitoneum, or

 hemarthrosis (in joints): Large accumulations of blood in

 one of the body cavities
Petechial hemorrhages of   Intracerebral bleeding
  the colonic mucosa
Subarachnoid Haemorrhage:
Petechiae &
Ecchymoses
Conjunctival Petechiae
Hemorrhage: Epidural hematoma
Hemothorax
4- Thrombosis
Hemostasis and Thrombosis
Normal hemostasis result of a set of well-regulated

  processes that accomplish two important functions:

(1) They maintain blood in a fluid, clot-free state in

  normal vessels.

(2) They are aimed to induce a rapid and localized

  hemostatic plug at a site of vascular injury.
•   Thrombosis: an inappropriate activation of

    normal   hemostatic    processes,   such as   the

    formation of a blood clot (thrombus) in

    uninjured vasculature or thrombotic occlusion of

    a vessel after relatively minor injury.
Both hemostasis and thrombosis are regulated by

 three general components:-

  – the vascular wall

  – platelets

  – the coagulation factors.
6  hemodynamic disorders
•   Three primary causes for thrombus formation,

    the so-called Virchow triad:

     (1) Endothelial injury

     (2) Stasis or slowing of blood flow

     (3) Blood hyper-coagulability
•   Virchow triad in thrombosis. Endothelial integrity is the single most important
    factor. Note that injury to endothelial cells can affect local blood flow and/or
    coagulability; abnormal blood flow (stasis or turbulence) can, in turn, cause
    endothelial injury. The elements of the triad may act independently or may
    combine to cause thrombus formation.
• Thrombi    may    develop    anywhere     in   the

 cardiovascular system, but stasis is a major factor

 in the development of venous thrombi

• An area of attachment to the underlying vessel

 or heart wall, frequently firmest at the point of

 origin, is characteristic of all thromboses.
• The propagating tail may not be well attached and,

  particularly in veins, is prone to fragmentation,

  creating an embolus.

• Mural thrombi - arterial thrombi that arise in heart

  chambers or in the aortic lumen, that usually adhere

  to the wall of the underlying structure
• Mural thrombi. Thrombus in the left and right ventricular

  apices, overlying a white fibrous scar.
Thrombosis
• Fate of the Thrombus.

     1. Propagation.

     2. Embolization.

     3. Dissolution.

     4. Organization and recanalization.
• Potential outcomes of venous thrombosis.
Mural thrombi.




Laminated thrombus in a dilated abdominal aortic
                  aneurysm.
6  hemodynamic disorders
Lines of Zahn: alternating

layers of platelets and

fibrin in the thrombus
5- Embolism
• An embolus is a detached intravascular solid,

 liquid, or gaseous mass that is carried by the

 blood to a site distant from its point of origin.

• Emboli lodge in vessels too small to permit

 further passage, resulting in partial or complete

 vascular occlusion
Pulmonary Thrombo-embolism



• 95% of venous emboli originate from deep

 leg vein thrombi
• Large   embolus    derived

  from a lower extremity deep

  venous thrombosis and now

  impacted in a pulmonary

  artery branch.
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 embolization are:

      1. Lower extremities (75%)

      2. Brain (10%)
A- Fat Embolism

• Microscopic fat globules may be found in the

 circulation after fractures of long bones (which

 have fatty marrow) or, rarely, in the setting of soft

 tissue trauma and burns.
• Bone marrow embolus in the pulmonary circulation. The
  cleared vacuoles represent marrow fat that is now
  impacted in a distal vessel along with the cellular
  hematopoietic precursors.
Fat embolus in a glomerulus (kidney)
B- Air Embolism

• Gas bubbles within the circulation can obstruct vascular flow.

• Enter the circulation during obstetric procedures or as a

  consequence of chest wall injury.

• In excess of 100 cc is required to have a clinical effect
C- Amniotic Fluid Embolism

• Underlying cause is the infusion of amniotic fluid or fetal

  tissue into the maternal circulation via a tear in the placental

  membranes or rupture of uterine veins.

• Characterized by sudden severe dyspnea, cyanosis, and

  hypotensive shock, followed by seizures and coma.
6- Infarction
• An infarct is an area of ischemic necrosis caused by

  occlusion of either the arterial supply or the venous

  drainage in a particular tissue.

• Nearly 99% of all infarcts result from thrombotic or

  embolic events, and almost all result from arterial

  occlusion.
• Infarcts are classified on the basis of their color

  (reflecting the amount of hemorrhage) and the

  presence or absence of microbial infection
• Red (hemorrhagic) infarcts occur



(1) with venous occlusions (such as in ovarian torsion);

(2) in loose tissues (such as lung)

(3) in tissues with dual circulations (e.g., lung and small

   intestine).
•    White (anemic) infarcts occur




1.   with arterial occlusions in solid organs with end-

     arterial circulation (such as heart, spleen, and kidney)


2.   Solid tissues
Examples of infarcts. (A) Hemorrhagic, roughly wedge-shaped

  pulmonary infarct. (B) Sharply demarcated white infarct in

  the spleen.
• The dominant histologic characteristic of infarction is

  ischemic coagulative necrosis

• most infarcts are ultimately replaced by scar tissue.

• The brain is an exception to these generalizations;

  ischemic injury in the central nervous system results

  in liquefactive necrosis
• Remote kidney infarct,

  now replaced by a large

  fibrotic cortical scar.
• Septic infarctions may develop when embolization

  occurs by fragmentation of a bacterial vegetation

  from a heart valve or when microbes seed an area

  of necrotic tissue.
6  hemodynamic disorders
7- Shock
• Shock, or cardiovascular collapse, is the final

  common pathway for a number of potentially

  lethal clinical events, including severe hemorrhage,

  extensive trauma or burns, large myocardial

  infarction, massive pulmonary embolism, and

  microbial sepsis.
• gives rise to systemic hypo-perfusion caused by

 reduction in:

     1. cardiac output

     2. the effective circulating blood volume.

• The end results are hypotension, followed by

 impaired tissue perfusion and cellular hypoxia.
Type of Shock            Clinical Examples              Principal Mechanism
                -   Ventricular rupture               Failure     of   myocardial
                -   Arrhythmia                        pump      owing to intrinsic
Cardiogenic
                -   Cardiac tamponade                 myocardial          damage,
                -   Pulmonary embolism                extrinsic pressure,
                -   Myocardial infarction             or obstruction to outflow

                -   Hemorrhage                        Inadequate blood or plasma
                -   Fluid loss, e.g., vomiting,       volume
Hypo-volemic
                    diarrhea, burns, or trauma
                - Overwhelming microbial infections   Peripheral vasodilation and
                - Endotoxic shock                     pooling of             blood;
                - Gram-positive septicemia            endothelial
   Septic       - Fungal sepsis                       activation/injury;
                                                       leukocyte-induced
                                                      damage;         disseminated
                                                      intravascular coagulation;
                                                      activation    of     cytokine
                                                      cascades
Less commonly:

1. Neurogenic shock -in the setting of anesthetic
   accident or spinal cord injury, owing to loss of
   vascular tone and peripheral pooling of blood.

2. Anaphylactic shock, initiated by a generalized
   IgE-mediated     hypersensitivity      response,    is
   associated    with   systemic     vasodilatation   and
   increased vascular permeability
Clinical Course
• The clinical manifestations depend on the precipitating
  insult.
• In hypovolemic and cardiogenic shock, the patient
  presents with hypotension; a weak, rapid pulse;
  tachypnea; and cool, clammy, cyanotic skin.
• In septic shock, the skin may initially be warm and
  flushed because of peripheral vasodilation.
END

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6 hemodynamic disorders

  • 2. • Normal fluid homeostasis is maintained by vessel wall integrity, intravascular pressure and osmolarity within certain physiologic ranges. • Changes in intravascular volume, pressure, or protein content, or alterations in endothelial function will affect the movement of water across the vascular wall.
  • 3. 1- Edema Increased fluid in the interstitial tissue spaces.
  • 4. Patho-physiologic Causes of Edema - Increased Hydrostatic Pressure: Impaired venous return - Reduced plasma osmotic pressure (Hypo-proteinemia): Liver cirrhosis, nephrotic syndrome - Lymphatic Obstruction: Neoplastic, or postsurgical - Sodium Retention: Excessive salt intake with renal insufficiency - Inflammation: Acute inflammation, Chronic inflammation
  • 5. Types of edema • Anasarca: Generalized edema • Dependent edema: Prominent feature of congestive heart failure, particularly of the right ventricle. • Renal edema: Edema as a result of renal dysfunction or nephrotic syndrome is generally more severe than cardiac edema and affects all parts of the body equally.
  • 6. • Peri-orbital edema: is a characteristic finding in severe renal disease. • Pitting edema: finger pressure over substantially edematous subcutaneous tissue displaces the interstitial fluid and leaves a finger-shaped depression • Pulmonary edema: most typically seen in the setting of left ventricular failure
  • 10. 2- Hyperemia and Congestion • Both indicate a local increased volume of blood in a particular tissue.
  • 11. Hyperemia versus congestion. In both cases there is an increased volume and pressure of blood in a given tissue with associated capillary dilatation and a potential for fluid extravasation.
  • 12. In hyperemia, increased inflow leads to engorgement with oxygenated blood, resulting in erythema. In congestion, diminished outflow leads to a capillary bed swollen with deoxygenated venous blood and resulting in cyanosis.
  • 15. 3- Hemorrhage Extravasation of blood due to vessel rupture
  • 16. Types • Hematoma: accumulation of blood within tissue. • Petechiae: minute 1 to 2mm hemorrhages into skin, mucous membranes, or serosal surfaces. • Purpura: slightly larger (≥3 mm) hemorrhages.
  • 17. • Ecchymoses: larger (>1 to 2 cm) subcutaneous hematomas (i.e., bruises) • Hemothorax, hemopericardium, hemoperitoneum, or hemarthrosis (in joints): Large accumulations of blood in one of the body cavities
  • 18. Petechial hemorrhages of Intracerebral bleeding the colonic mucosa
  • 25. Hemostasis and Thrombosis Normal hemostasis result of a set of well-regulated processes that accomplish two important functions: (1) They maintain blood in a fluid, clot-free state in normal vessels. (2) They are aimed to induce a rapid and localized hemostatic plug at a site of vascular injury.
  • 26. Thrombosis: an inappropriate activation of normal hemostatic processes, such as the formation of a blood clot (thrombus) in uninjured vasculature or thrombotic occlusion of a vessel after relatively minor injury.
  • 27. Both hemostasis and thrombosis are regulated by three general components:- – the vascular wall – platelets – the coagulation factors.
  • 29. Three primary causes for thrombus formation, the so-called Virchow triad: (1) Endothelial injury (2) Stasis or slowing of blood flow (3) Blood hyper-coagulability
  • 30. Virchow triad in thrombosis. Endothelial integrity is the single most important factor. Note that injury to endothelial cells can affect local blood flow and/or coagulability; abnormal blood flow (stasis or turbulence) can, in turn, cause endothelial injury. The elements of the triad may act independently or may combine to cause thrombus formation.
  • 31. • Thrombi may develop anywhere in the cardiovascular system, but stasis is a major factor in the development of venous thrombi • An area of attachment to the underlying vessel or heart wall, frequently firmest at the point of origin, is characteristic of all thromboses.
  • 32. • The propagating tail may not be well attached and, particularly in veins, is prone to fragmentation, creating an embolus. • Mural thrombi - arterial thrombi that arise in heart chambers or in the aortic lumen, that usually adhere to the wall of the underlying structure
  • 33. • Mural thrombi. Thrombus in the left and right ventricular apices, overlying a white fibrous scar.
  • 35. • Fate of the Thrombus. 1. Propagation. 2. Embolization. 3. Dissolution. 4. Organization and recanalization.
  • 36. • Potential outcomes of venous thrombosis.
  • 37. Mural thrombi. Laminated thrombus in a dilated abdominal aortic aneurysm.
  • 39. Lines of Zahn: alternating layers of platelets and fibrin in the thrombus
  • 41. • An embolus is a detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin. • Emboli lodge in vessels too small to permit further passage, resulting in partial or complete vascular occlusion
  • 42. Pulmonary Thrombo-embolism • 95% of venous emboli originate from deep leg vein thrombi
  • 43. • Large embolus derived from a lower extremity deep venous thrombosis and now impacted in a pulmonary artery branch.
  • 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 embolization are: 1. Lower extremities (75%) 2. Brain (10%)
  • 45. A- Fat Embolism • Microscopic fat globules may be found in the circulation after fractures of long bones (which have fatty marrow) or, rarely, in the setting of soft tissue trauma and burns.
  • 46. • Bone marrow embolus in the pulmonary circulation. The cleared vacuoles represent marrow fat that is now impacted in a distal vessel along with the cellular hematopoietic precursors.
  • 47. Fat embolus in a glomerulus (kidney)
  • 48. B- Air Embolism • Gas bubbles within the circulation can obstruct vascular flow. • Enter the circulation during obstetric procedures or as a consequence of chest wall injury. • In excess of 100 cc is required to have a clinical effect
  • 49. C- Amniotic Fluid Embolism • Underlying cause is the infusion of amniotic fluid or fetal tissue into the maternal circulation via a tear in the placental membranes or rupture of uterine veins. • Characterized by sudden severe dyspnea, cyanosis, and hypotensive shock, followed by seizures and coma.
  • 51. • An infarct is an area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage in a particular tissue. • Nearly 99% of all infarcts result from thrombotic or embolic events, and almost all result from arterial occlusion.
  • 52. • Infarcts are classified on the basis of their color (reflecting the amount of hemorrhage) and the presence or absence of microbial infection
  • 53. • Red (hemorrhagic) infarcts occur (1) with venous occlusions (such as in ovarian torsion); (2) in loose tissues (such as lung) (3) in tissues with dual circulations (e.g., lung and small intestine).
  • 54. White (anemic) infarcts occur 1. with arterial occlusions in solid organs with end- arterial circulation (such as heart, spleen, and kidney) 2. Solid tissues
  • 55. Examples of infarcts. (A) Hemorrhagic, roughly wedge-shaped pulmonary infarct. (B) Sharply demarcated white infarct in the spleen.
  • 56. • The dominant histologic characteristic of infarction is ischemic coagulative necrosis • most infarcts are ultimately replaced by scar tissue. • The brain is an exception to these generalizations; ischemic injury in the central nervous system results in liquefactive necrosis
  • 57. • Remote kidney infarct, now replaced by a large fibrotic cortical scar.
  • 58. • Septic infarctions may develop when embolization occurs by fragmentation of a bacterial vegetation from a heart valve or when microbes seed an area of necrotic tissue.
  • 61. • Shock, or cardiovascular collapse, is the final common pathway for a number of potentially lethal clinical events, including severe hemorrhage, extensive trauma or burns, large myocardial infarction, massive pulmonary embolism, and microbial sepsis.
  • 62. • gives rise to systemic hypo-perfusion caused by reduction in: 1. cardiac output 2. the effective circulating blood volume. • The end results are hypotension, followed by impaired tissue perfusion and cellular hypoxia.
  • 63. Type of Shock Clinical Examples Principal Mechanism - Ventricular rupture Failure of myocardial - Arrhythmia pump owing to intrinsic Cardiogenic - Cardiac tamponade myocardial damage, - Pulmonary embolism extrinsic pressure, - Myocardial infarction or obstruction to outflow - Hemorrhage Inadequate blood or plasma - Fluid loss, e.g., vomiting, volume Hypo-volemic diarrhea, burns, or trauma - Overwhelming microbial infections Peripheral vasodilation and - Endotoxic shock pooling of blood; - Gram-positive septicemia endothelial Septic - Fungal sepsis activation/injury; leukocyte-induced damage; disseminated intravascular coagulation; activation of cytokine cascades
  • 64. Less commonly: 1. Neurogenic shock -in the setting of anesthetic accident or spinal cord injury, owing to loss of vascular tone and peripheral pooling of blood. 2. Anaphylactic shock, initiated by a generalized IgE-mediated hypersensitivity response, is associated with systemic vasodilatation and increased vascular permeability
  • 65. Clinical Course • The clinical manifestations depend on the precipitating insult. • In hypovolemic and cardiogenic shock, the patient presents with hypotension; a weak, rapid pulse; tachypnea; and cool, clammy, cyanotic skin. • In septic shock, the skin may initially be warm and flushed because of peripheral vasodilation.
  • 66. END