Hemodinamic Disorder, Thrombosis, and Shock

HEMODINAMIC DISORDER, THROMBOSIS, AND SHOCK
dr. Duti S. Aziz, SpPA SUBDEP PA RUMKITAL DR. RAMELAN
EDEMA
The term edema signifies increased fluid in the interstitial tissue spaces extravasation of fluid from vessels into interstitial spaces; the fluid may be protein poor (transudate) or may be protein rich (exudate). Anasarca is a severe and generalized edema with profound subcutaneous tissue swelling. There are several pathophysiologic categories of edema The mechanism of inflammatory edema mostly involves increased vascular permeability
Edema results from any of the following conditions:

Increased hydrostatic pressure, caused by a reduction in venous return (as in heart failure) Decreased colloid osmotic pressure, caused by reduced concentration of plasma albumin (due to decreased synthesis, as in liver disease, or increased loss, as in kidney disease) Lymphatic obstruction that impairs interstitial fluid clearance (as in scarring, tumors, or certain infections) Primary renal sodium retention (in renal failure) Increased vascular permeability (in inflammation)
Table 4-1. Pathophysiologic Categories of Edema Increased Hydrostatic Pressure

Impaired venous return Congestive heart failure Constrictive pericarditis Ascites (liver cirrhosis) Venous obstruction or compression Thrombosis External pressure (e.g., mass)
Lower extremity inactivity with prolonged dependency

Arteriolar dilation Heat Neurohumoral dysregulation
Reduced Plasma Osmotic Pressure (Hypoproteinemia) Protein-losing glomerulopathies (nephrotic syndrome) Liver cirrhosis (ascites) Malnutrition Protein-losing gastroenteropathy Lymphatic Obstruction Inflammatory Neoplastic Postsurgical Postirradiation Sodium Retention Excessive salt intake with renal insufficiency Increased tubular reabsorption of sodium Renal hypoperfusion Increased renin-angiotensin-aldosterone secretion Inflammation Acute inflammation Chronic inflammation Angiogenesis
Morphology
Subcutaneous edema Dependent edema Periorbital edema Pitting edema Pulmonary edema Edema of the brain herniation
Hydrothorax Hydropericardium Hydroperitoneum Anasarca
HYPEREMIA AND CONGESTION

Hyperemia is an active process resulting from augmented blood flow due to arteriolar dilation. Congestion is a passive process resulting from impaired venous return out of a tissue.
HEMORRHAGE
Hemorrhage is extravasation of blood from vessels into the extravascular space.
external confined within a tissue
The clinical significance of hemorrhage depends on the volume and rate of blood loss.
Hematoma Petechiae Ecchymoses Hemothorax Hemopericardium Hemoperitoneum
HEMOSTASIS AND THROMBOSIS

Normal hemostasis is a consequence of tightly regulated processes that maintain blood in a fluid, clot-free state in normal vessels while inducing the rapid formation of a localized hemostatic plug at the site of vascular injury. The pathologic form of hemostasis is thrombosis; it involves blood clot (thrombus) formation in uninjured vessels or thrombotic occlusion of a vessel after relatively minor injury.
Both hemostasis and thrombosis involve three components:
1. Vascular wall 2. Platelets 3. The coagulation cascade.
COAGULATION CASCADE
Thrombosis
process of hemostasis dysregulation that underlies thrombus formation.
Virchow's triad
embolus. lines of Zahn mural thrombi Arterial thrombi Venous thrombosis Postmortem clots vegetations nonbacterial thrombotic endocarditis
Table 4-2. Hypercoagulable States

Primary (Genetic) Common Mutation in factor V gene (factor V Leiden) Mutation in prothrombin gene Mutation in methyltetrahydrofolate gene
Rare
Antithrombin III deficiency Protein C deficiency Protein S deficiency Very rare Fibrinolysis defects
Secondary (Acquired) High risk for thrombosis Prolonged bedrest or immobilization Myocardial infarction Atrial fibrillation Tissue damage (surgery, fracture, burns)
Cancer
Prosthetic cardiac valves Disseminated intravascular coagulation Heparin-induced thrombocytopenia
Antiphospholipid antibody syndrome (lupus anticoagulant syndrome)

Lower risk for thrombosis Cardiomyopathy Nephrotic syndrome
Hyperestrogenic states (pregnancy)

Oral contraceptive use Sickle cell anemia
Fate of the Thrombus

Propagation. Embolization. Dissolution. Organization and recanalization
DIC (Disseminated Intravascular Coagulation)?
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.
99% of all emboli represent some part of a dislodged thrombus, hence the term thromboembolism.
The consequences of thromboembolism include ischemic necrosis (infarction) of downstream tissue. Depending on the site of origin, emboli may lodge anywhere in the vascular tree; the clinical outcomes are best understood from the standpoint of whether emboli lodge in the pulmonary or systemic circulations.
Pulmonary Thromboembolism
Systemic Thromboembolism Fat Embolism Air Embolism Amniotic Fluid Embolism
Pulmonary emboli derive primarily from lower extremity deep vein thrombosis; their effect (sudden death, right heart failure, pulmonary hemorrhage, or infarction) depends on the size of the embolus. Systemic emboli derive primarily from cardiac mural or valvular thrombi, aortic aneurysms, or atherosclerotic plaque; whether an embolus causes tissue infarction depends on the site of embolization and collateral circulation.
NFARCTION
An infarct is an area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage in a particular tissue.
Red infarcts
occur (1) with venous occlusions (such as in ovarian torsion) (2) in loose tissues (such as lung) that allow blood to collect in the infarcted zone (3) in tissues with dual circulations such as lung and small intestine, permitting flow of blood from an unobstructed parallel supply into a necrotic area (such perfusion not being sufficient to rescue the ischemic tissues )
(4) in tissues that were previously congested because of sluggish venous outflow (5) when flow is re-established to a site of previous arterial occlusion and necrosis (e.g., fragmentation of an occlusive embolus or angioplasty of a thrombotic lesion).
White infarcts
occur with arterial occlusions or in solid organs (such as heart, spleen, and kidney), where the solidity of the tissue limits the amount of hemorrhage that can seep into the area of ischemic necrosis from adjoining capillary beds .
The dominant histologic characteristic of infarction is ischemic coagulative necrosis Septic infarctions ? Factors That Influence Development of an Infarct ?
SHOCK
( or Cardiovascular Collaps )
Shock 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.
Regardless of the underlying pathology, shock gives rise to systemic hypoperfusion; it can be caused either by reduced cardiac output or by reduced effective circulating blood volume. The end results are hypotension, impaired tissue perfusion, and cellular hypoxia.
3 general categories of shock : 1. Cardiogenic 2. Hypovolemic 3. Septic
Table. 3 Major Types of Shock

Type of Shock
Cardiogenic Myocardial infarction Ventricular rupture Arrhythmia Cardiac tamponade Pulmonary embolism Failure of myocardial pump resulting from intrinsic myocardial damage, extrinsic pressure, or obstruction to outflow Inadequate blood or plasma volume
Clinical Examples
Principal Mechanisms
Hypovolemic
Hemorrhage Fluid loss (e.g., vomiting, diarrhea, burns, or trauma) Septic Overwhelming microbial infections Endotoxic shock Gram-positive septicemia Fungal sepsis Superantigens (e.g. toxic shock syndrome) Peripheral vasodilation and pooling of blood; endothelial activation/injury; leukocyteinduced damage; disseminated intravascular coagulation
Stages of Shock
1. An initial nonprogressive stage during which reflex compensatory mechanisms are activated and perfusion of vital organs is maintained. 2. A progressive stage characterized by tissue hypoperfusion and onset of worsening circulatory and metabolic imbalances. 3. An irreversible stage that sets in after the body has incurred cellular and tissue injury so severe that even if the hemodynamic defects are corrected, survival is not possible
Patogenesa ?
Morphology
Since shock is characterized by failure of many organ systems. The cellular changes may appear in any tissue.
adrenal changes Kidneys gastrointestinal tract diffuse alveolar damage
CHAPTER 4. Page 79 102.
SELAMAT BELAJAR

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HEMODINAMIC DISORDER, THROMBOSIS, AND SHOCK

dr. Duti S. Aziz, SpPA SUBDEP PA RUMKITAL DR. RAMELAN

Edema results from any of the following conditions:

Table 4-1. Pathophysiologic Categories of Edema Increased Hydrostatic Pressure

Lower extremity inactivity with prolonged dependency

Hydrothorax Hydropericardium Hydroperitoneum Anasarca

HYPEREMIA AND CONGESTION

Hematoma Petechiae Ecchymoses Hemothorax Hemopericardium Hemoperitoneum

HEMOSTASIS AND THROMBOSIS

Both hemostasis and thrombosis involve three components:

1. Vascular wall 2. Platelets 3. The coagulation cascade.

Table 4-2. Hypercoagulable States

Antiphospholipid antibody syndrome (lupus anticoagulant syndrome)

Hyperestrogenic states (pregnancy)

Fate of the Thrombus

DIC (Disseminated Intravascular Coagulation)?

Systemic Thromboembolism Fat Embolism Air Embolism Amniotic Fluid Embolism

3 general categories of shock : 1. Cardiogenic 2. Hypovolemic 3. Septic

Table. 3 Major Types of Shock

adrenal changes Kidneys gastrointestinal tract diffuse alveolar damage

CHAPTER 4. Page 79 102.

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