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Hemodynamic Disorders,

Thromboembolism, and
Shock
By Kassa B.(MD, pathology rsident)

1
Outline
• Hyperemia and Congestion
• Edema
• Hemorrhage
• Hemostasis and Thrombosis
• Embolism
• Infarction
• Shock
Basic Physiology of the circulatory system
• Health of cells and tissues depends on the circulation of blood
• The circulatory system consists of two subdivisions:
• The cardiovascular system consists of the heart and blood vessels, and
• The lymphatic system, which includes lymphatic vessels and lymphoid tissues
within the spleen, thymus, tonsils, and lymph nodes
• The three basic functions of this system are:
• Transportation
• Regulation
• Protection
• To achieve this functions heart must pump blood adequately, blood
vessels should maintain their integrity and hemostasis kept
Hyperemia and Congestion
• Hyperemia and congestion both refer to an increase in blood volume
within a tissue
• Hyperemia is an active process resulting from arteriolar dilation and
increased blood inflow
• Eg. At sites of inflammation or in exercising skeletal muscle
• Congestion is a passive process resulting from impaired outflow of
venous blood from a tissue
• Eg. In cases of local venous obstruction or systemically as in cardiac failure
• Long-standing chronic congestion, inadequate tissue perfusion and
persistent hypoxia may lead to parenchymal cell death
EDEMA
• Edema is an accumulation of interstitial fluid within tissues
• Accumulation of fluid in body cavities is called effusion such as in the
• Pleural cavity (hydrothorax),
• Pericardial cavity (hydropericardium), or
• Peritoneal cavity (hydroperitoneum, or ascites)
• Anasarca is severe, generalized edema marked by profound swelling
everywhere
• Based on the cause edema can be broadly categorized as:
• Inflammatory edema; largely related to increased vascular permeability
• Non-Inflammatory edema
EDEMA cont’d
• The effects of edema vary, ranging from merely annoying to rapidly
fatal
• Subcutaneous edema is important to recognize primarily because it
signals potential underlying cardiac or renal disease
• Pulmonary edema is a common clinical problem that most frequently
is seen in the setting of left ventricular failure
• It can cause death by interfering with normal ventilatory function
• Brain edema is life-threatening; if the swelling is severe, the brain can
herniate injuring the medullary centers and cause death
HEMORRHAGE
• Hemorrhage, defined as the extravasation of blood from vessels
• Hemorrhage may be external or accumulate within a tissue as a
hematoma
• Hemorrhage occurs due to trauma, inflammation, tumor or bleeding
diatheses
• The clinical significance of any particular hemorrhage depends on the
volume of blood lost, the rate of bleeding and site of bleeding
• Rapid loss of large amount of blood can lead to hemorrhagic shock
• Small amount of blood into the brain could lead to death
• Chronic or recurrent external blood loss leads to iron deficiency anemia
HEMOSTASIS
• Normal hemostasis comprises a series of regulated processes that
maintain blood in a fluid, clot-free state in normal vessels while
rapidly forming a localized hemostatic plug at the site of vascular
injury
• Simply put hemostasis is the fine balance between pro and anti-
coagulants
• Elements of this complex system are:
• Blood vessels
• Platelets
• Coagulation cascade
HEMOSTASIS cont’d
HEMOSTASIS cont’d
HEMOSTASIS cont’d
Thrombosis
• Thrombosis is the formation of blood clot (thrombus) within intact
vessels
• Abnormalities that lead to thrombus formation are called Virchow’s
triad
Thrombosis cont’d
• Components of Virchow’s triad:
• Endothelial injury (e.g., by toxins, hypertension, inflammation, or metabolic
products)
• Abnormal blood flow, stasis or turbulence (e.g., due to aneurysms,
atherosclerotic plaque)
• Hypercoagulability: either primary (e.g., factor V Leiden, increased
prothrombin synthesis, antithrombin III deficiency) or secondary (e.g., bed
rest, tissue damage, malignancy)
Thrombosis cont’d
• After its formation a thrombus has four fates:
• Propagation enlarges through the accretion of additional platelets and fibrin,
increasing the odds of vascular occlusion or embolization
• Embolization Part or all of the thrombus is dislodged and transported
elsewhere in the vasculature
• Dissolution newly formed thrombus can be removed; activation of
fibrinolytic factors may lead to its rapid shrinkage and complete dissolution
• Organization and recanalization through time new blood vessels can grow
into the thrombus and reestablish the continuity of the vessel
Thrombosis cont’d
• Thrombi are significant because they cause obstruction of arteries and
veins and may give rise to emboli
• Clinical importance depends on the site of thrombosis
• Thrombi in the venous system can cause congestion leading to local
swelling and pain; but their feared complication is embolization to the
lungs
• Arterial thrombi are far more dangerous especially those involving the
coronaries and cerebrovascular system; which is the leading cause of
death world wide
EMBOLISM
• An embolus is an intravascular solid, liquid, or gaseous mass that is
carried by the blood to a site distant from its point of origin
• Sources of emboli can be:
• Dislodged thrombus- the commonest
• Atherosclerotic debris (cholesterol emboli)
• Fat droplets,
• Bubbles of air or nitrogen,
• Tumor fragments,
• Bits of bone marrow, and
• Amniotic fluid
EMBOLISM cont’d
• Emboli lodge in vessels too small to permit further passage, resulting
in partial or complete vascular occlusion
• Their effects depend mainly on the size of the embolus and the
location in which it lodges
• For example pulmonary embolism may lead to right-sided heart
failure, pulmonary hemorrhage, pulmonary infarction, or sudden
death
Disseminated Intravascular Coagulation
(DIC)
• DIC is the sudden or insidious onset of widespread thrombosis within
the microcirculation.
• DIC is not a primary disease but rather a potential complication of
numerous conditions associated with widespread activation of
thrombin
• The thrombi are generally microscopic in size, yet so numerous as to
often cause circulatory insufficiency, particularly in the brain, lungs,
heart, and kidneys
• DIC consumes platelets and coagulation proteins; hence also leads to
a bleeding catastrophe
INFARCTION
• An infarct is an area of ischemic necrosis caused by occlusion of the
vascular supply to the affected tissue
• The process is called infarction
• Causes of infarction are:
• Thromboembolism
• Arterial vasospasm
• Extrinsic compression of a vessel eg. By a growing tumor, compartment
syndrome
• Vessel twisting
• Traumatic vascular rupture
INFARCTION cont’d
• Infarcts can be:
• Hemorrhagic (red) caused by venous occlusion or occurring in spongy tissues;
• Pale (white) caused by arterial occlusion in compact tissues
• Septic or bland based on the presence or absence of bacterial infection
• Whether or not vascular occlusion lead to infarction depends on:
• Collateral blood supplies,
• The rate at which an obstruction develops,
• Intrinsic tissue susceptibility to ischemic injury, and blood oxygenation
SHOCK
• Shock is defined as a state of systemic tissue hypoperfusion
• The consequences are impaired tissue perfusion and cellular hypoxia
• If left uncorrected leads to irreversible tissue injury that often proves
fatal
• The four pathogenic groups of shock are:
• Hypovolemic shock eg. Hemorrhage, vomiting and diarrhea
• Cardiogenic shock eg. Myocardial infarction, arrhythmia
• Distributive shock eg. Septic shock, neurogenic shock, anaphylactic shock
• Obstructive shock eg. Tension pneumothorax, hemothorax, cardiac
tamponade
SHOCK cont’d
• Shock is a progressive disorder that leads to death if the underlying
problems are not corrected
• Stages of shock:
• Non-progressive stage, during which reflex compensatory
mechanisms are activated and vital organ perfusion is maintained
• Progressive stage, characterized by tissue hypoperfusion and onset of
worsening circulatory and metabolic derangement, including acidosis
• Irreversible stage, in which cellular and tissue injury is so severe that
even if the hemodynamic defects are corrected, survival is not
possible
SHOCK cont’d
REFERENCE

PAGES 97-119
Thank You

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