HEMODYNAMIC DISORDERS,

THROMBOSIS AND SHOCK

Dr.khadeja Mohammed abdallah

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 Hyperemia and Congestion Edema
 Hemorrhage
 Homeostasis and Thrombosis
 Normal Homeostasis
 Thrombosis
 Disseminated Intravascular Coagulation
 Pulmonary Thromboembolism
 Systemic Thromboembolism
 Infarction
 Shock
 Pathogenesis of Septic Shock
 Stages of Shock
Integrity of the blood vessel is necessary to carry
blood to tissues.
Damage to the wall is repaired by homeostasis,
which involves formation of a thrombus (clot) at the
site of vessel injury.
Hemostasis occurs in two stages:
primary .
secondary.
Primary Hemostasis forms a weak platelet plug and
is mediated by interaction between platelets and
the vessel wall.
Secondary Hemostasis stabilizes the platelet plug
and is mediated by the coagulation cascade.
PRIMARY HEMOSTASIS
Step 1 Transient vasoconstriction of damaged vessel
Mediated by reflex neural stimulation and endothelin release
from endothelial cells.
Step 2 Platelet adhesion to the surface of disrupted vessel
Von Willebrand factor (vWF) binds exposed subendothelial
collagen.
Platelets bind vWF using the GPlb receptor.
vWF is derived from the Weibel-Palade bodies of endothelial
cells and a-granules of platelets.
Step 3 Platelet degranulation
Adhesion induces shape change in platelets and
degranulation with release of multiple mediators.
ADP is released from platelet dense granules; promotes
exposure of GPIIb/ IIIa receptor on platelets.
TXA, is synthesized by platelet cyclooxygenase (COX) and
released, promotes platelet aggregation.
Step 4 Platelet aggregation
Platelets aggregate at the site of injury via
GPIIb/IIIa using fibrinogen (from plasma) as a
linking molecule; results in formation of platelet
plug.
Platelet plug is weak; coagulation cascade
(secondary Hemostasis) stabilizes it.
DISORDERS OF PRIMARY HEMOSTASIS
 Usually due to abnormalities in platelets.
 divided into quantitative or qualitative disorders.
 Clinical features include mucosal and skin
bleeding.
 Symptoms of mucosal bleeding include:
 Epistaxis (most common overall symptom).
 Hemoptysis.
 GI bleeding, hematuria.
 menorrhagia.
 Intracranial bleeding occurs with severe
thrombocytopenia.
 Symptoms of skin bleeding include:
 petechiae (1-2 mm).
 ecchymoses (> 3 mm).
 purpura (> 1 cm).
 and easy bruising.
 petechiae are a sign of thrombocytopenia and are
not usually seen with qualitative disorders.
 Useful laboratory studies include
 Platelet count.
normal 150-400.
Count < 50 leads to symptoms.
 Bleeding time
 normal 2-7 minutes.
 prolonged with quantitative and qualitative
platelet disorders.
 Blood smear used to assess number and size of
platelets.
 Bone marrow biopsy used to assess
megakaryocytes, which produce platelets.
SECODARY HEMOSTASiS
 Stabilizes the weak platelet plug via the
coagulation cascade.
 Coagulation cascade generates thrombin,
which converts fibrinogen in the platelet plug
to fibrin.
 Fibrin is then cross-linked, yielding a stable
platelet-fibrin thrombus.
 Factors of the coagulation cascade are
produced by the liver in an inactive state.
 Then activated .
Thrombosis
 Pathologic formation of an intravascular blood
clot (thrombus).
 Can occur in an artery or vein.
 Most common location is the deep veins
(DVT) of the leg below the knee.
 Three major risk factors for thrombosis
are(virchaw triad) :
 disruption in blood flow.

 Endothelial cell damage.

 Hypercoagulablestate .
EMBOLISM
 Intravascular mass that travels and occludes
downstream vessels.
 Symptoms depend on the vessel involved.
 Thromboembolus is due to thrombus that
dislodges most common type of embolus
(>95%).
 Atherosclerotic embolus is due to an
atherosclerotic plaque that dislodges.
 Fat embolus is associated with bone fractures,
particularly long bones, and soft tissue trauma .
 Develops while fracture is still present or shortly
after repair.
 Gas embolus may occurring during
laparoscopic surgery .
 Amniotic fluid embolus enters maternal
circulation during labour or delivery
 Presents with:
 Shortness of breath.
 Neurologic symptoms.
 DIC .
Pulmonary embolus (PE)
 Usually due to thrombus embolism the most
common source is deep venous thrombosis .
 (DVT) of the lower extremity, usually involving
the femoral, iliac, or popliteal veins.
 Pulmonary infarction occurs if a large or
medium-sized artery is obstructed in patients
with preexisting cardiac or pulmonary
compromise.
 only 10% of PEs cause infarction.
CLINICAL PRESENTATION
 Presents with :
 Shortness of breath.
 Hemoptysis.
 Pleuritic chest pain.
 pleural effusion.
INVESTIGATION
 V/Q lung scan shows mismatch.
 Spiral CT shows a vascular defect in the lung.
 Lower extremity Doppler US is useful to
detect DVT.
 D dimmer is elevated.
 Gross examination reveals a hemorrhagic,
wedge-shaped infarct.
Systemic embolism
 Usually due to thromboembolism .
 Most commonly arise in the left heart .
 Travel down systemic circulation to occlude
flow to organs, most commonly lower
extremities .
SHOCK
 Shock is the final common pathway for several
potentially
lethal events, including extensive trauma or burns,
myocardial infarction, pulmonary embolism, and
sepsis.
 Shock is characterized by systemic hypoperfusion
of tissues.
 The consequences are impaired tissue perfusion
and cellular hypoxia .
 Although shock initially is reversible, prolonged
shock eventually leads to irreversible tissue injury
that
often proves fatal.
most common forms of shock
 Cardiogenic shock : results from low cardiac
output due
to myocardial pump failure.
 It may be caused by :
 Myocardial damage (infarction).
 Ventricular arrhythmias.
 Extrinsic compression (cardiac tamponade) .
 Outflow obstruction (pulmonary embolism).
 Hypovolemic shock : results from low cardiac
output due
to loss of blood or plasma volume (e.g., due to
hemorrhage or fluid loss from severe burns).
 Septic shock : results from arterial
vasodilation and venous blood pooling that
stems from the systemic immune response to
microbial infection.
 Neurogenic shock: Less commonly, shock can
result from loss of vascular tone associated
with anesthesia or secondary to a spinal cord
injury .
 Anaphylactic shock results from systemic
vasodilation and increased vascular
permeability that is triggered by an IGE
mediated hypersensitivity reaction.
Stages of Shock
 Shock is a progressive disorder that leads to
death if the
underlying problems are not corrected.
 Death typically follows the failure of multiple
organs.
 Unless the insult is massive and rapidly lethal
from a shock tends to evolve through three
general stages.
 An initial non progressive stage: during which
reflex compensatory mechanisms are activated
and vital organ perfusion is maintained.
 The net effect is:
 Tachycardia.
 Peripheral vasoconstriction.
 Renal fluid conservation.
 Cutaneous vasoconstriction causes the
characteristic “shocky” skin coolness and
pallor.

 .
 A progressive stage: characterized by tissue
hypoperfusion and onset of worsening
circulatory and metabolic derangement,
including acidosis.
 An irreversible stage, in which cellular and
tissue injury is so severe that even if the
hemodynamic defects are corrected, survival
is not possible In the early non progressive
phase of shock
Clinical Course
 The clinical manifestations of shock depend on the
precipitating insult.
 In hypovolemic and cardiogenic shock:
 Hypotension.
 A weak rapid pulse.
 Tachypnea.
 Cool, clammy, cyanotic skin.
 In septic shock:
 The skin may be warm and flushed due to peripheral
vasodilation.
 Prognosis varies with the origin of shock and its duration.
 More than 90% of young, otherwise healthy patients with
hypovolemic shock survive with appropriate management.
 Septic or cardiogenic shock is associated with substantially
worse outcomes, even with state-of-the-art care.
Thank you