Hemodynamic Disorders,Thromboembolic
Disease, and Shock
I. HEMORRHAGE
 Escape of blood from the vasculature
into surrounding tissues
 Most common cause is TRAUMA
Forms of Hemorrhage:
A. Hematoma
 Localized hemorrhage within a tissue or
organ (bruise or pasa)
 1cm hemorrhage in skin or subcutis
B. Hemothorax = Blood Is Chest Cavity
Hemopericardium = Blood in pericardial
space
Hemoperitoneum = Blood in adbominal
cavity
Hemarthrosis = blood is synovial space
(joints)
C. Petichial hemorrhages and Purpura
 Small punctate hemorrhage in the skin,
mucous membrane and serosal
surfaces.
Petichiae: 1-3 mm hemorrhages skin,
mucosa - Purpura: 3-10 mm hemorrhage
skin, mucosa
D. Ecchymosis: Diffuse hemorrhage
usually in skin and SQ tissue
II. HYPEREMIA
 localized increase in the volume of
blood in capillaries and small vessels
TWO TYPES
• A. Active Hyperemia -results from local
arteriolar dilatation (inflammation and
blushing)
• B. Passive Congestion / Passive Hyperemia -
Results from obstructed venous blood flow or
increased back pressure from congestive heart
failure
Two Subtypes: -
1. Acute Passive Congestion
 Occurs of shock, acute inflammation or
sudden right sided heart failure
 Active passive congestion of liver
2. Chronic Passive Congestion
 Involves the lungs and the liver
 In lungs: caused by left sided heart
failure or mitral stenosis
 there is distention of alveolar
capillaries leading to capillary
rupture and escape of blood
into alveoli
 Heart Failure cells: Hemosiderin-Laden
macrophages
 In Liver: caused by right sided heart
failure
 NUTMEG Liver: liver appears
speckled, nutmeg like in color ;
can lead to cirrhosis
III. INFARCTION
 Necrosis of an organ (solid) resulting
from ischemia caused by obstruction of
bood supply.
 Infarct: necrotic tissue
Causes:
 Occlusive thrombi or emboli (99%)
 Compromised venous drainage
 Decreased blood flow
Types:
A. Anemic infarct:
 white or pale infarcts caused by arterial
occlusion in the heart, spleen or kidney
B. Hemorrhagic infarcts
 AKA red infracts – RBCs ooze into
necrotic tissue
 Occurs in the lungs and gastrointestinal
tract • Caused by venous occlusion
 Associated with volvulus, incarcerated
hernia and post-operative adhesions
Factors that Influence formation of Infarction:
 Rapidity of vascular inadequacy
 Availability of collateral flow
 Duration of occlusion
 Susceptibility of tissue to anoxia
IV. THROMBOSIS
 Intravascular coagulation of blood often
causing significant interruption of blood
flow
 Predisposing factors: Immobilization,
CHF, Polycythemia, Sickle cell disease,
Malignancies, smoking and OCP use
 Thrombus: A mass of blood
constituents, platelets, red cells, fibrin,
and white cells formed in the circulating
blood stream
Hemostasis and Thrombosis: Dependent on
Three Factors
•1. Vascular endothelium
•2. Platelets
•3. Coagulation system
1. Endothelial Cells: 3. 3. Coagulation Cascade
A. Antithrombotic Properties  Release of tissue factor from
 Antiplatelet effects injured endothelial cells
 Anticoagulant properties initiates coagulation cascade.
 Fibrinolytic properties  Ultimately forms a more stable
B. Prothrombotic Properties plug (secondary hemostasis).
 Adhesion of platelets  Classic, alternative and manna-
 Synthesis of von Willebrand’s binding lectin Pathways
factor (VWF)
 Synthesis of tissue factor (TF)
2. Platelets/Thrombocytes
 Recognize sites of endothelial
injury
 Adhere to subendothelial
collagen and become activated
 Release chemicals stored within
granules (ADP, Thromboxane
A2) Anticoagulants
 These molecules recruit
additional platelets (primary  Antithrombins inhibit serine protease
hemostasis) factors
 Proteins C and S inactivate factors Va
Reaction of platelets: Steps and VIIIa
 Plasminogen-plasmin system results in
1. Adhesion: mediated by von
fibrinolysis
Willebrand factor
Thrombi: Arterial
2. Release of reaction: release of ADP,
Histamine, serotonin, PDGF • Often attached to an atherosclerotic lesion

3. Activation of coagulation cascade • Most occur in coronary, cerebral, and femoral

4. Arachidonic acid metabolism:
cyclooxygenase pathway produces
Thromboxane A2
5. Platelet aggregation
arteries.
• Occlusive and alter blood flow
• Lines of Zahn alternate dark gray layers of
platelet and fibrin (in areas of active blood flow

6. Stabilization of platelet plug - Eventually liquifies and disappear

7. Limitation of Platelet plug formation:

played by prostacyclin
 Coronary Artery Occlusion Deep Vein Thrombosis (DVT)

Thrombi: Venous

• Occlusive cast of the vessel

• 90% in veins of lower extremities

Abdominal Aortic Aneurysm Thrombus
 Femoral
 Popliteal
 Iliac

Plaque with Recent Thrombus

Thrombus in Vessel: Lines of Zahn

Early Organizing Thrombus

Thrombus Potential Sequelae :

•Propagate

•Embolize

•Dissolve

•Recanalize
Disseminated intravascular coagulation (DIC)
• Not a primary disease, but complication of
diseases with widespread activation of
thrombin
• Pathophysiology:
 Fibrin-platelet thrombi in
microcirculation, with concurrent
consumption of platelets and
coagulation proteins.
 RBCs may be torn and fragmented by
fibrin thrombi.
 Diffuse activation of fibrinolysis,
generating increased FDPs & D-dimer
(lab evidence DIC)
• Treatment: diagnose and treat underlying
disease; buy time (not cure) with administration
of platelets and fresh frozen plasma
Peripheral smear in DIC
V. Embolus
• A detached solid, liquid, or gaseous mass that
is carried by the blood stream to a site distal
from its point of origin.
• 90% originate from thrombi
• Either arterial or venous
 Arterial: 85% arise from heart
 Venous: Majority arise from leg veins
• Occlude vessels resulting in varying pathology
Types of Emboli
1. Thromboemboli:
 Comes from fragments of a thrombus
 Caused by prolonged immobilization
leading to venous thrombosis
 Thrombus dislodges and deposits into
pulmonary vessel leading into
pulmonary infarct (wedge-shaped on
xray)
2. Arterial Emboli
 Origin:
 Mural thrombi from mitral
stenosis with atrial fibrillation
 Mural thrombi from a
myocardial infarction
 Deposits: Branches of coronary artery
specifically the MIDDLE CEREBRAL
ARTERY; MESENTERIC ARTERY and
RENAL ARTERY
3. Paradoxical Emboli
 Left sided emboli from patent foramen
ovale or ASD
Other Forms of Emboli
1. Fat Emboli
 From particles of bone marrow or fatty
tissue within bone; secondary to
fractures
 Deposits: lung, kidney, brain, etc
2. Air Embolism
 Introduction of air into the circulation
 Bends/Caisson’s Disease:
decompression sicknes – Nitrogen
bubble formation in blood due to rapid
ascent during scuba diving
3. Amniotic fluid Embolism Pulmonary Infarction

 Escape of amniotic fluid and its content

into the mother’s circulatin. Causes DIC

4. Miscellaneous Emboli

 From atheromatous plaques,

inflammed tissue

Thrombus in Leg Vein

Atheromatous Embolus

Tumor Embolus

Right Ventricle Embolus from Leg Vein

Fat Embolus to Lung

Distal Pulmonary Embolus

 Fat Embolus to Kidney Mechanism of Edema

• Increased hydrostatic pressure

• Loss of plasma colloid

• Increased vascular permeability

• Impaired lymphatic drainage

• Salt and water retention

Fat Embolus to Brain: Macro
Pitting edema of legs (decreased oncotic
pressure)

Fluid Droplets in Trachea/Bronchi

VI. EDEMA

EDEMA

• The accumulation of abnormal amounts of

fluid in intercellular spaces of body cavities.

• Inflammation and release of mediators

(exudate: contains inflammatory cells).

• Alterations in hemodynamic forces

(transudate: consists of fluid without cells).
Types of Edema VII. SHOCK

1. Anazarca  Systemic hypoperfusion due to reduced

cardiac output or reduced effective
 Generalized edema blood volume.
2. Hydrothorax  Major causes:

 Accumulation of fluid in chest cavity 1. Myocardial pump failure

3. Hydropericardium 2. Loss blood/plasma volume

 Accumulation of fluid in pericardial 3. Systemic microbial infection

space
4. Hydroperitoneum / Ascites
 Accumulation of fluid in abdominal
cavity
5. Pleural effusion
6. Transudate
 Results from disturbance of Starling
forces
 Specific gravity < 1.012
 Protein content < 3 g/dl, LDH LOW
7. Exudate
 Results from damage to the capillary
wall
 Specific gravity > 1.012
 Protein content > 3 g/dl, LDH HIGH
4. Spinal cord injury
5. Generalized IgE-mediated
hypersensitivity response, with widespread
vasodilation, increased capacitance, &
increased vascular permeability
TYPES of SHOCK
• CARDIOGENIC: AMI, Chronic Heart Failure
• HYPOVOLEMIC: Hemorrhage or Leakage
• SEPTIC: “ENDOTOXIC” shock
• NEUROGENIC: Loss of vascular tone
• ANAPHYLACTIC: IgE-mediated systemic
vasodilation and increased vascular
permeability
Clinical sequelae of sepsis

Ascites
Stages of shock

• Nonprogressive phase

 Reflex mechanisms activated

and perfusion of vital organs
maintained

• Progressive stage

 Persistent tissue hypoperfusion

leads to widespread hypoxic
cell damage, metabolic acidosis,
prolonged vasodilation

• Irreversible stage

 Severe cellular injury with

multiorgan failure, dominated
by renal, lungs, heart