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HEMODYNAMIC
DYSFUNCTION
May 19, 2008
Pathophysiology
Premed 2
Dr. ROOPA
FLUID DISTRIBUTION
60% of lean body weight is water
 -2/3 is intracellular
 -1/3 is extracellular
 5% of total body water is in blood plasma

DEFINITION OF TERMS

Hemmorhage: escape of blood from the vessels
-surrounding tissues
-body cavity
-outside of the body
HEMATOMA:
THE TISSUE
BLOOD TRAPPED WITHIN
Hemopericardium
Hemoperitoneum
Petechiae
Purpura
Ecchymosis

A petechia (pronounced plural petechiae is a
small (1-2mm) red or purple spot on the body,
caused by a minor hemorrhage (broken capillary
blood vessels

Purpura (from the Latin, purpura, meaning
"purple") is the appearance of red or purple
discolorations on the skin that do not blanch on
applying pressure. They are caused by bleeding
underneath the skin. Purpura measure 0.3-1 cm,
whereas petechiae measure less than 3 mm, and
ecchymoses greater than 1 cm.[1]
An ecchymosis is a spot caused by loss of blood
from a vessel.
 It implies a larger size than a petechia.[1]
 It has a more diffuse border than purpura.[2]
 It can be caused by a bruise (which implies
trauma), but can also be caused by bleeding
diathesis.[
 Ecchymosis: The skin discoloration caused by the
escape of blood into the tissues from ruptured
blood vessels. Ecchymoses can similarly occur in
mucous membranes as, for example, in the
mouth.

INFARCTION
An infarction is the process of tissue death
caused by blockage of the tissues blood
supply.The supplying artery may be blocked by
an obstruction.
 Types:
1. anemic/ white/ pale infarcts
- arterial occlusion
- heart, spleen and kidney
2. hemorrhagic / red infarct
- venous occlusion
-intestines and lungs
-areas with redundant blood supply

NORMAL HEMOSTASIS
A well regulated process
 maintains blood in a fluid, clot free state in
normal vessels
 induces the rapid formation of a localized
hemostatic plug at the site of vascular injury

NORMAL SEQUENCES OF HEMOSTASIS
1. Arteriolar vasoconstriction
 2. Exposure of subendothelial ECM when there is
endothelial injury
 3. Tissue factor released at site of injury
 4. Formation of permanent plug

THROMBOSIS
 Blood
coagulates inside the blood vessels
 Interruption of blood flow
 Predisposing factors:
smoking
OCP
immobilization
sickle cell disease
polycythemia
cancer
congestive heart failure
THROMBOGENESIS
Formation of a thrombus
 Depends on:
 1. platelets
 2. endothelial cells
 3. coagulation cascade

PLATELET PLUG
Injury to the blood vessel exposes collagen in the
vessel wall
 Von Willebrand factor allows the platelets to
adhere
 Conformational change in the platelets
 Activation of the coagulation cascade
 Also, formation of TxA2: constricts blood vessels,
platelets aggregate


Von Willebrand factor (vWF) is a blood
glycoprotein involved in hemostasis.
PLATELET PLUG
Fibrinogen links strengthen the plug
 Fibrin formation occurs
 Prostacyclin is secreted by endothelial cells; limit
the plug

COAGULATION CASCADE
2 pathways. Intrinsic pathway(contact activation
pathway)
 Extrinsic pathway(tissue factor pathway)
 Lead to fibrin formation
 Extrinsic pathway
-initiated by tissue factor
-final product: formation of fibrin
-prothrombin time
-factors II, V, VII and X
-fibrinogen

COAGULATION CASCADE
 Intrinsic
pathway
 Involves all the clotting factors except VII
and XIII
 Involves contact activation with:
-Hageman factor (factor XII)
-prekallikrein
-high molecular weight
kininogen(HMWK)
-factor XI
THROMBOTIC DISORDERS
Hereditary thrombophilia
 Antiphospholipid antibody syndrome
 Disseminated intravascular coagulopathy

HEREDITARY THROMBOPHILIA
Adolescents, young women
 Recurrent venous thrombosis
 Thromboembolism
 Deficiency: antithrombin III
protein S
protein C
 Most frequent cause: Factor V Leiden

DISSEMINATED INTRAVASCULAR
COAGULATION
Is a pathological activation of coagulation
mechanisms that happens in response to a
variety of diseases.
 Consumption of platelets and coagulation factors
 Widespread thrombosis and hemorrhage


Disseminated intravascular coagulation
(DIC), is a pathological activation of coagulation
(blood clotting) mechanisms that happens in
response to a variety of diseases. As its name
suggests, it leads to the formation of small blood
clots inside the blood vessels throughout the
body.[1] As the small clots consume all the
available coagulation proteins and platelets,
normal coagulation is disrupted and abnormal
bleeding occurs from the skin critically ill, and
may participate in the development of multiple
organ failure, which may lead to death.[4]
KINDS OF THROMBI

Arterial thrombi
-areas with active blood flow
-lines of Zahn

Lines of Zahn are a characteristic of thrombi[1]
that appear when formed in the heart or aorta.
They have visible and microscopic laminations
produced by alternating pale layers of platelets
mixed with fibrin and darker layer containing red
blood cells. Their presence implies thrombosis at
a site of rapid blood flow. In veins or smaller
arteries, where flow is not as constant, they are
less apparent
VENOUS THROMBI
Areas with less blood flow
 Veins of lower extremities
 Venous stasis
 Dark red; no lines of Zahn

EMBOLISM

In medicine, an embolism (plural embolisms)
occurs when an object migrates from one part of
the body (through circulation) and causes a
blockage (occlusion) of a blood vessel in another
part of the body.
PULMONARY EMBOLISM
Sudden death
 Immobilized patients, heart disease (CHF)
 Saddle emboli: bifurcation of the pulmonary
artery
 Leads to pulmonary infarcts

ARTERIAL EMBOLI




1.
2.
3.
Originates from a mural thrombus
Left atrium: mitral stenosis
Left ventricle: Myocardial infarction
Sites of arrest:
Middle cerebral artery: most common
Mesenteric arteries
Renal arteries
PARADOXICAL EMBOLI
Emboli comes from venous side
 Passes though right-to –left shunt
atrial septal defect
patent foramen ovale
 Reaches arterial circulation

OTHER FORMS OF EMBOLI

Fat emboli: bone marrow particles; fractures
-go to brain, lungs, kidney
-fat embolism syndrome:
difficulty breathing
petechiae
neurologic manifestations

Air emboli: air goes into the blood vessels
-trauma to the chest; abortion
-decompression sickness: “the bends”
or muscle pains
-caissons disease: infarcts in the CNS, bones,
tissues
-due to nitrogen bubbles in the blood

Amniotic fluid embolism: amniotic fluid in the
blood
-can lead to DIC, death
EDEMA
Abnormal fluid in the interstitial tissues spaces
or body cavities
 Caused by:
-increased hydrostatic pressure
right sided heart failure: peripheral
edema
left sided heart failure: pulmonary
edema

EDEMA

Causes:
-increased capilary permeability
-decreased oncotic pressure
-increased sodium retention
-blocked lymphatics
TYPES OF EDEMA
Anasarca: generalized form
 Hydrothorax
 Hydropericardium
 Hydroperitoneum (ascites)

Transudate
-non inflammatory
-abnormal hyrdostatic
or osmotic pressure
-low protein
-sp.gr. < 1.012
-high glucose

Exudate
-inflammation
-increased vascular
permeability
-high protein content
-sp.gr. >1.020
-many WBC
-low glucose

SHOCK
Circulatory collapse
 Hypoperfusion
 Decreased oxygenation of tissues
 Caused by:
-decreased cardiac output
-widespread peripheral vasodilatation
 Organ most affected: kidney
-acute tubular necrosis

TYPES OF SHOCK
Hypovolemic shock
-loss in blood volume
-massive hemorrhage
-burns
-vomiting, diarrhea

Cardiogenic shock
-massive MI
-pump failure of the left ventricle
 Septic shock
-bacterial infections; endotexemia

Neurogenic shock
-severe trauma
-peripheral vasodilatation

STAGES OF SHOCK
 1.
nonprogressive (early stage)
-compensatory mechanisms
-increased heart rate; increased
peripheral resistance
2. progressive stage
-compensatory mechanisms not
adequate
-tissue hypoperfusion
-circulatory and metabolic imbalance

3. Irreversible stage
-organ damage
-metabolic imbalance
-death