PM_HEMODYNAMIC_DYSFUNCTION
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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