Transcript HEMODYNAMIC DYSFUNCTION

HEMODYNAMIC
DYSFUNCTION
Pathophysiology
Premed 3
Dr. ROOPA
Hemodynamics, literally meaning
blood movement, is the study of blood
flow or the circulation.
Definition of terms
Hemmorhage:The escape or
extravasation of blood from the
vessels into
-surrounding tissues
-body cavity
-outside of the body
Different types of hemorrhages.
1. hematoma
2.hemothorax, hemopericardium,
hemoperitoneum, hemoarthrosis
3. petechial hemorrhages.
Hematoma: localized hemorrhage
within a tissue or organ
Hemopericardium
Hemoperitoneum
Petechiae
Purpura
Ecchymosis
petechiae
Minute 1 -2 mm hemorrhages into
skin,mucous membrane, or serosal
surfaces are called petechiae.
purpura
Slightly equal or more than 3 mm
hemorrhages.
Causes are same of the petechiae,
also vasculitis.
Ecchymosis
Larger >1 to 2 cm subcutaneous
hematomas(bruises)
Red cells in this lesions are degraded
and phagocytosed by macrophages
Hb is enzymatically converted into
bilirubin
Eventually into hemosiderin.
Infarction
Necrosis due to ischemia or poor blood supply
The necrotic tissue is referred to an Infarct
Types:
1. anemic/ white/ pale infarcts
- arterial occlusion
- heart, spleen and kidney
2. hemorrhagic / red infarct
-arterial or venous occlusion
-GIT and lungs
-areas with redundant blood supply
Thrombosis
Blood coagulates inside the blood vessels
Interruption of blood flow
pathologically Predisposed by many
conditions:
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
How is thePlatelet plug
stabilised?
Fibrinogen links strengthen the plug
Fibrin formation occurs
Prostacyclin is secreted by
endothelial cells; limit the plug
Prostacyclin is product of
cyclooxygenase pathway,is
synthesised by endothelial cells.
Endothelial cells
Normally are resistant to the
formation of a platelet plug
Synthesis of thrombomodulin: inhibit
coagulation
Vitamin K-dependent clotting factors
Factor II, VII, IX, and X
Prothrombin time (PT test)Measures function of extrinisic
pathway factors (VII, X, II, V,
fibrinogen)
Partial thromboplastin time (PTT test)
Measures function of intrinsic
pathway factors (XII, XI, IX, VIII, X, II,
fribrinogen
Proteins C and S
Vitamin-K dependent proteins that act
in a complex to inactivate factors Va
and VIIIa.
Antithrombin: Bind heparin-like
molecules on endothelial cells and act
to inhibit the activity of thrombin and
other serine proteases.
Thrombotic disorders
Hereditary thrombophilia
Antiphospholipid antibody syndrome
is associated with SLE
Disseminated intravascular
coagulopathy
Hereditary thrombophilia
Adolescents, young women
Characterrised by Recurrent venous
thrombosis
Thromboembolism
Deficiency: antithrombin III
protein S
protein C
Disseminated Intravascular
Coagulation
Consumption of platelets and
coagulation factors
Widespread thrombosis and
hemorrhage
Kinds of thrombi
Arterial thrombi
-areas with active blood flow
-lines of Zahn
Venous thrombi
Areas with less blood flow
Most often in Veins of lower
extremities
Are predisposed by Venous stasis
Dark red; no lines of Zahn not
prominent or absent.
Thrombophlebitis: inflammation of the
veins + thrombus
Embolism
Passage and trapping in the blood
vessels of mass objects
Breaking up of a thrombi: embolism
Types:
a. pulmonary
b. arterial
c. paradoxical
Pulmonary embolism
Pulmonary embolism (PE) is a
blockage of the main artery of the
lung or one of its branches by a
substance that has travelled from
elsewhere in the body through the
bloodstream (embolism). PE most
commonly results from DVT.Emboli to
the lungs; usually occuring in
immobilized postoperative patients
and those with CHF.
Symptoms of pulmonary embolism
include difficulty breathing, chest pain
on inspiration, and palpitations.
Clinical signs include low blood
oxygen saturation and cyanosis, rapid
breathing, and a rapid heart rate.
Severe cases of PE can lead to
collapse, abnormally low blood
pressure, and sudden death.
Saddle Embolus
A large thrombus lodged at an arterial
bifurcation, where blood flows from a
large-bore vessel to a smaller one.
The ‘classic’ saddle embolus—which
occurs at the bifurcation of the
pulmonary arteries in fatal pulmonary
embolism.
Arterial emboli
Originates from a mural thrombus
Left atrium: mitral stenosis
Left ventricle: Myocardial infarction
Sites of arrest:
1. Middle cerebral artery: most
common
2. Mesenteric arteries
3. Renal arteries
Paradoxical emboli
The obstruction of a systemic artery
by an embolus that originates in the
venous system and reaches the
arterial system through a septal
defect or an open oval foramen of the
heart.
Other forms of emboli
Fat emboli:Occurs when particles of
bone marrow and other fatty
intraosseous tissue enter the
circulation as a result of severe
fractures OR
obstruction by a fat embolus,
occurring especially after fractures of
large bones.
-go to brain, lungs, kidney
Fat embolism syndrome:
difficulty breathing
petechiae
neurologic manifestations
Air emboli:
- Introduction of air into the
circulation; can occur as a result of
obstetric procedures, chest wall
injury, decompression sickness
Caisson disease: Chronic
decompression sickness, gas emboli
in the bones, small infarcts in the
CNS.
Amniotic fluid embolism: Amniotic
Fluid Emboli Caused by escape of
amniotic fluid into maternal circulation
leading to sudden severe dyspnea,
cyanosis, hypotension and shock, can
also cause pulmonary edema and
DIC amniotic fluid in the blood.
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 hydrostatic pressure
-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
Represents circulatory collapse with
resultant hypoperfusion and
decreased oxygenation of tissues
or the organs and tissues of the body
are not receiving an adequate flow of
blood. Shock can result in serious
damage or even death.
Caused by:
-decreased cardiac output
-widespread peripheral vasodilatation
Types of shock
Hypovolemic shock
-loss in blood volume, it can occur with
-massive hemorrhage or fluid loss from
burns
-vomiting, diarrhea
Cardiogenic shock
Results from low cardiac output due
to myocardial failure.
Due to massive MI.
Septic shock
Results from vasodilation and
peripheral pooling of blood as part of
systemic reaction to bacterial or
fungal infection.
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