hemodynamic dysfunction pathophysiology premed 3 dr. roopa
TRANSCRIPT
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HEMODYNAMIC DYSFUNCTION
PathophysiologyPremed 3
Dr. ROOPA
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Hemodynamics, literally meaning blood movement, is the study of blood flow or the circulation.
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Definition of terms
Hemmorhage:The escape or extravasation of blood from the vessels into
-surrounding tissues
-body cavity
-outside of the body
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Different types of hemorrhages.
1. hematoma
2.hemothorax, hemopericardium, hemoperitoneum, hemoarthrosis
3. petechial hemorrhages.
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Hematoma: localized hemorrhage within a tissue or organ
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Hemopericardium
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Hemoperitoneum
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Petechiae Purpura
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Ecchymosis
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petechiae
Minute 1 -2 mm hemorrhages into skin,mucous membrane, or serosal surfaces are called petechiae.
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purpura
Slightly equal or more than 3 mm hemorrhages.
Causes are same of the petechiae, also vasculitis.
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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.
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Infarction
Necrosis due to ischemia or poor blood supplyThe necrotic tissue is referred to an InfarctTypes: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
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Thrombosis
Blood coagulates inside the blood vesselsInterruption of blood flowpathologically Predisposed by many conditions:smokingOCPimmobilizationsickle cell diseasepolycythemiacancercongestive heart failure
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Thrombogenesis
Formation of a thrombus
Depends on:
1. platelets
2. endothelial cells
3. coagulation cascade
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Platelet plug
Injury to the blood vessel exposes collagen in the vessel wallVon Willebrand factor allows the platelets to adhere Conformational change in the plateletsActivation of the coagulation cascadeAlso, formation of TxA2: constricts blood vessels, platelets aggregate
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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.
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Endothelial cells
Normally are resistant to the formation of a platelet plug
Synthesis of thrombomodulin: inhibit coagulation
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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
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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.
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Thrombotic disorders
Hereditary thrombophilia
Antiphospholipid antibody syndrome is associated with SLE
Disseminated intravascular coagulopathy
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Hereditary thrombophilia
Adolescents, young women
Characterrised by Recurrent venous thrombosis
Thromboembolism
Deficiency: antithrombin III
protein S
protein C
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Disseminated Intravascular Coagulation
Consumption of platelets and coagulation factors
Widespread thrombosis and hemorrhage
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Kinds of thrombi
Arterial thrombi
-areas with active blood flow
-lines of Zahn
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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
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Embolism
Passage and trapping in the blood vessels of mass objects
Breaking up of a thrombi: embolism
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Types:
a. pulmonary
b. arterial
c. paradoxical
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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.
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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.
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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.
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Arterial emboli
Originates from a mural thrombusLeft atrium: mitral stenosisLeft ventricle: Myocardial infarctionSites of arrest:
1. Middle cerebral artery: most common
2. Mesenteric arteries3. Renal arteries
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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.
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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
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Fat embolism syndrome:
difficulty breathing
petechiae
neurologic manifestations
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Air emboli:
- Introduction of air into the circulation; can occur as a result of obstetric procedures, chest wall injury, decompression sickness
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Caisson disease: Chronic decompression sickness, gas emboli in the bones, small infarcts in the CNS.
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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.
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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
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EDEMA
Causes:
-increased hydrostatic pressure
-increased capilary permeability
-decreased oncotic pressure
-increased sodium retention
-blocked lymphatics
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Types of edema
Anasarca: generalized form
Hydrothorax
Hydropericardium
Hydroperitoneum (ascites)
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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
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SHOCK
Represents circulatory collapse with resultant hypoperfusion and decreased oxygenation of tissuesor 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
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Types of shock
Hypovolemic shock
-loss in blood volume, it can occur with
-massive hemorrhage or fluid loss from
burns
-vomiting, diarrhea
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Cardiogenic shock
Results from low cardiac output due to myocardial failure.
Due to massive MI.
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Septic shock
Results from vasodilation and peripheral pooling of blood as part of systemic reaction to bacterial or fungal infection.
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Neurogenic shock
-severe trauma
-peripheral vasodilatation
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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
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3. Irreversible stage
-organ damage
-metabolic imbalance
-death