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.main artery of the lungembolism

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.difficulty breathingchest pain on inspirationpalpitations Clinical signs oxygen saturationcyanosisrapid breathinga rapid heart rate collapseabnormally low blood pressuresudden deat

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. < high glucose Exudate -inflammation -increased vascular permeability -high protein content -sp.gr. > 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.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