HEMODYNAMIC DISORDERS - SRM Institute of Science · PDF file2015-11-07 · Acute...

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Transcript of HEMODYNAMIC DISORDERS - SRM Institute of Science · PDF file2015-11-07 · Acute...

  • HEMODYNAMIC DISORDERS

    Jv = ([Pc Pi] [c i])

  • Hemodynamic Disorders

    Thromboembolic Disease

    Shock

  • Overview Edema Hyperemia Congestion Hemorrhage Hemostasis Thrombosis Embolism Infarction Shock

  • EDEMA ONLY 4 POSSIBILITIES!!!

    Increased Hydrostatic PressureReduced Oncotic PressureLymphatic ObstructionSodium/Water Retention

  • WATER 60% of body 2/3 of body water is INTRA-cellular The rest is INTERSTITIAL Only 5% is INTRA-vascular

    EDEMA is SHIFT to the INTERSTITIAL SPACE

    HYDRO- -THORAX, -PERICARDIUM, -PERICARDIUM

    EFFUSIONS, ASCITES, ANASARCA

  • INCREASED HYDROSTATIC PRESSURE

    Impaired venous return Congestive heart failure Constrictive pericarditis Ascites (liver cirrhosis) Venous obstruction or compression Thrombosis External pressure (e.g., mass) Lower extremity inactivity with prolonged dependency Arteriolar dilation Heat Neurohumoral dysregulation

  • REDUCED PLASMA ONCOTICPRESSURE (HYPOPROTEINEMIA) Protein-losing glomerulopathies

    (nephrotic syndrome) Liver cirrhosis (ascites) Malnutrition Protein-losing gastroenteropathy

  • LYMPHATIC OBSTRUCTION(LYMPHEDEMA)

    Inflammatory Neoplastic Postsurgical Postirradiation

  • Na+ RETENTION Excessive salt intake with renal

    insufficiency Increased tubular reabsorption of

    sodium

    Renal hypoperfusion Increased renin-angiotensin-aldosterone secretion

  • INFLAMMATION Acute inflammation Chronic inflammation Angiogenesis

  • Jv = ([Pc Pi] [c i])

  • CHF EDEMA INCREASED VENOUS PRESSURE

    DUE TO FAILURE

    DECREASED RENAL PERFUSION, triggering of RENIN-ANGIOTENSION-ALDOSTERONE complex, resulting ultimately in SODIUM RETENTION

  • HEPATIC ASCITES

    PORTAL HYPERTENSION

    HYPOALBUMINEMIA

  • ASCITES

  • RENAL EDEMA SODIUM RETENTION

    PROTEIN LOSING GLOMERULOPATHIES (NEPHROTIC SYNDROME)

  • EDEMA SUBCUTANEOUS (PITTING) DEPENDENT ANASARCA LEFT vs RIGHT HEART PERIORBITAL (RENAL) PULMONARY CEREBRAL (closed cavity, no expansion)

    HERNIATION of cerebellar tonsils HERNIATION of hippocampal uncus over tentorium HERNIATION, subfalcine

  • Pitting Edema

  • Transudate vs Exudate Transudate

    results from disturbance of Starling forces specific gravity < 1.012 protein content < 3 g/dl

    Exudate results from damage to the capillary wall specific gravity > 1.012 protein content > 3 g/dl

  • HYPEREMIA/(CONGESTION)

  • HYPEREMIAActive Process

    CONGESTIONPassive ProcessAcute or Chronic

  • CONGESTION LUNG

    ACUTECHRONIC

    LIVERACUTECHRONIC

    CEREBRAL

  • ACUTE PASSIVE HYPEREMIA/CONGESTION,

    LUNG

  • Kerley B

    Air Bronch-ogram

  • CHRONIC PASSIVE HYPEREMIA/CONGESTION,

    LUNG

  • Acute Passive Congestion, Liver

  • Acute Passive Congestion, Liver

  • CHRONIC PASSIVE HYPEREMIA/CONGESTION, LIVER

  • HEMORRHAGE EXTRAVASATION beyond vessel HEMORRHAGIC DIATHESIS HEMATOMA (implies MASS effect) DISSECTION PETECHIAE (1-2mm) (PLATELETS) PURPURA 1cm (BRUISE) HEMO-: -thorax, -pericardium, -peritoneum, HEMARTHROSIS

    ACUTE, CHRONIC

  • EVOLUTION of HEMORRHAGE

    ACUTE CHRONIC PURPLE GREEN BROWN HGB BILIRUBIN HEMOSIDERIN

  • HEMATOMAvs.

    CLOT

  • HEMOSTASIS OPPOSITE of THROMBOSIS

    PRESERVE LIQUIDITY OF BLOODPLUG sites of vascular injury

    THREE COMPONENTSVASCULAR WALL, i.e., endoth/ECMPLATELETSCOAGULATION CASCADE

  • SEQUENCE of EVENTSfollowing VASCULAR INJURY

    ARTERIOLAR VASOCONSTRICTION Reflex Neurogenic Endothelin, from endothelial cells

    THROMBOGENIC ECM at injury site Adhere and activate platelets

    Platelet aggregation (1 HEMOSTASIS) TISSUE FACTOR released by endothelium

    Activates coagulation cascade thrombin fibrin (2HEMOSTASIS)

    FIBRIN polymerizes, TPA limits plug

  • PLAYERSENDOTHELIUMPLATELETSCOAGULATION CASCADE

  • ENDOTHELIUM NORMALLY

    ANTIPLATELET PROPERTIESANTICOAGULANT PROPERTIESFIBRINOLYTIC PROPERTIES

    IN INJURYPRO-COAGULANT PROPERTIES

  • ENDOTHELIUM ANTI-Platelet PROPERTIES

    Protection from the subendothelial ECM Degrades ADP (inhib. Aggregation)

    ANTI-Coagulant PROPERTIES Membrane HEPARIN-like molecules Makes THROMBOMODULIN Protein-C TISSUE FACTOR PATHWAY INHIBITOR

    FIBRINOLYTIC PROPERTIES (TPA)

  • ENDOTHELIUM PROTHROMBOTIC PROPERTIES

    Makes vWF, which binds Plats CollMakes TISSUE FACTOR (with plats)Makes Plasminogen inhibitors

  • ENDOTHELIUM ACTIVATED by INFECTIOUS AGENTS ACTIVATED by HEMODYNAMICS ACTIVATED by PLASMA

  • PLATELETS ALPHA GRANULES

    Fibrinogen Fibronectin Factor-V, Factor-VIII Platelet factor 4, TGF-beta

    DELTA GRANULES (DENSE BODIES) ADP/ATP, Ca+, Histamine, Serotonin, Epineph.

    With endothelium, form TISSUE FACTOR

  • NORMAL platelet on LEFT, DEGRANULATING ALPHA GRANULE ON RIGHT AT OPEN WHITE ARROW

  • PLATELET PHASES ADHESION SECRETION (i.e.,

    release or activation or degranulation)

    AGGREGATION

  • PLATELET ADHESION Primarily to the

    subendothelial ECM

    Regulated by vWF, which bridges platelet surface receptors to ECM collagen

  • PLATELET SECRETION

    BOTH granules, and Binding of agonists to

    platelet surface receptors AND intracellular protein PHOSPHORYLATION

  • PLATELET AGGREGATION ADP TxA2 (Thromboxane A2) THROMBIN from coagulation

    cascade also FIBRIN further strengthens

    and hardens and contracts the platelet plug

  • PLATELET EVENTS

    ADHERENCE to ECM SECRETION of ADP and TxA2 EXPOSE phospholipid

    complexes Express TISSUE FACTOR PRIMARY SECONDARY PLUG STRENGTHENED by FIBRIN

  • COAGULATION CASCADE

    INTRINSIC(contact)/EXTRINSIC(TissFac) Proenzymes Enzymes Prothrombin(II) Thrombin(IIa) Fibrinogen(I) Fibrin(Ia) Cofactors

    Ca++ Phospholipid (from platelet membranes) Vit-K dep. factors: II, VII, IX, X, Prot. S, C, Z

  • COAGULATION TESTS (a)PTT INTRINSIC (HEP Rx) PT (INR) EXTRINSIC (COUM Rx) BLEEDING TIME (PLATS) (2-9min) Platelet count (150,000-400,000/mm3) Fibrinogen Factor assays

  • THROMBOSIS Pathogenesis Endothelial Injury Alterations in Flow Hypercoagulability Morphology Fate Clinical Correlations Venous Arterial (Mural)

  • THROMBOSIS Virchows TRIANGLE

    ENDOTHELIAL INJURY

    ABNORMAL FLOW(NON-LAMINAR)

    HYPER-COAGULATION

  • ENDOTHELIAL INJURY

    Jekyll/Hyde disruptionany perturbation in the dynamic

    balance of the pro- and antithrombotic effects of endothelium, not only physical damage

  • ENDOTHELIUM ANTI-Platelet PROPERTIES

    Protection from the subendothelial ECM Degrades ADP (inhib. Aggregation)

    ANTI-Coagulant PROPERTIES Membrane HEPARIN-like molecules Makes THROMBOMODULIN Protein-C TISSUE FACTOR PATHWAY INHIBITOR

    FIBRINOLYTIC PROPERTIES (TPA)

  • ENDOTHELIUM PROTHROMBOTIC PROPERTIES

    Makes vWF, which binds Plats CollMakes TISSUE FACTOR (with plats)Makes Plasminogen inhibitors

  • ABNORMAL FLOW NON-LAMINAR FLOW TURBULENCE EDDIES STASIS DISRUPTED ENDOTHELIUMALL of these factors may bring

    platelets into contact with endothelium and/or ECF

  • 1 HYPERCOAGULABILITY(INHERITED)

    COMMONEST: Factor V and Prothrombin defects

    Common: Mutation in prothrombin gene, Mutation in methyltetrahydrofolate gene

    Rare: Antithrombin III deficiency, Protein C deficiency, Protein S deficiency

    Very rare: Fibrinolysis defects

  • 2 HYPERCOAGULABILITY(ACQUIRED)

    Prolonged bed rest or immobilization Myocardial infarction Atrial fibrillation Tissue damage (surgery, fracture, burns) Cancer (TROUSSEAU syndrome, i.e., migratory thrombophlebitis) Prosthetic cardiac valves Disseminated intravascular coagulation Heparin-induced thrombocytopenia Antiphospholipid antibody syndrome (lupus anticoagulant syndrome)

    Lower risk for thrombosis: Cardiomyopathy Nephrotic syndrome Hyperestrogenic states (pregnancy) Oral contraceptive use Sickle cell anemia Smoking, Obesity

  • MORPHOLOGY ADHERENCE TO VESSEL WALL

    HEART (MURAL) ARTERY (OCCLUSIVE/INFARCT) VEIN

    OBSTRUCTIVE vs. NON-OBSTRUCTIVE RED, YELLOW, GREY/WHITE ACUTE, ORGANIZING, OLD

  • MURAL THROMBI, HEART

  • FATE of THROMBI PROPAGATION (Downstream) EMBOLIZATION DISSOLUTION ORGANIZATION RECANALIZATION

  • OCCLUSIVE ARTERIAL THROMBUS

  • D. (CALF, THIGH, PELVIC) V.T. CHF a huge factor

    INACTIVITY!!! Trauma Surgery Burns Injury to vessels, Procoagulant substances from tissues Reduced t-PA activity

  • ARTERIAL/CARDIAC THROMBI ACUTE MYOCARDIAL INFARCTION =

    OLD ATHEROSCLEROSIS + FRESH THROMBOSIS

    ARTERIAL THROMBI also may send fragments DOWNSTREAM, but these fragments may contain flecks of PLAQUE also

    LODGING is PROPORTIONAL to the % of cardiac output the organ receives, i.e., brain, kidneys, spleen, legs, or the diameter of the downstream vessel

  • ATHEROEMBOLI CHOLESTEROL clefts are

    components of atherosclerotic plaques, NOT thrombi!!!

  • Disseminated Intravascular Coagulation

    D.I.C. OBSTETRIC COMPLICATIONS ADVANCED MALIGNANCYNOT a primary diseaseCONSUMPTIVE coagulopathy, e.g.,

    reduced platelets, fibrinogen, F-VIII and other consumable clotting factors, brain, heart, lungs, kidneys, MICROSCOPIC ONLY

  • EMBOLISMPulmonary Systemic (Mural Thrombi and

    Aneurysms) Fat Air Amniotic Fluid

  • PULMONARY EMBOLISM U