Minarcik robbins 2013_ch4-hemodyn
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Transcript of Minarcik robbins 2013_ch4-hemodyn
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HEMODYNAMIC DISORDERS
Jv = ([Pc − Pi] − σ[πc − πi])
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•Hemodynamic Disorders
•Thromboembolic Disease
•Shock
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Overview• Edema (increased fluid in the ECF)
• Hyperemia (INCREASED flow)
• Congestion (INCREASED backup)
• Hemorrhage (extravasation)
• Hemostasis (opposite of thrombosis)
• Thrombosis (clotting blood)
• Embolism (downstream travel of a clot)
• Infarction (death of tissues w/o blood)
• Shock (circulatory failure/collapse)
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EDEMA• ONLY 4 POSSIBILITIES!!!
–Increased Hydrostatic Pressure–Reduced Oncotic Pressure–Lymphatic Obstruction–Sodium/Water Retention
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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, -PERITONEAL
• EFFUSIONS, ASCITES, ANASARCA
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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
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REDUCED PLASMA ONCOTICPRESSURE (HYPOPROTEINEMIA)• Protein-losing glomerulopathies
(nephrotic syndrome)
• Liver cirrhosis (ascites)
• Malnutrition
• Protein-losing gastroenteropathy
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LYMPHATIC OBSTRUCTION(LYMPHEDEMA)
• Inflammatory
• Neoplastic
• Postsurgical
• Postirradiation
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Na+ RETENTION• Excessive salt intake with renal
insufficiency
• Increased tubular reabsorption of sodium
• Renal hypoperfusion Increased renin-angiotensin-aldosterone secretion
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INFLAMMATION• Acute inflammation
• Chronic inflammation
• Angiogenesis
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Jv = ([Pc − Pi] − σ[πc − πi])
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CHF EDEMA• INCREASED VENOUS PRESSURE
DUE TO FAILURE
• DECREASED RENAL PERFUSION, triggering of RENIN-ANGIOTENSION-ALDOSTERONE complex, resulting ultimately in SODIUM RETENTION
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HEPATIC ASCITES
• PORTAL HYPERTENSION
• HYPOALBUMINEMIA
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ASCITES
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RENAL EDEMA• SODIUM RETENTION
• PROTEIN LOSING GLOMERULOPATHIES (NEPHROTIC SYNDROME)
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EDEMA• SUBCUTANEOUS (“PITTING”)
• “DEPENDENT”
• ANASARCA
• LEFT vs RIGHT HEART
• PERIORBITAL
• PULMONARY
• CEREBRAL (closed cavity, no expansion)– HERNIATION of cerebellar tonsils– HERNIATION of hippocampal uncus over tentorium– HERNIATION, subfalcine
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“Pitting” Edema
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Transudate vs Exudate• Transudate
– results from disturbance of Starling forces– specific gravity < 1.012– protein content < 3 g/dl, LDH LOW
• Exudate– results from damage to the capillary wall– specific gravity > 1.012– protein content > 3 g/dl, LDH HIGH
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HYPEREMIA/(CONGESTION)
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HYPEREMIAActive Process
CONGESTIONPassive ProcessAcute or Chronic
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CONGESTION• LUNG
–ACUTE
–CHRONIC
• LIVER–ACUTE
–CHRONIC
• CEREBRAL
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ACUTE PASSIVE HYPEREMIA/CONGESTION,
LUNG
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Kerley B
Air Bronch-ogram
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CHRONIC PASSIVE HYPEREMIA/CONGESTION,
LUNG
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Acute Passive Congestion, Liver
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Acute Passive Congestion, Liver
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CHRONIC PASSIVE HYPEREMIA/CONGESTION, LIVER
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HEMORRHAGE• EXTRAVASATION beyond vessel
• “HEMORRHAGIC DIATHESIS”
• HEMATOMA (implies MASS effect)
• “DISSECTION”
• PETECHIAE (1-2mm) (PLATELETS)
• PURPURA <1cm
• ECCHYMOSES >1cm (BRUISE)• HEMO-: -thorax, -pericardium, -peritoneum, HEMARTHROSIS
• ACUTE, CHRONIC
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EVOLUTION of HEMORRHAGE
• ACUTE CHRONIC
• PURPLE GREEN BROWN
• HGB BILIRUBIN HEMOSIDERIN
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HEMATOMAvs.
“CLOT”
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HEMOSTASIS• OPPOSITE of THROMBOSIS
–PRESERVE LIQUIDITY OF BLOOD
–“PLUG” sites of vascular injury
• THREE COMPONENTS–VASCULAR WALL, i.e., endoth/ECM
–PLATELETS
–COAGULATION CASCADE
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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, plats.
– Activates coagulation cascadethrombinfibrin (2˚ HEMOSTASIS)
• FIBRIN polymerizes, TPA limits plug
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PLAYERS•ENDOTHELIUM
•PLATELETS
•COAGULATION “CASCADE”
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ENDOTHELIUM• NORMALLY
–ANTIPLATELET PROPERTIES
–ANTICOAGULANT PROPERTIES
–FIBRINOLYTIC PROPERTIES
• IN INJURY–PRO-COAGULANT PROPERTIES
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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)
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ENDOTHELIUM• PROTHROMBOTIC PROPERTIES
–Makes vWF, which binds PlatsColl
–Makes TISSUE FACTOR (with plats)
–Makes Plasminogen inhibitors
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ENDOTHELIUM• ACTIVATED by INFECTIOUS AGENTS
• ACTIVATED by HEMODYNAMICS
• ACTIVATED by PLASMA
• ACTIVATED by ANYTHING which disrupts it
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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
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NORMAL platelet on LEFT, “DEGRANULATING” ALPHA GRANULE ON RIGHT AT OPEN WHITE ARROW
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PLATELET PHASES
• ADHESION
• SECRETION (i.e., “release” or “activation” or “degranulation”)
• AGGREGATION
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PLATELET ADHESION
• Primarily to the subendothelial ECM
• Regulated by vWF, which bridges platelet surface receptors to ECM collagen
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PLATELET SECRETION
• BOTH granules, α and δ• Binding of agonists to
platelet surface receptors AND intracellular protein PHOSPHORYLATION
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PLATELET AGGREGATION
• ADP
• TxA2 (Thromboxane A2)
• THROMBIN from coagulation cascade also
• FIBRIN further strengthens and hardens and contracts the platelet plug
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PLATELET EVENTS
• ADHERENCE to ECM
• SECRETION of ADP and TxA2
• EXPOSE phospholipid complexes
• Express TISSUE FACTOR
• PRIMARYSECONDARY PLUG
• STRENGTHENED by FIBRIN
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COAGULATION “CASCADE”
• INTRINSIC(contact)/EXTRINSIC(TissFac)
• ProenzymesEnzymes
• 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
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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
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THROMBOSIS• Pathogenesis
• Endothelial Injury
• Alterations in Flow
• Hypercoagulability
• Morphology
• Fate
• Clinical Correlations
• Venous
• Arterial (Mural)
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THROMBOSIS• Virchow’s TRIANGLE
ENDOTHELIAL INJURY
ABNORMAL FLOW(NON-LAMINAR)
HYPER-COAGULATION
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ENDOTHELIAL “INJURY”
• Jekyll/Hyde disruption–any perturbation in the dynamic
balance of the pro- and antithrombotic effects of endothelium, not only physical “damage”
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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)
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ENDOTHELIUM• PROTHROMBOTIC PROPERTIES
–Makes vWF, which binds PlatsColl
–Makes TISSUE FACTOR (with plats)
–Makes Plasminogen inhibitors
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ABNORMAL FLOW• NON-LAMINAR FLOW
• TURBULENCE
• EDDIES
• STASIS
• “DISRUPTED” ENDOTHELIUM
ALL of these factors may bring platelets into contact with endothelium and/or ECF
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1˚ HYPERCOAGULABILITY(INHERITED)
• COMMONEST: Factor V and
Prothrombin defects
• Common: Mutation in prothrombin gene, Mutation in methylenetetrahydrofolate gene
• Rare: Antithrombin III deficiency, Protein C deficiency, Protein S deficiency
• Very rare: Fibrinolysis defects
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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
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MORPHOLOGY• ADHERENCE TO VESSEL WALL
– HEART (MURAL)
– ARTERY (OCCLUSIVE/INFARCT)
– VEIN
• OBSTRUCTIVE vs. NON-OBSTRUCTIVE
• RED, YELLOW, GREY/WHITE
• ACUTE, ORGANIZING, OLD
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MURAL THROMBI, HEART
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FATE of THROMBI• PROPAGATION (Downstream)
• EMBOLIZATION
• DISSOLUTION
• ORGANIZATION
• RECANALIZATION
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OCCLUSIVE ARTERIAL THROMBUS
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D.V.T.• 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
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ARTERIAL/CARDIAC THROMBI• ACUTE MYOCARDIAL INFARCTION =
OLD ATHEROSCLEROSIS + FRESH THROMBOSIS
• ARTERIAL THROMBI also may send fragments DOWNSTREAM, but these fragments may contain flecks of calcified or cholesterol 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
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ATHEROEMBOLI• “CHOLESTEROL” clefts are
components of atherosclerotic arterial plaques, NOT venous thrombi!!!
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Disseminated Intravascular Coagulation
D.I.C.• OBSTETRIC COMPLICATIONS
• ADVANCED MALIGNANCY
• SHOCK (Shock and DIC are joined at the hip)
NOT a primary disease
CONSUMPTIVE coagulopathy, e.g., reduced platelets, fibrinogen, F-VIII and other consumable clotting factors, brain, heart, lungs, kidneys, MICROSCOPIC ONLY
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EMBOLISM•Pulmonary• Systemic (Mural Thrombi and
Aneurysms)
• Fat
• Air
• Amniotic Fluid
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PULMONARY EMBOLISM• USUALLY SILENT, USUALLY SILENT• CHEST PAIN, LOW PO2, S.O.B.• Sudden OCCLUSION of >60% of pulmonary
vasculature, presents a HIGH risk for sudden death, i.e., acute cor pulmonale, ACUTE right heart failure
• “SADDLE” embolism often/usually fatal• PRE vs. POST mortem blood clot:
– PRE: Friable, adherent, lines of “ZAHN”
– POST: Current jelly or chicken fat
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SYSTEMIC EMBOLI• “PARADOXICAL” EMBOLI
• 80% cardiac/20% aortic
• Embolization lodging site is proportional to the degree of flow (cardiac output) that area or organ gets, i.e., brain (15%), kidneys (~25%), legs, splanchnic (~25%), liver (~25%)
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OTHER EMBOLI•FAT (long bone fx’s, also
bones with marrow)
•AIR (SCUBA “bends”)
•AMNIOTIC FLUID, very prolonged or difficult delivery, high mortality
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Amniotic Fluid Embolism
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INFARCTION• Defined as an area of necrosis*
secondary to decreased blood flow
• HEMORRHAGIC vs. ANEMIC• RED vs. WHITE
– END ARTERIES vs. DUAL ARTERY SUPPLY
• ACUTEORGANIZATIONFIBROSIS
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INFARCTION FACTORS• NATURE of VASCULAR SUPPLY
– Single end arteries such as kidney, spleen?– Dual blood supply such as lung, liver?
• RATE of DEVELOPMENT–SLOW (BETTER)
–FAST (WORSE)
• VULNERABILITY to HYPOXIA–MYOCYTE vs. FIBROBLAST
• CHF vs. NO CHF
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HEART
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SHOCK• Pathogenesis
–Cardiac
–Septic
–Hypovolemic
• Morphology
• Clinical Course
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SHOCK• Definition: CARDIOVASCULAR COLLAPSE
• Common pathophysiologic features:– INADEQUATE CARDIAC OUTPUT and/or– INADEQUATE BLOOD VOLUME
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GENERAL RESULTS• INADEQUATE TISSUE PERFUSION
• CELLULAR HYPOXIA
• If UN-corrected, a FATAL outcome
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TYPES of SHOCK• CARDIOGENIC: (Acute, Chronic Heart
Failure)
• HYPOVOLEMIC: (Hemorrhage or Leakage)
• SEPTIC: (“ENDOTOXIC” shock, #1 killer in ICU)
• NEUROGENIC: (loss of vascular tone)• ANAPHYLACTIC: (IgE mediated systemic vasodilation and increased
vascular permeability)
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CARDIOGENIC shock• MI
• VENTRICULAR RUPTURE
• ARRHYTHMIA
• CARDIAC TAMPONADE
• PULMONARY EMBOLISM (acute RIGHT heart failure or “cor pulmonale”)
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HYPOVOLEMIC shock
• HEMORRHAGE, Vasc. compartmentH2O
• VOMITING, Vasc. compartmentH2O
• DIARRHEA, Vasc. compartmentH2O
• BURNS, Vasc. compartmentH2O
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SEPTIC shock
• OVERWHELMING INFECTION• “ENDOTOXINS”, i.e., LPS (Usually Gm-)• Gm+• FUNGAL• “SUPERANTIGENS”, (Superantigens are polyclonal T-lymphocyte
activators that induce systemic inflammatory cytokine cascades similar to those occurring downstream in septic shock, “toxic shock” superantigens by staph are the prime example.)
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SEPTIC shock events*(overwhelming infection)
• Peripheral vasodilation• Pooling• Endothelial Activation• DIC
* Think of this as a TOTAL BODY inflammatory response, or early total body infarct!
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ENDOTOXINS• Usually Gm-
• Degraded bacterial cell wall products
• Also called “LPS”, because they are Lipo-
Poly-Saccharides
• Attach to a cell surface antigen known as CD-14
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ENDOTOXINS
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SEPTIC shock events(linear sequence)
• SYSTEMIC VASODILATION (hypotension)
• ↓ MYOCARDIAL CONTRACTILITY• DIFFUSE ENDOTHELIAL ACTIVATION• LEUKOCYTE ADHESION• ALVEOLAR DAMAGE (ARDS)
• DIC
• VITAL ORGAN FAILURE CNS
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CLINICAL STAGES of shock
•NON-PROGRESSIVE (compensatory mechanisms)
•PROGRESSIVE (acidosis, early organ failure)
• IRREVERSIBLE
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NON-PROGRESSIVE• COMPENSATORY MECHANISMS
•CATECHOLAMINES• VITAL ORGANS PERFUSED
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PROGRESSIVE• HYPOPERFUSION
• EARLY “VITAL” ORGAN FAILURE
• OLIGURIA
•ACIDOSIS
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IRREVERSIBLE
•HEMODYNAMIC CORRECTIONS of no use
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PATHOLOGY• MULTIPLE ORGAN FAILURE
• SUBENDOCARDIAL HEMORRHAGE (why?)
• ACUTE TUBULAR NECROSIS (why?)
• DAD (Diffuse Alveolar Damage, lung) (why?)
• GI MUCOSAL HEMORRHAGES (why?)
• LIVER NECROSIS (why?)
• DIC (why?)
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ARDS/DAD
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MYOCARDIAL NECROSIS
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ATN
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DIC
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CLINICAL PROGRESSIONof SYMPTOMS
• Hypotension • Tachycardia • Tachypnea • Warm skin Cool skin Cyanosis
• Renal insufficiency• Obtundance
• Death