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128 Cards in this Set
- Front
- Back
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NORMAL FLUID HOMEOSTASIS -REQUIREMENTS-
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VESSEL WALL INTEGRITY
MAINTENANCE OF INTRAVASCULAR: PRESSURE, OSMOLARITY |
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STARLING’S LAW
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ARTERIAL FLUID
EQUALS VENOUS + LYMPHATIC FLUID |
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FLUID IMBALANCES
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REDUCTION – HYPOVOLEMIC (ABSOLUTE, RELATIVE)
INCREASE - HYPERVOLEMIC |
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ABNORMAL FLUID HOMEOSTASIS
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MAJOR MORBIDITY/MORTALITY: MYOCARDIAL INFARCTION, PULMONARY EMBOLISM, STROKE
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FLUID & HEMODYNAMIC DERANGEMENTS -TOPICS-
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HYPEREMIA
CONGESTION EDEMA DEHYDRATION HEMORRHAGE THROMBOSIS EMBOLISM ISCHEMIA INFARCTION SHOCK |
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HYPEREMIA IS
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INCREASED REDNESS OF A TISSUE CAUSED BY AN INCREASED AMOUNT OF BLOOD
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ACTIVE HYPEREMIA
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INCREASED BLOOD SUPPLY
ACTIVE ARTERIAL DILATION (“ACTIVE” HYPEREMIA) TISSUE APPEARS RED MAY BE ACCOMPANIED BY EDEMA BLUSHING, FLUSHING, INFLAMMATION (“HEART FAILURE CELLS”) |
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CONGESTION
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IMPAIRED VENOUS OUTFLOW
ACCUMULATION OF VENOUS BLOOD “PASSIVE” HYPEREMIA TISSUE IS BLUE-RED (CYANOTIC) OFTEN ACCOMPANIED BY EDEMA CAN LEAD TO HYPOXIA AND TISSUE DEATH |
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LOCAL CONGESTION
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VENOUS OBSTRUCTION
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SYSTEMIC CONGESTION
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“NUTMEG” LIVER (RIGHT VENTRICULAR FAILURE)
“BROWN INDURATION” OF LUNGS (LEFT VENTRICULAR FAILURE) |
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EDEMA IS
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THE ACCUMULATION OF FLUID IN INTERSTITIAL SPACES OR BODY CAVITIES
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TOTAL BODY WATER -DISTRIBUTION-
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60% OF TOTAL BODY WEIGHT:
66% INTRACELLULAR 33% EXTRACELLULAR (95 % INTERSTITIAL, 5% PLASMA) |
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CONTROL OF FLUID MOVEMENT
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OPPOSING EFFECTS OF: VASCULAR HYDROSTATIC PRESSURE, PLASMA COLLOID OSMOTIC PRESSURE
NORMALLY BALANCED BETWEEN: EXIT FROM ARTERIOLES INTO INTERSTITIUM, INFLOW AT VENULES, LYMPHATIC DRAINAGE |
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MECHANISM OF EDEMA
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ARTERIAL FLUID
IS GREATER THAN VENOUS + LYMPHATIC FLUID |
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TYPES OF EDEMA FLUID
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TRANSUDATE
EXUDATE |
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TRANSUDATE
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NON-INFLAMMATORY
MOST COMMON LOW PROTEIN CONTACT SPECIFIC GRAVITY < 1.020 |
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EXUDATE
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INFLAMMATORY
HIGH PROTEIN CONTENT SPECIFIC GRAVITY > 1.020 |
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EDEMA -MECHANISMS-
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INCREASED VASCULAR PERMEABILITY
INCREASED INTRAVASCULAR PRESSURE REDUCED PLASMA ONCOTIC PRESSURE INCREASED INTERSTITIAL ONCOTIC PRESSURE LYMPHATIC OBSTRUCTION |
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EDEMA -INCREASED VASCULAR PERMEABILITY-
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INFLAMMATION
MEDIATED BY VASOACTIVE AMINES POSTCAPILLARY VENULE FLUID ESCAPES THROUGH GAPS BETWEEN CONTRACTED ENDOTHELIAL CELLS |
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EDEMA -INCREASED INTRAVASCULAR PRESSURE
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INCREASED HYDROSTATIC PRESSURE
IMPAIRED VENOUS RETURN: RIGHT HEART FAILURE (PERIPHERAL EDEMA); LEFT HEART FAILURE (PULMONARY EDEMA); PREGNANCY (EDEMA OF LEGS) ARTERIOLAR DILATATION |
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EDEMA -DECREASED PLASMA ONCOTIC PRESSURE-
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RENAL DISEASE (NEPHROTIC SYNDROME)
LIVER DISEASE (HEPATIC CIRRHOSIS) |
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EDEMA -LYMPHATIC OBSTRUCTION-
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SURGICAL REMOVAL OF LYMPH NODES
INFECTION – ELEPHANTIASIS… |
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SYSTEMIC EDEMA -IMPORTANT CAUSES-
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CARDIAC FAILURE
RENAL FAILURE LIVER FAILURE |
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LOCAL EDEMA -IMPORTANT CAUSES-
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TRAUMA
INFECTION PREGNANCY HYPERSENSITIVITY NEOPLASMS |
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EDEMA -SPECIFIC TYPES-
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ANASARCA
ASCITES HYDROTHORAX HYDROPERICARDIUM |
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ANASARCA
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GENERALIZED SUBCUTANEOUS EDEMA
DEPENDENT PORTIONS RIGHT-SIDED HEART FAILURE CARDIAC, PEDAL, PITTING EDEMA |
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ASCITES
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EDEMA
PERIOTONEAL CAVITY HEPATIC PORTAL OBSTRUCTION CIRRHOSIS |
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CONSEQUENCES OF EDEMA
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INCONSEQUENTIAL… FATAL
SUBQ EDEMA: INDICATES UNDERLYING DISEASE PULMONARY EDEMA: INTERFERES WITH VENTILATION, PREDISPOSES TO INFECTION CEREBRAL EDEMA: HERNIATES BRAIN INTO VERTEBRAE, COMPRESSES MEDULLARY CENTERS, COMPRESSES BLOOD VESSELS |
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CEREBRAL EDEMA CONSEQUENCES
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HERNIATES BRAIN INTO VERTEBRAE
COMPRESSES MEDULLARY CENTERS COMPRESSES BLOOD VESSELS |
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PULMONARY EDEMA CONSEQUENCES
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INTERFERES WITH VENTILATION
PREDISPOSES TO INFECTION |
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DEHYDRATION
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ABNORMAL LOSS OF BODY WATER
DECREASED INTAKE INCREASED LOSS (SWEATING, VOMITING, DIARRHEA) |
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HEMORRHAGE IS
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DISCHARGE OF BLOOD FROM A RUPTURED BLOOD VESSEL
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HEMORRHAGE -CAUSES-
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TRAUMA
INVASION BY NEOPLASMS… INCREASED CAPILLARY FRAGILITY THROMBOCYTOPENIA HEMOPHILIA AND OTHER BLEEDING DISORDERS |
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HEMORRHAGE -TYPES-
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INTERNAL OR EXTERNAL
HEMATOMA (LOCALIZED HEMORRHAGE) HEMORRHAGE INTO BODY CAVITIES SPECIFIC TYPES |
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HEMORRHAGE -TYPES OF HEMATOMAS-
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PETECHIAE – SMALL (1-2mm)
PURPURA – LARGER (3-5mm) ECCHYMOSIS – LARGEST (1-2CM) |
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ECCHYMOSIS HEMATOMA
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LARGEST (1-2CM)
BRUISE HEMOGLOBIN→ BILIRUBIN→HEMOSIDERIN RED-BLUE→BLUE-GREEN→GOLDEN BROWN |
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HEMORRHAGE -INTO BODY CAVITIES-
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HEMOTHORAX
HEMOPERICARDIUM HEMOPERITONEUM HEMARTHROSIS |
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HEMORRHAGE -SPECIFIC TYPES-
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EPISTAXIS (NOSE BLEED)
HEMOPTYSIS (COUGHING UP BLOOD) HEMATEMESIS (VOMITING BLOOD) MELENA (BLOOD IN THE STOOL) |
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EPISTAXIS
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HEMORRHAGE
NOSE BLEED |
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HEMOPTYSIS
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HEMORRHAGE
COUGHING UP BLOOD |
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HEMATEMESIS
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HEMORRHAGE
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MELENA
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HEMORRHAGE
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HEMORRHAGE -FACTORS IN SIGNIFICANCE-
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RATE & VOLUME OF BLOOD LOST (RAPID LOSS OF 20% SURVIVABLE; SLOW LOSS OF > 20% SURVIVABLE; HYPOVOLEMIC SHOCK MAY ENSUE)
LOCATION OF HEMORRHAGE (SUBCUTANEOUS BEST, BRAIN WORST) CHRONIC EXTERNAL BLOOD LOSS (PEPTIC ULCER, MENSTRUAL; RISK OF IRON DEFICIENCY ANEMIA) |
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HEMOSTASIS IS
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PHYSIOLOGIC BLOOD CLOTTING TO REPAIR INJURY TO A BLOOD VESSEL
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HEMOSTASIS -GENERAL INFORMATION-
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TIGHTLY REGULATED (MAINTAINS FLUID STATE OF BLOOD; RAPIDLY FORM HEMOSTATIC PLUG)
THROMBOSIS = PATHOLOGIC HEMOSTASIS HEMOSTASIS AND THROMBOSIS INVOLVE: VESSEL WALL, PLATELETS, AND COAGULATION CASCADE |
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HEMOSTASIS -STEPS-
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VASOCONSTRICTION
HEMOSTATIC PLUG FORMATION (PRIMARY HEMOSTASIS) FIBRIN CLOT FORMATION (SECONDARY HEMOSTASIS) THROMBOLYSIS |
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HEMOSTASIS -VASOCONSTRICTION-
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ARTERIOLAR CONSTRICTION
NEUROGENIC REACTION TO INJURY RELEASE OF ENDOTHELIN (VASOCONSTRICTOR) TRANSIENT (SECONDS TO MINUTES) BLEEDING WILL RESUME UNLESS OTHER EVENTS OCCUR |
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PRIMARY HEMOSTASIS
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NORMAL ENDOTHELIUM
ENDOTHELIAL INJURY CYTOKINES PRODUCTION SECRETION OF PLASMINOGEN ACTIVATOR INHIBITORS |
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PRIMARY HEMOSTASIS -NORMAL ENDOTHELIUM-
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ANTIPLATELET
ANTICOAGULANT PROMOTES LIQUID BLOOD FLOW BLOCKS PLATELET ACTIVITY (BLOCKS ADHESION/AGGREGATION; PROSTACYCLIN AND NO) INHIBITS COAGULATION CASCADE (HEPARIN-LIKE MOLECULES INACTIVATE THROMBIN; THROMBOMODULIN MAKE THROMBIN AN ANTICOAGULANT) |
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PRIMARY HEMOSTASIS -ENDOTHELIAL INJURY-
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PLATELET ATTRACTION TO ENDOTHELIAL EXTRACELLULAR MATRIX
PLATELETS ADHERE TO VON WILLEBRAND FACTOR PLATELETS RELEASE THROMBOXANE A2 AGGRAGATION OF PLATELETS |
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PRIMARY HEMOSTASIS -CYTOKINE EXPRESSION-
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TNF AND IL-1
ENDOTHELIAL PRODUCTION OF TISSUE FACTOR ACTIVATES EXTRINSIC CLOTTING SYSTEM |
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PRIMARY HEMOSTASIS -FIBRINOLYTIC INHIBITION-
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PLASMINOGEN ACTIVATOR INHIBITORS (FROM ENDOTHELIUM)
INHIBITS FIBRINOLYSIS (ALLOWS CLOTTING TO CONTINUE) |
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HEMOSTASIS -SECONDARY HEMOSTASIS-
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ACTIVATION OF TISSUE FACTOR (FACTOR III; AMPLIFYING SERIES OF RNXs)
THROMBIN FORMATION THROMBIN CONVERTS SOLUBLE FIBRINOGEN INTO INSOLUBLE FIBRIN FIBRIN ENCASES PLATELETS STABLE HEMOSTATIC PLUG FORMED |
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HEMOSTASIS -THROMBOLYSIS-
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DISSOLUTION OF THE CLOT
TISSUE PLASMINOGEN ACTIVATOR PRODUCED PLASMIN PLASMIN CLEAVES FIBRIN ANTITHROMBIN III (INACTIVATES THROMBIN & FACTOR X) PROTEINS S AND C (DISABLES FACTORS V AND VII) |
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PRIMARY HEMOSTASIS -ANTITHROMBOTIC ACTIVITY-
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FIBRINOLYTIC SYSTEM
ANTITHROMBINS INHIBIT ACTIVITY OF THROMBIN PLASMIN BREAKS DOWN FIBRIN |
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A CLOT IS
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BLOOD WHICH HAS CLOTTED POSTMORTEM OR IN AN EXTRAVASCULAR LOCATION
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THROMBOSIS IS
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FORMATION OF AN ANTEMORTEM BLOOD CLOT (THROMBUS) IN A BLOOD VESSEL OR IN THE HEART
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THROMBOSIS -VIRCHOW’S TRIAD-
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ENDOTHELIAL INJURY
BLOOD FLOW DISTURBANCES HYPERCOAGULBILITY |
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VIRCHOW’S TRIAD -ENDOTHELIAL INJURY-
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DOMINANT INFLUENCE
ATHEROSCLEROSIS, MI… SHEARING EFFECTS OF FLOW COAGULATION FACTORS ELABORATED PLATELET ADHESION, AGGREGATION |
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VIRCHOW’S TRIAD -ABNORMAL BLOOD FLOW-
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TUBULENCE AND STASIS
ATHEROTIC PLAQUES, DAMAGES HEART VALVES… PLATELETS CONTACT ENDOTHELIUM PREVENTS DILUTION OF COAGULATION FACTORS MAY DAMAGE ENDOTHELIUM |
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VIRCHOW’S TRIAD -HYPERCOAGULABILITY-
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LEAST IMPORTANT
MANY 1º AND 2º CAUSES MANAGED WITH ANTICOAGULANT DRUGS |
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THROMBOSIS -LOCATION-
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ANYWHERE IN CARDIOVASCULAR SYSTEM
SITES OF ENDOTHELIAL INJURY OR FLOW TURBULANCE (ARTERIAL THROMBI, CARDIAC THROMBI) SITES OF STASIS (VENOUS THROMBI) |
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THROMBI -COMMON LOCATIONS-
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LEG VEINS (90%)
LEG ARTERIES HEART CHAMBERS ANEURYSMS CORONARY ARTERIES CEREBRAL ARTERIES MESENTERIC ARTERIES |
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THROMBOSIS -MORPHOLOGY-
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LAMINATED STRUCTURE (LINES OF ZAHN, PALE LAYERS OF PLATELETS/FIBRIN, DARK LAYERS OF ERYTHROCYTES)
PROPAGATE: “HEAD” – ENDOTHELIAL ATTACHMENT “TAIL” – EXTENSION INTO LUMEN ARTERIAL – RETROGRADE TO FLOW VENOUS – IN DIRECTION OF FLOW |
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THROMBOSIS PROPOGATION
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“HEAD” – ENDOTHELIAL ATTACHMENT
“TAIL” – EXTENSION INTO LUMEN ARTERIAL – RETROGRADE TO FLOW VENOUS – IN DIRECTION OF FLOW |
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THROMBUS -COMPONENTS-
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ERYTHROCYTES
LEUKOCYTES PLATELETS FIBRIN |
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POSTMORTEM CLOT
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WET & ELASTIC
HOMOGENOUS (“CHICKEN FAT”) NOT ATTACHED |
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ANTEMORTEM THROMBUS
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DRY & FRIABLE
LAMINATED (LINES OF ZAHN) ATTACHED |
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THROMBI CLASSIFICATION CRITERIA
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BY DEGREE OF OCLUSION
BY COLOR AND COMPOSITION |
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THROMBOSIS -CLASSIFICATION-
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MURAL THROMBUS
ARTERIAL THROMBUS VENOUS THROMBUS HEARY VALVE VEGETATIONS |
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MURAL THROMBUS
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NON-OCCLUSIVE
LARGE VESSELS HEART CHAMBERS MAY EMBOLIZE |
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ARTERIAL THROMBUS
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OFTEN OCCLUSIVE
ATHEROSCLEROTIC PLAQUES FRIABLE LINES OF ZAHN PALE IN COLOR (“WHITE” THROMBUS; LOTS OF FIBRIN) MAY CAUSE INFARCTION (MI, STROKE) MAY EMBOLIZE (BRAIN, KIDNEYS, SPLEEN) |
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VENOUS THROMBUS
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PHLEBOTHROMBOSIS
DUE TO STASIS OF BLOOD ALMOST ALWAYS OCCLUSIVE SOFTER THAN ARTERIAL THROMBI LINES OF ZAHN NOT PROMINENT RED IN COLOR (“RED” THROMBUS; LOTS OF ERYTHROCYTES) 90% IN VEINS OF LEGS (POPITEAL, FEMORAL, ILIAC VEINS) ASYMPTOMATIC… PAINFUL CONGESTION AND EDEMA PREDISPOSE TO VARICOSE FORMATION MAY EMBOLIZE (USUALLY TO LUNGS) |
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THROMBOSIS -LEG VEINS-
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MOST COMMON SITE
DUE TO STASIS OF BLOOD (CARDIAC FAILURE; INACTIVITY/IMMOBILIZATION) MAY BECOME INFLAMED (THROMBOPHLEBITIS) MAY PRODUCE HOMAN’S SIGN (PAINFUL DORSIFLECTION) |
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HEART VALVE VEGETATIONS
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INFECTIVE ENDOCARDITIS (AREAS OF MICROBIAL COLONIZATION OR DAMAGE)
ALSO THROMBOTIC ENDOCARDITIS (STERILE, NON-BACTERIAL) MURMUR AND DYSFUNCTION |
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THROMBOSIS -TREATMENT-
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ANTICOAGULANTS
SURGICAL REMOVAL |
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THROMBOSIS -FATE-
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FIBRINOLYSIS (DISSOLVES)
PROPAGATION (GETS LARGER) ORGANIZATION (SCARS… RECANALIZATION) EMBOLIZATION (COMES LOOSE) |
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EMBOLISM IS
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OCCLUSION OF A VESSEL BY IMPACTION OF A FOREIGN MASS (EMBOLUS)
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EMBOLISM -GENERAL INFORMATION-
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SOLID, LIQUID OR GAS
99% DISLODGED THROMBI (THROMBOEMBOLISM) LODGE IN SMALL VESSEL MAY CAUSE INFARCTION |
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EMBOLISM -TYPES-
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THROMBOEMBOLISM
FAT (MARROW) EMBOLISM AMNIOTIC FLUID EMBOLISM AIR EMBOLISM TUMOR EMBOLISM |
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THROMBOEMBOLISM
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THROMBUS COMES LOOSE
VENOUS EMBOLI (95% FROM DEEP CALF VEINS; LODGE IN THE LUNGS) ARTERIAL EMBOLI (MURAL THROMBUS OF LEFT HEART; LODGE IN SPLEEN, KIDNEYS, BRAIN) |
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PULMONARY THROMBOEMBOLISM
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20-25/100,000 HOSPATILIZATIONS
2% FATAL – 200,000/YR IN U.S. 95% FROM DEEP LEG VEINS 60-80% CLINICALLY SILENT OFTEN FATAL |
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PULMONARY THROMBOEMBOLISM
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PULMONARY INFARCTION
PULMONARY HEMORRHAGE PULMONARY HYPERTENSION |
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SADDLE EMBOLUS
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CLINICALLY SILENT
PULMONARY THROMBOEMBOLISM |
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SYSTEMIC THROMBOEMBOLISM
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EMBOLI IN ARTERIAL CIRULATION
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SYSTEMIC THROMBOEMBOLISM
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80% FROM CARDIAC MURAL THROMBI
60% LEFT VENTRICLE 25% LEFT ARTIA 15% VALVULAR VEGETATIONS |
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SYSTEMIC THROMBOEMBOLISM
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WIDE VARIETY OF SITES
75% LOWER EXTREMITIES 10% BRAIN INTESTINES, KIDNEYS, SPLEEN |
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SYSTEMIC THROMBOEMBOLISM
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TISSUE VULNERABILITY TO ISCHEMIA
CALIPER OF OCCLUDED VESSEL COLLATERAL BLOOD SUPPLY USUALLY CAUSES INFARCTION |
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FAT (MARROW) EMBOLISM
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FOLLOWS LONG BONE FRACTURE (90% INCIDENCE; 10% PRODUCE CLINICAL FINDINGS)
FATTY MARROW ENTERS CIRCULATION USUALLY GO TO LUNGS AND/OR BRAIN MULTIPLE SMALL EMBOLI (DEVASTATING COLLECTIVE EFFECT) 10% FATALITY RATE |
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FAT (MARROW) EMBOLISM
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OCCLUSION OF VESSELS
BIOCHEMICAL FROM FFA RELEASE |
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FAT (MARROW) EMBOLISM
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PULMONARY INSUFFICIENCY 1-3 DAYS POST FX
NEUROLOGIC… DELIRIUM… DEATH |
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GAS EMBOLISM
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BUBBLES OBSTRUCT VASCULAR FLOW
OVER 100 mL FOR CLINICAL EFFECT |
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GAS EMBOLISM CAUSES
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OBSTETRIC PROCEDURES
CHEST WALL INJURY DECOMPRESSION SICKNESS |
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GAS EMBOLISM SIGNS AND SYMPTOMS
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ISCHEMIC IN VARIOUS TISSUES
PAINFUL “BENDS” IN SKELETAL MUSCLE/JOINTS “CHOKES” IN LUNGS |
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GAS EMBOLISM TREATMENT
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INCREASE BAROMETRIC PRESSURE
FORCE BUBBLES BACK INTO SOLUTION ALLOW PATIENT TO EXHALE GASSES GRADUALLY REDUCE PRESSURE |
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EMBOLISM -TREATMENT-
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ANTICOAGULANTS
OXYGEN (IF PULMONARY) SURGICAL REMOVAL |
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AMNIOTIC FLUID EMBOLISM
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RARE LABOR COMPLICATION
AMNIOTIC FLUID ENTERS CIRCULATION (TEARS IN PLACENTAL MEMBRANES, TEARS IN UTERIVE VEINS) VISCOUS FLUID EMBOLIZES TO LUNGS ACUTE DYSPNEA, CYANOSIS, SHOCK 20-40% FATAL PULMONARY EDEMA PULMONARY EMBOLI WITH FETAL HAIR, HAIR |
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EMBOLISM -PROGNOSTIC FACTORS-
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SITE OF EMBOLUS
SIZE OF THE VESSEL OCCLUDED NUMBER OF EMBOLI |
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ISCHEMIA IS
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REDUCTION IN BLOOD SUPPLY TO A TISSUE
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INFARCTION IS
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TISSUE NECROSIS RESULTING FROM CIRCULATORY INSUFFICIENCY
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INFARCTION -EPIDEMIOLOGY-
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COMMON CAUSE OF ILLNESS
50% OF DEATHS DUE TO CVD: MYOCARDIAL INFARCTION, CEREBRAL INFARCTION, PULMONARY INFARCTION, BOWEL, EXTREMITIES |
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INFARCTION -CAUSES-
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99% THROMBOTIC OR EMBOLIC
DUE TO ARTERIAL OCCLUSION INFARCTION RARE WITH VENOUS OCCLUSION OPENING OF BY-PASS VASCULAR CHANNELS MAY PREVENT OR LIMIT NECROSIS |
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INFARCTION NATURE OF VASCULAR SUPPLY
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ALTERNATE BLOOD SUPPLY IMPORTANT
ORGANS WITH DUAL SUPPLY DO BETTER “END-ARTERIAL” ORGANS DO WORST |
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INFARCTION RATE OF DEVELOPMENT OF OCCLUSION
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SLOW BETTER THAN RAPID
ALLOWS COLLATERAL VESSELS TO OPEN |
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INFARCTION VULNERABILITY TO HYPOXIA
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NEURONS/MYOCARDIUM MORE SUSCEPTIBLE
FIBROBLASTS LESS SUSCEPTIBLE |
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INFARCTION OXYGEN CONTENT OF BLOOD
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LOW CONTENT FAVORS INFARCTION
HIGH CONTENT RESISTS INFARCTION |
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INFARCTS -CLASSIFICATION-
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BASED ON COLOR
BASED ON SHAPE BASED ON TYPE OF NECROSIS |
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ANEMIC (WHITE) INFARCT
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LITTLE HEMORRHAGE
ARTERIAL OCCLUSIONS SOLID ORGANS |
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HEMORRHAGIC (RED) INFARCT
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CONTAIN HEMORRHAGE
VENOUS OCCLUSION LOOSE TISSUES (LUNGS) TISSUES WITH DUAL CIRCULATION TISSUE PREVIOUSLY CONGESTED OCCURS WHEN FLOW RE-ESTABLISHED |
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INFARCTS -SHAPE-
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MOST WEDGE-SHAPED (OCCLUDED VESSEL AT APEX; BASE AT PERIPHERY OF ORGAN)
SOME IRREGULAR (ORGANS WITH COLLATERAL CIRCULATION; BRAIN, HEART) |
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INFARCTION -TYPE OF NECROSIS-
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COAGULATIVE NECROSIS (DOMINANT PATTERN; WELL-DEFINED MARGINS)
SEPTIC INFARCTION (BACTERIAL VEGETATIONS ON HEART VALVES; INFARCT CONVERTED INTO ABSCESS) |
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INFARCTS -FACTORS DETERMINING DAMAGE-
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COLLATERAL CIRCULATION
RATE OF OCCLUSION TISSUE VULNERABILITY BLOOD OXYGEN LEVEL |
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SHOCK IS
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A CLINICAL STATE OF CIRCULATORY FAILURE RESULTING IN TISSUE HYPOXIA
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SHOCK -PATHOGENESIS-
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CIRCULATORY FAILURE->
INADEQUATE O2 SUPPLY-> ACIDOSIS-> SHOCK-> COMA-> DEATH |
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SHOCK -CLASSIFICATION-
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HYPOVOLEMIC: MASSIVE FLUID LOSS, TRAUMA, HEMORRHAGE, BURNS
CARDIOGENIC: HEART FAILURE, MYOCARDIAL INFARCTION SEPTIC (ENDOTOXIC) |
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CARDIOGENIC SHOCK
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FAILURE OF THE CARDIAC PUMP
MYOCARDIAL INFARCTION, ARRHYTHMIAS INADEQUATE TISSUE PERFUSION |
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HYPOVOLEMIC SHOCK
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LOSS OF BLOOD OR PLASMA
HEMORRHAGE, BURNS, TRAUMA INADEQUATE PERFUSION |
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SEPTIC SHOCK
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BACTERIAL ENDOTOXINS->
RELEASE OF CYTOKINES-> VASCULAR DILATATION INCREASED PERMEABILITY-> PERIPHERAL POOLING-> DIC |
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SEPTIC (ENDOTOXIC) SHOCK
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OVERWHELMING INFECTIONS (70% GRAM NEGATIVE BACILLI; PRODUCING ENDOTOXIN)
PERIPHERAL POOLING OF BLOOD (LPS ATTACHES TO INF CELLS; CYTOKINASE PRODUCTION) INADEQUATE PERFUSION #1 CAUSE OF DEATH IN INTENSIVE CARE UNITS |
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SHOCK -CLINICAL STAGES-
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NON-PROGRESSIVE STAGE
PROGRESSIVE STAGE IRREVERSIBLE STAGE |
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SHOCK NON-PROGRESSIVE STAGE
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REFLEX COMPENSATORY MECHANISMS ACTIVATED
NEUROHUMEROL MECHANISMS ORGAN PERFUSION MAINTAINED |
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SHOCK NON-PROGRESSIVE STAGE
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BARORECPTIVE REFLEXES
CATECHOLAMINE RELEASE RENIN-ANGIOTENSIN ACTIVATION ANTIDIURETIC HORMONE RELEASE SYMPATHETIC STIMULATION |
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SHOCK NON-PROGRESSIVE STAGE ORGAN PERFUSION MAINTAINED
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TACHYCARDIA
PERIPHERAL VASOCONSTRICTION RENAL FLUID CONSERVATION |
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SHOCK PROGRESSIVE STAGE
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TISSUE HYPOPERFUSION
WIDESPREAD TISSUE HYPOXIA AEROBIC RESPIRATION REPLACED WITH ANAEROBIC GLYCOLYSIS LACTIC ACIDOSIS (VASOMOTOR RESPONSE REDUCED; PERIPHERAL POOLING OF BLOOD; LOWER CARDIAC OUTPUT) DIC DEVELOPS…HEMORRHAGE |
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SHOCK IRREVERSIBLE STAGE
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SEVERE CELLULAR/TISSUE INJURY
ORGANS FAIL SURVIVAL NOT POSSIBLE |
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SHOCK -MORPHOLOGY-
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FIBRIN THROMBI ALL OVER
KIDNEYS (ACUTE TUBULAR NECROSIS; OLIGURIA, ANURIA) ADRENALS (CORTICAL LIPID DEPLETION) GASTROINTESTINAL TRACT (MUSOCAL HEMORRHAGE/NECROSIS) LUNGS (DIFFUSE ALVEOLAR DAMAGE) |
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SHOCK -SYMPTOMS-
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DEPENDS ON CAUSE
HYPOTENSION WEAK, RAPID PULSE TACHYCARDIA COOL, CLAMMY, CYANOTIC SKIN (EXCEPT SEPTIC SHOCK) CARDIAC, CEREBRAL, PULMONARY CHANGES |
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SHOCK -PROGNOSIS-
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HYPOVOLEMIC SHOCK:
80-90% SURVIVE WITH TX; IF OTHERWISE HEALTHY CARDIOGENIC AND SEPTIC SHOCK: BAD PROGNOSIS |
