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Hemodynamics Disorders, Hemodynamic Disorders EMBOLISM -99% thromboembolism ->infaction of distal tissue Amniotic Fluid Embolism 1/50K deliveries, 80% mort Tear in placental memb, uterine vv rupture-> -amniotic fluid and contents into mom -therefore, find epith squamous cells in mom's lungs -sudden severe dypsnea, cyanosis, hypoTN shock ->seizures, coma if surviving initial crisis->pulm edema, DIC, Hemodynamic Disorders HEMOSTASIS & THROMBOSIS Hemostasis on Clotting Map, Hemodynamic Disorders EMBOLISM -99% thromboembolism ->infaction of distal tissue Systemic Thromboembolism -emboli w/in aa circ. -80% from cardiac mural thrombi -most from LV, some from LA -small amt of paradoxical emb. -embolism esp in lower extremities, brain ->usually infarction -can be saved due to collaterals, Hemodynamic Disorders EMBOLISM -99% thromboembolism ->infaction of distal tissue Fat Embolism -usually after long bone Fx or soft tissue trauma/burns -fat released from marrow or adipose->vasc -occurs in 90% pts w/ severe trauma but Sx in % -cause dz due to obstruction, aggregation, toxic injury Fat Embolism Syndrome-1-3 d post-injury -sudden onset of tachypnea, dyspnea, tachycardia -neuro sx-restlessness, irritability->delirium, coma -diffuse petechiae (no TCP) in 20-50% pts -TCP-plts adhere to fat, removed from circ -anemia via RBC aggregation/hemolysis -FATAL in 10% of full blown cases, Hemodynamic Disorders HEMOSTASIS & THROMBOSIS Thrombosis MORPHOLOGY- Occur anywhere -Cardiac, aa. usually due to endoth injury/turbulence-OBSTRUCTION -grows retrograde -vv. due to stasis, grow in direction of flow->EMBOLIZE -Characteristed firm attachment to point of origin -Propagating tail prone to breaking(esp. vv)->embolus -Lines of Zahn in heart and aorta=pale plt/fibrin; RBCs Mural thrombi-adhere to wall in heart/aorta -heart due to stasis from abnl contraction (MI, arrhyth) -aorta due to ulcerated plaque/aneurysm Arterial Thrombi-usually occlusive-in coronary, cerebral, fem aa. -usually superimposed on plaque -embolisms go to brain, kidney, spleen Venous/phlebothrombosis-occlusive-red/stasis thrombi -90% in legs (DVTs at or above knee more serious) SVT in saphenous -both cause local pain, distal edema -50% of DVTs asymptomatic->embolize->death Heart valves-bac/fungal infx can make foothold infx, nonbacterial thrombotic, and verrucous endocarditis -verrucous (Libman-Sacks) due to immune complezes (SLE) THROMBUS FATE-days to wks 1. Propagation via accum of plts, fibrin->obstruct vessel 2. Embolization-dislodged thrombi 3. Dissolution-removed via fibrinolytic activity(older throm are tougher) 4. Organization(inflamm, fibrosis)/Recanalization(new flow) -vascularizes thrombus, then enzs released from trapped WBCS ->degrades plaque, but ideal for bacterial growth (mycotic aneurysm), Hemodynamic Disorders EMBOLISM -99% thromboembolism ->infaction of distal tissue Pulmonary Thromboembolism -95% from DVT Saddle Embolus at PA bifurc Paradoxical Embolus-pass thru ASD or VSD->left side->systemic TE -60-80% are small, silent -Sudden death, cor pulmonale, CV collapse -when ᡴ% fo pulm circ obstructed ->pulm hemorrhage, not infarction b/c dual blood flow -multiple emboli over time->pulm HTN, right heart failure, Hemodynamic Disorders HYPEREMIA & CONGESTION -both=local increased blood in tissue Congestion-PASSIVE -impaired outflow Systemic-cardiac failure Local-isolated vv. obstruction ->blue-red tissue color (deox Hgb) -Commonly occurs w/ edema Chronic Passive Congestion ->blood stasis->chronic hypoxia ->parenchymal dmg, scarring ->small foci of hemorrhage -RBCs phagocytized ->clusters of hemosiderin-laden macs, Hemodynamic Disorders INFARCTION ~99% from embolism/thrombus Some via twisting of vessels, vasospasm Vv thrombosis usually causes congestion, not infarct Histology-ischemic coagulative necrosis- -no change in appearance if recent -inflam edges hours after insult, then degradation ->repair starting at edges, mostly scar tissue -in brain, always LIQUEFACTIVE, however Septic infarcts from vegetation of heart valve or seeding of necrotic tissue->ABSCESS -greater inflam response, Hemodynamic Disorders EMBOLISM -99% thromboembolism ->infaction of distal tissue Air Embolism cc to have Sx -air enters circ via OB procedures, chest wall injury -air coalesces as physical obstructions Decompression sickness-N2 gas bubbles out of sol'n on ascent too quickly -the BENDS-bubbles in sk mm., joints ->focal ischemia in brain, heart Tx-barometric chamber then slow decompression Caisson Dz-chronic form of decompression sickness -ischemic necrosis in head of femur, tibia, humeri, Hemodynamic Disorders INFARCTION Factors influencing development 1. Nature of vasc supply -lungs/liver vs spleen/kidney 2. Rate of occlusion development -slow-time to develop collaterals 3. Vulnerability of tissue to hypoxia -neurons, myocardium quite vuln 4. Blood oxygen content -if ventilation low, infarction more likely