1 cardiac

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Unformatted text preview: Cardiovascular Physiology •  Cardiovascular disease is #1 cause of death •  Major underlying cause is ischemia due to: atherosclerosis (plaquing) white thrombus red thrombus artery spasm •  It ain't what you don't know that gets you into trouble. It's what you know for sure that just ain't so. Mark Twain Symptoms of myocardial infarction are present after 70% of occlusion Connective Tissue •  Ordinary –  Loose connective tissue (areolar tissue) –  Dense ordinary connective tissue •  Regular vs. Irregular Events in Hemostasis •  Hemostasis-prevention of blood loss •  Mechanisms –  vascular spasm –  formation of a platelet plug –  blood coagulation –  fibrous tissue growth to seal Platlets in a clotting cascade Vasoconstriction first •  Special –  Adipose tissue (fat) –  Blood cells –  Blood cell forming tissue •  Myeloid or lymphatic tissue –  Cartilage –  Bone Hemostasis •  Vascular Constriction-associated w/ trauma –  neural reflexes •  SNS induced constriction from pain Platelet Plug Platelets function as whole cells but cannot divide Platelets contain: actin & myosin enzymes & calcium ADP & ATP Thromboxane A2 serotonin growth factor –  local myogenic spasm •  responsible for most of the constriction –  local humoral factors •  thromboxane A2 from platelets •  Spasm ∝ trauma Sympathetics are activated to constrict 1 Platelet Cell Membrane Contains: Glycoproteins that avoid the normal endothelium but adhere to damaged area Phospholipids containing platelet factor 3 a.k.a. thromboplastin-initiates clotting Initiates platlet cascade for clotting Mechanism of Platelet Activation When platelets contact damaged area they 1) swell 2) irregular form w/ irradiating processes protruding from surface 3) contractile proteins contract causing granule release 4) secrete ADP, Thromboxane A2 & serotonin Thromboxane A2 1) Vasoconstrictor Potent Platelets •  Important in minute ruptures –  lack of platelets associated with small hemorrhagic areas under skin and throughout internal tissues –  half-life of 8-12 days •  eliminated primarily by macrophage action –  (greater than 1/2 of all macrophages in spleen) 2) Potentiates the release of granule contents (not essential for release to occur) (but it intensifies the release) •  150,000-300,000 per µl Plasma Role of Endothelium •  Chelators •  Prevents platelet aggregation •  produces PGI2 (prostacyclin)–  vasodilator –  stimulates platelet adenyl cyclase which suppresses release of granules –  limits platelet extension Anticoagulants –  citrate & oxalate •  tye up calcium No Ca = no contractile protiens = no release of granules •  Heparin –  enhances the action of antithrombin III •  principal inhibitor of thrombin Cant convert fibrinogen to fibrin •  Dicumarol (Warfarin) –  inhibition of vitamin K dependent factors produced by the liver •  II, VII, IX, X Factors •  produces factor VIII (clotting) Platlet aggregation could reel off vessels Stimulating adenylcyclase surpresses activation of platlets 2 Enzymes required fomr the reactions Prostaglandin synthesis •  •  •  •  •  Phospholipid to Arachidonic acid- Lipase Arachidonic acid to PGG2-PGH2- FA cyclo PGG2-PGH2 to Thromb. A2- Thromb. synt PGG2-PGH2 to PGI2- Prostacyclin synt. Aspirin and Ibuprofen block Fatty acid cyclooxygenase ~ blocks prostaglandin production ~ prevents blockage of vessels Blood Coagulation-Thrombosis •  Extrinsic mechanism-initiated by chemical factors released by damaged tissues •  Intrinsic mechanism-requires only comp...
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This note was uploaded on 05/03/2011 for the course PHYS 339 taught by Professor Free during the Spring '11 term at Palmer Chiropractic.

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