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248 Cards in this Set
- Front
- Back
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Cardiovascular system consists of... |
heart, blood vessels, and blood. contains nervous tissues, muscles tissue, connective tissue,and epithelial |
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functions of cardiovascular system |
transport hormones through the blood, maintain homeostasis, protection |
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functions of blood |
transport dissolved gasses nutrients and hormones. distribute nutrients, regulate pH an dion composition of interstitial fluid, restrict fluid loss at injury site (thrombocutes) defend against toxins, stabilize body temp. -38 C, avg pH 7.4 |
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cardiovascular transport function |
-carries nutrients from digestive system to cells throughout body. -carries waste products from cells of body to kidneys -carried hormones from endocrine to target cells -carries resp gasses: O2 from lungs to cells and CO2 from cells to lungs |
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how does cardiovascular system maintain homeostasis? |
-participates in maintenance of body temp by absorbing and redistributing heat, body fluids and pH levels and electrolyte concentrations. |
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how does cardiovascular system protect? |
-protects body from bacteria and other pathogens through immune system (leukocytes) -prevents excess fluid loss as injury sites through clotting |
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blood is ____% of body weight |
7% |
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female versus male volume of blood? |
males have 5-6 liters while females have 4-5 liters of blood. pH is between 7.35 and 7.45, slightly alkaline.
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Acidosis |
can be common during exercise, blood become too acidic, CO2 builds up, loses extra H+ ions in urine. |
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alkalosis |
anythign above 7.45, blood gets more basic every time you eat a meal |
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blood is ___X as viscous as ___ |
5X as viscous as water |
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what is fluid connective tissue |
cells and cell frgaments surrounded in liquid extracellular matrix |
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whole blood composition |
55% plasma, 45% formed elements. plasma is 92% water, 7% plasma proteins (albumins, fibrinogens, and globulins) and 1% ions, nutrients, gases, hormones, and waste. |
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albumins |
make up 60% of plasma proteins responsible for viscosity and osmotic pressure of blood. also responsible for transporting fatty acids, thyroid hormones, and some steroid hormones. |
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globulins |
35% of plasma proteins includes immunoglobulins-antibodies-that attack foreign proteins and pathogens binds ions and hormones, cholesterol, and other proteins that move cholesterol through blood stream |
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fibrinogens |
make up approx 5% and includes clotting proteins serum=plasma that has all of the clotting proteins removed. if clotting does not happen, fibrinogen converts to fibrin leaving behind serum which also removes Ca ions |
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which plasma protein would be elevated during viral infection? |
globulins because they produce immunoglobulins whihc as antibodies to help the body fight against infection. |
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where are plasma proteins synthesized? |
liver synthesizes and released more than 90% of PP liver disorders can alter composition and functional properties of blood. |
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define hematocrit |
the percentage of blood sample that consists of the formed elements determined by centrifuging blood sample so all formed elements come out of suspension -low hematocrit can account for fatigue, anemia, tired, etc. not making enough ATP |
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hemopoiesis |
the production of formed elements in red bone marrow hemocytoblast: stem cell |
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RBC's |
-slightly less than 1/3 the blood volume, -99.9% of the formed elements -4-6 million RBC's per microliter of blood. -destroyed and replaced constantly at approx same rate -travel 700 miles in 120 days -destroyed by phagocytosis in liver and spleen -liver takes over for spleen to break down RBC's if spleen has been removed |
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Structure of RBC |
-7.8um -no nucleus when mature and few other organelles -densely packed with hemoglobin -biconcave shape allows surface volume, stacks (rouleaux) to pass through blood vessels easier, bend and flex when entering capillaries, -short life span, 120 days bc lacking organelles. receive energy though anaerobic metabolism of glucose. |
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hemoglobin |
-account for 95% of proteins in RBC's -formed from 4 subunits -red pigment that gives blood color -each subunit contains one molecule of heme (the pigment molecule containing ionized iron which can reversibly bind an oxygen molecule-very weak -responsible for cells ability to transport oxygen and CO2 |
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heme |
colors lots of things, blood, vomit, feces, etc. |
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When O2 is high in lungs... |
heme forms complex with O2 oxyhemoglobin-bright red color |
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when O2 is low in tissues |
O2 dissociates from heme iron deoxyhemoglobin- darker red blue color |
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What does carbon monoxide do to heme? |
CO irreversibly binds to heme iron, preventing O2 binding. |
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Deoxyhemoglobin |
hemoglobin molecule not bound to O2 |
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Thalassemia |
-abnormal hemoglobin inherited disorder -inability to produce sufficient alpha or beta chains of hemoglobim -common in mediterranean descent -rate of RBC prod is slower. -mature RBC are fragile and short lived. |
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Sickle Cell anemia |
-inherited chain -beta chain of hemoglobin is abnormal -in low O2, hemoglobin molecules interacted causing cells to become stiff and curved -sickled cells are not able to make it through capillary beds, can block beds and be painful. deadly
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Turnover of Hemoglobin: |
Globulin protein: can be disassembled into amino acids and re-used Heme pigments: converted to biliverdin, then converted to bilirubin and excrete in urine and feces, bile Heme iron: is recycled, stored in phagocytes, or transported throughout blood bound to transferrin |
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erythropoiesis |
the formation of RBC's, occurs only in red bone marrow or myeloid tissue (located in vertebrae, sternum, ribs, skull, scapulae, pelvis, etc) |
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Stages of RBC maturation |
Proerythroblasts-->various erythroblast stages-->sheds nucleus and becomes reticulocyte (immature RBC eners blood stream and has no nucleus, eventually becomes mature.) -reticulocyte still contains RNA. after2 days in marrow retic enters blood stream. after 24 hours in circulation they become mature (approx 7 days total) |
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amino acids, iron and vitamins.... |
-are needed in adequate supply to regulate erythropoiesis -B6 and B12 and folic acid needed for protein synthesis (used to cause pernicious anemia but is not common anymore.) -cant make hemoglobin if protein deficient |
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erythropoiesis stimulated... |
directly by erythropoietin and indirectly by several hormones (thyroxine, androgens, and growth hormones. |
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thyroxin |
increases metabolic rate and acts on mitochondria when ATP is produced |
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Androgens: |
testosterone, growth hormone. |
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erythropoietin |
stimulating hormone released by kidneys in response to low O2, stimulates erythroblast stimulation, and accelerated Hb synthesis and RBC maturation. |
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Hemolytic |
breaking down RBC's faster than normal |
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Pernicious |
B12 deficiency |
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aplastic |
mutation from exposure to radiation |
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iron deficiency |
very common, low iron in diet |
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hemorrhagic |
rare, occurs in short turn situations with internal hemorrhaging |
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polycythemia |
makes too many RBC's |
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hematuria |
blood in urine |
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hemogloinuria |
hemoglobin in urine |
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juandice |
bilirubin build up in body and tissues, appearing yellow |
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dehydration |
would cause increase in hematocrit due to reduction in plasma volume -formed elements=hematocrit. -hematocrit usually lower in females 40-43, men is 45-48 |
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each RBC contains 280 million hemoglobin molecules... |
so one hb molecule contains 4 heme units, each RBC can potentially carry more than a billion molecules of O2 |
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structure of hemoglobin allows 98.5 percent of oxygen carried by blood is bound to hb molecules inside RBC's |
structure of hemoglobin |
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antigens |
-substances that can trigger a protective defense mechanism called an immune response -most antigens are proteins |
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surface antigens |
-contained in plasma membrane, , the immune system recognizes as normal. immune system ignores these rather than attacking. -integral membrane glycoproteins or glycolipids whose characteristics are genetically determined. |
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blood type |
determined by the presence or absence of certain antigens in RBC plasma membranes. |
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Type A blood |
surface antigen A only |
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Type B blood |
surface antigen B only, |
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type AB blood |
both A and B surface antigens |
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Type O blood |
neither A or B antigens (agglutinogens) |
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Rh + or Rh- |
positive means presence of Rh surface antigen, negative means absence of Rh antigen. |
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Plasma contains... |
antibodies-agglutinins, opposite antigens for whatever surface antigens you have. Type A blood has Anti-B antibodies in their plasma that agglutinate or clump when attacking B antigens on |
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hemolysis |
attack and destruction of rbc with wrong antigens |
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Rh negative individual... |
does not have Rh+ antibodies in plasma. present only if sensitized by accident during transfusion or pregnancy with rh- mother and rh + fetus |
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•HemolyticDisease of the Newborn can occur in + fetus carried by - mother |
rh factor |
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WBC's |
-less than .1% formed elements -have nuclei and other organelles -more abundant in loose and dens connective tissues of body, use blood to travel from organ to organ and rapidly to areas of infection |
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characteristics of WBC's |
-migrate out of blood stream, margination adhere to blood vessel walls. squeeze between adjacent endothelial cells and enter surrounding tissue (emigration) -capable of amoeboid movement or gliding motion made possible by cytoplasm. -attracted to specific chemical stimuli (positive chemotaxis) -capable of phagocytosis |
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most wbcs are... |
neutrophils. neu-numerous |
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specific defenses |
t cells and b cells |
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Neutrophils |
50-70% of circulating WBC polymorph-2-5 heads, segmented nucleus short life span of 10 hours phagocytic- engluf pathogens or debris in tissue |
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eosinophils |
2-4% circulating increase in number during allergic reactions and parasitic infection phagocytic-engluf antibody labeled materials and reduce inflammation |
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monocytes |
2-8% circulating migrate out of blood vessels and become macrophages macrophages are aggressive phagocytes that attempt to engulf items even larger than self. -release chem that attracts other phagocytic cells, and draws fibroblasts to region to begin producing scar tissue |
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basophil |
less than 1% of circulating WBC migrate to damaged tissue and release histamine and heparin promotes inflammation |
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Lymphocytes |
20-30% circulating provide defense against pathogens or toxins T-cells: cell mediated immunity-specific defense mechanism for invading foreign cells B cells: humoral immunity thaty involves production of antibodies NK cells: natural killer cells destroy abnormal cells, sometimes in preventing cancer |
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Leukopenia |
decreased number of WBCS |
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Leukocytosis |
Increased number of WBC's -extreme leukocytosis generally indicates presence of leukemia-cancer of the WBC's |
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hemocytoblasts |
produce WBC's |
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Eosinophils,basophils, neutrophils and monocytes are produced in.... |
bone marrow by myeloid stem cells |
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lymphocytes |
produced by lymphoid stem cells in red bone marrow. many lymphoid stem cells migrate from red bone marrow to peripheral lympthatic tissues like the thymus, lymph nodes, and spleen. |
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thrombocytopenia |
low number of platelets |
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thrombocytosis |
high number of platelets |
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megakaryocytes |
pieces of cell pinch off as platelets occurs in red bone marrow platelets are then released into circulating blood |
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platelet function |
-release chemicals important to clotting process, enzymes and other factors -forming temporary patch in walls of damaged cells -reducing size of break in the vessel wallby using platelet filaments |
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reduced blood flow to the kidneys (blockage in the kidneys) triggers... |
erythropoeitin which stimulates an increase in RBC formation |
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someone who is producing large amounts of antibodies to combat a virus would have a lot of... |
Lymphocytes, bc B cells produce circulating antibodies |
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histamine |
dilates blood vessels |
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heparin |
prevents blood clotting |
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4 characteristics of WBC's |
1. emigration (squeezing between cells and capillary walls 2. amoeboid movement-gliding movement that transports the cell 3. positive chemotaxis-attraction to specific chemical stimuli 4.phagocytosis- engulfing particles for neut, eos, and mono |
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T-cells B cells NK cells |
-cell mediated immunity-specific defense mechanism for invading foreign cells -humoral immunity that involves production of antibodies -natural killer cells destroy abnormal cells, sometimes in preventing cancer. immune surveillance |
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hemostasis |
the stopping of bleeding, halts blood loss through the walls of damaged vessels. also establishes framework for tissue repair |
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Three phases of hemostasis |
vascular phase platelet phase coagulation phase |
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Vascular phase |
-contraction in smooth muscle fibers of the vessel wall called vascular spasm. decreases diameter of vessel at injury site -last about 30 minutes -endothelium releases chemical factors and hormones to trigger clotting -endothelium plasma membrane becomes sticky to prevent blood flow along damaged vessel and help platelets attach as platelet phase begins |
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Platelet phase |
-starting marked by attachments of platelets to sticky endothelial surfaces and to exposed collagen fibers -called platelet adhesion -as more platelets stick it is called platelet aggregation -during platelet activation change shape, actin starts contracting, release factors stimulating aggregation and vascular spasm, releases clotting factors and calcium ions |
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coagulation phase |
-complex sequence of steps requiring Ca2+ and eleven or more proteins (clotting factors) -triggering initiates a positive feedback loop chain reaction. -several clotting factors synthesized in liver and always present in blood -tissue damage and platelet activation releases triggering factors |
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coagulation phase continued |
-chain rxn leads to conversion of prothrombin to thrombin -thrombin causes the clotting of blood by converting fibrinogen to fibrin |
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prothrombin |
–inactiveenzyme made in liver, always present in plasma. converted to thrombin during coagulation |
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Fibrinogen |
–solubleprotein made in liver, always present in plasma |
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Fibrin |
insolublestrands of protein, form clot, trapping platelets and RBC’s |
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clot retraction |
-pulls town edges of vessel closer together -reduces risidual bleeding and stabilizes injury site -reduces size of damaged area |
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fibrinolysis |
clot gradually dissolves, this process begins when 2 enzymes activate plasminogen. |
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plasminogen |
isconverted to plasmin (by thrombin) Plasminogen- inactive enzyme made in liver, always present in plasma |
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Plasmin |
an active enzyme that breaks down fibrin strands • |
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unusually low megakaryocytes means what? |
would interfere with bloods ability to clot properly bc fewer megakaryocytes would produce fewer platelets |
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no fat diet= |
no fat means vitamin k is not being absorbed. without vitamin k, you would have decreased production of several clotting factors -most notably prothrombin |
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activation of factor XII |
initiates the intrinsic pathway |
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severalanti-coagulants – enzymes that inhibit clotting by inhibiting one or more clotting factors |
•Antithrombin III•Thrombomodulin•Heparin(accelerates activation of Antithrombin III) |
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•Drugsthat depress the clotting response |
–heparin–Coumadin(warfarin)–aspirin |
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•Drugsthat dissolve existing clots |
–Tissueplasminogen activator (t-PA)–Streptokinaseand urokinase |
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Coagulationphase requires |
•Ca+2 and Vitamin K –Lowplasma concentrations of Ca+2impairs blood clotting–VitaminK deficiency leads to bleeding disorders - needed in liver for synthesis offour of the clotting factors •Intestinalbacteriaproduce vitamin K •Fatsoluble vitamin K requires dietary fat for absorption |
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•Hemophilia– inherited, sex linked |
–Inadequateproduction of clotting factor VIII –Excessivebleeding, treated with transfusion of clotting factors –1in 10,000 births |
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•VonWillebranddisease |
–Abnormalproduction of vWFprotein that binds to factor VIII –Symptomsvary , usually not as severe as hemophilia |
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•Embolus |
–Ablood clot circulating inblood system–Embolism– embolus becomes stuck and blocks a blood vessel |
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Thrombus |
–Bloodclot attached toblood vessel wall–Enlargingthrombus can block blood vessel or pieces can break off becoming embolus |
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Infarct |
–tissuedeath due to circulatory interruption (stroke, heart attack, pulmonaryembolism) |
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Atria |
•thinwalled chambers–receiveblood from the veins and pump blood through valves to the ventricles |
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Ventricles |
•thickwalled chambers–receiveblood from atria and pump blood through valves into arteries–leftventricle is more muscular than right side – needs to generate more force topump blood through systemic circuit |
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•Atrioventricularvalves: |
–Arein open position when atria and ventricles are relaxed–Are open when atria are contracting–Are forcedCLOSED when ventricles contract to prevent backflow of blood fromventricles to atria |
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Semilunarvalves |
–Arein closed position when atria and ventricles are relaxed, and when atriacontract–Areforced open whenventricles contract enough to raise pressure higher than blood pressure in thearteries –Closeagain when whenventricles stop contracting |
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ValvularDisorders |
AorticValve is location of the majority of all valvular disorders •Bicuspid(Mitral) Valve •MitralValve Prolapse •PulmonaryValve and Tricuspid Valve (very rare) |
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serous membrane covering outer surface of heart |
visceral pericardium |
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simple squamous epithelium covering heart valves is the |
endocardium |
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the cardiac skeleton of the heart does.... |
physciallly isolates muscle fibers of atria from the ventricles, and it maintains normal shape of the heart |
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blood flow of the heart depends on which 2 things |
1. opening and closing of the 4 valves 2. contraction of the myocardum (atria and ventricles) |
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Myocardialcells (cardiac muscle cells) |
•Small •Singlenucleus •Abundantmitochondria •Veryextensive blood supply •Interconnectedby intercalated discs –gap junctions provide electrical interconnection –desmosomes provide structural connection |
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why do cardiac muscle cells have so many mitochondria? |
Cardiacmuscles need a lot of mitochondria because they continuously need ATP because they are always contracting. |
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2 types of cardiac muscle cells |
1.Contractilemyocardial cells 2.Myocardial cells of conducting system -these work together to produce heartbeat. -The conducting system acts likenervous tissue, but its not. |
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Conducting system |
•Consistsof specialized, non-contractile, cardiac muscle cells –Nodalmyocardial cells (pacemakers) produce spontaneous action potentials –Conductingmyocardial cells propagate the electrical signal (action potential) rapidlythrough out the mass of heart muscle cells (conducting cells pass action potential extremely quickly.) |
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•Sinoatrial(SA)node |
–Locatedin wall of right atrium–Initiatesaction potential that starts the cardiac contraction cycle |
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•Atrioventricular(AV)node |
–Locatedat junction between atria and ventricle–Conductselectrical signal acrossatrial-ventricular septum |
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•Atrialconducting cells |
–Internodalpathways–Rapidlyconduct action potential from SA node to atrial muscle cells and to AV node |
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•Ventricularconducting cells |
–Rapidlyconduct action potential from AV node to ventricle muscle cells–AVbundle (bundle of His), Bundle branches, Purkinje fibers |
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•Actionpotential |
–Rapiddepolarizationcaused by opening of voltage gated sodium ionchannels–A plateau depolarized phase caused by opening ofslow acting voltage gated calcium ion channels–Repolarizationcaused by opening of potassium ion channels |
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calcium and myocardial contraction |
•Calciumions bind to troponin-tropomyosincomplex causing it to shift position–Ca2+ enters the cell membranes during the plateau phase •affectedby interstitial Ca2+ levels–AdditionalCa2+ is released from reserves in thesarcoplasmic reticulum |
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Acalcium channel blocking drug |
a)Shoulddecrease the force of cardiac muscle contractions |
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Bradycardia |
–slower thannormal |
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Tachycardia |
faster thannormal |
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•Conductiondeficits |
–AV nodecan take over if SA node is lost–Ectopicpacemaker – an area other than SA or AV node is generating action potentialsthat initiate contractions |
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•Arrhythmias |
–Abnormalpatterns ofcardiac electrical activity–Clinicallyimportant if pumping efficiency of heart is reduced–Atrialarrhythmias not as serious as ventricular arrhythmias |
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Pwave |
electricaldepolarization spreading from SA node through atrial musclecells |
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QRScomplex |
–depolarizationspreading from AV bundles and Purkinje fibers through ventriclemusclecells -rise in QRS could be due to enlarged heart, larger than normal amount of electrical activity |
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Twave |
–repolarization ofventricle muscle cells |
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Auscultation |
•listeningto heart sound via stethoscope |
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S1 – “lubb” |
closingof the AVvalves |
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S2 – “dupp" |
–closingof the semilunarvalves |
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•Twofaint heart sounds |
–S3 – blood flowing into the ventricles –S4 – associated with atrial contraction |
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CardiacCycle |
1.Cardiac contraction = heart beat 1.Atria contract, push remaining blood into ventricle,then atria relax 2.Ventricles contract, push blood into arteries,then ventricles relax atria systole atria diastole, ventricular systole ventricular diastole |
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1.Cardiac relaxation |
Bothatria and ventricles are in relaxed state until next heart beat starts |
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Systole |
•contraction –Atrialsystole pushes blood into ventricles –Ventricularsystole pushes blood into arteries |
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Diastole |
•relaxation –Duringdiastole, atria and ventricles fill with blood |
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Normalheart rate |
•75beats per minute–Eachcardiac cycle is 0.8 seconds (60 sec/75) or 800 milliseconds |
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• Asheart rate increases, all the phases of the cardiac cycle shorten |
–120bpm = 0.5 seconds = 500 milliseconds–greatestreduction is length of time spent in diastole |
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(EDV) |
•end-diastolicvolume (EDV) ofblood in the ventricles |
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•Atstart of cardiac cycle, atria and ventricles have blood received duringdiastole-–Ventriclesare ~70% filled |
•Atrialsystole pushes blood into the ventricle, filling ventricles to 100% |
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•Ventricularsystole occurs.... |
by building up pressure on blood until semilunar valves open |
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•Ventricularejection occurs... |
by pushing blood into arteries |
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strokevolume |
70-80milliliters ejected |
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ejection fraction |
60%ejected |
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–end-systolic volume (ESV ) |
40%remains in ventricle |
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automaticity |
ability of cardiac muscle tissue to contract without neural or hormonal stimulation |
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cardiac pacemaker/natural pacemaker |
SA node |
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Without SA node... |
heart would still function, AV node would take over and would just beat slower |
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why must impulse be delayed at AV node before passing to ventricles? |
because if it didnt, ventricles would start contracting immediately before atria were done contracting |
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trace pathway of electrical impulse thru conducting system of heart |
SA node, AV node, AV bundle, right and left bundle branches, Purkinje fibers into mass of ventricular muscle tissue |
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cardiac output is equal to... |
product of heart rate and stroke volume. the amount of blood pumped by left vent in 1 minute. |
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during diastole... |
a chamber of the heart relaxes and fills with blood |
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during cardiac cycle, amount of blood ejected from left ventricle when semilunar valve opens is... |
stroke volume. volume of blood ejected in single contraction |
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how do conducting system cells differ from contractile cells of the heart? |
contractile cells do not normally exhibit automaticity |
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what 3 factors regulate stroke volume? |
1. preload-stretch on heart before it contracts 2. contractility- forcefulness of contraction of individual ventricular muscle fibers 3. afterload- pressure that must exceed before blood can be ejected from ventricles. |
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refractory period of cardiac muscle or skeletal muscle is longer? |
Cardiac |
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difference between SA and AV node? |
SA node is pacemaker fo heart, AV node slows the impulse that signals contraction |
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sympathetic activation on the heart |
increases HR and force of contractions |
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parasympathetic stim on heart |
decreases HR and force of contractions |
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•Cardiodynamics |
•movementsand forces generated during cardiac contractions |
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•amountof blood in each ventricle at the of ventricular diastole (end of relaxing) |
•End-diastolicVolume (EDV) |
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•amountof blood remaining ineach ventricle at the end of ventricular systole |
•End-systolicVolume (ESV) |
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•EDV-ESV=SV |
•Volumeof blood before contraction-volume of blood after contraction= volume ejectedduring one contraction. |
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–Amountof blood pumped out of each ventricle during a single beat-volume of bloodejected during one contraction |
•StrokeVolume (SV) |
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•Ejectionfraction EF |
–Percentageof the EDV pumped out of each ventricle during a single beat–EF=SV/EDV (expressedas percent)-average is about 60% |
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•theamount of blood pumped by each ventricle in one minute |
Cardiacoutput |
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•CO=HRx SV |
–Cardiacoutput equals heart rate times stroke volume. •CO=75bpmX 80ml/beat•CO=6000ml/Min |
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Ifduring exercise the heart rate increases to 100bmp and the cardiac outputincreases to 10 liters per minute, what is the stroke volume |
•CO=HRX SV•SV=CO/HR•Convert10 liters to ml (1000ml=1L) 10kml/min•SV=10,000ml/min/ 100beats/m•SV=100ml/beat |
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•Autonomicnervous system control |
–Parasympathetic– Acetyl Choline (ACh) –when you are at rest PS delivers AChwhich slows your heart –Sympathetic– Norepinephrine (NE)does not kick in unless heart needs to go over 100 |
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•Endocrinecontrol |
–Epinephrine(E) & Norepinephrine (NE) (will act as hormones bc theyenter blood through adrenal medulla) |
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If,during exercise, the heart rate increasesto 100 beats per minute and thecardiac output increases to 10 litersperminute, what is the stroke volume? |
A.100milliliters per beat |
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FactorsAffecting Heart Rate |
•Dualinnervation - both sympathetic & parasympathetic ANS motor neuronsinnervate the SA and AV nodes –Parasympathetic- Acetyl Choline (ACh)•Decreasesslowsheart rate –Sympathetic- Norepinephrine (NE)•Increasesaccelerates heart rate |
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•RestingAutonomic Tone–Parasympatheticeffects dominate |
•Accelerationof heart rate– reduction inparasympathetic input–Increase insympathetic input•Slowingof heart rate–Increasein parasympathetic input–Reductionin sympathetic input |
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•AChfrom parasympathetic neurons |
–reducesrate of spontaneous depolarization in SA and AV nodal cells by increasing K+ion efflux |
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•NEfrom sympathetic neurons |
–Increasesrate of depolarization in nodal cells by increasing Ca+2ion influx |
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•CardiacCenters (inbrainstem) |
–Cardio-acceleratorycenter – controls sympathetic innervation of heart–Cardio-inhibitorycenter – controls parasympathetic innervation of heart–Receiveinput from chemoreceptors(detect all different kinds of chemicals) & baroreceptors(detects pressures and stretching)•Monitorblood pressure•MonitorO2 and CO2concentrations in blood |
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•Cardiacreflexes-similar to patellar reflex |
–Decreasein bloodpressure causesincrease in heart rate–Decreasein O2 or increase in CO2 causes increase in heart rate (this is areflex, it’s agood thing) |
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•Atrialreflex – adjustment in heart rate in response to an increase in venousreturn |
–Increasein rate of venous return causes stretch in walls of right atrium, stretchreceptors send signal to cardio-acceleratory center. Stretch baroreceptors topick up HR. |
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•StrokeVolume (SV) varies depending on |
–EndDiastolic Volume – how full theheart is when ventricles contract •Greatervenous return will increase EDV•Longerdiastole allows more blood into heart –EndSystolic Volume – the amount of blood left inthe ventricles aftercontraction•Strongercontraction of the ventricle ejects more blood•Weakheart will have low stroke volume, low ejection fraction.Heart doesn’t “squeeze" efficiently |
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HeartAttacks |
•Cardiacmuscle cells die, affecting ability of heart to contract |
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Anginapectoris |
•pain inthe chest–Developswhen workload of heart increases, trying to maintain homeostasis–Ischemia– inadequate blood supply to a region–Hypoxia – a low tissue oxygen levels |
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Treatments of heart blockages |
–Balloonangioplastyand insertion of stents w/ balloon and wire mesh, blow up balloon whichsquishes the plaque to the sides, removes balloon and mesh stays. Coronaryartery bypass graft-more intense/invasive |
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caffeine has effect on conducting and contracting cells similar to NE. what effect would a lot of caffeiene have on a heart? |
caffeiene acts directly on the heart, increasing the rate at which they polarize. this increases heart rate |
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if cardioinhibitory center of medulla oblongata was damaged which part of autonomic nerve system would be affected? |
bc it is part of the parasympathetic division of the ANS, parasympathetic stimulation of heart would decrease, sympathetic would take over increasing heart rate |
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how does increase in reploarization of pacemaker cells affect heart rate? |
this would slow down the heart rate bc the pacemaker cells would generate less action potentials |
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what affect does stimulating ACH receptors of heart have on cardiac output |
stim ACH would slow heart rate, meaning it would decrease cardiac output |
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effect of increase in venous return on stroke volume? |
venous return fills blood with heart stretching heart muscle, so a more forceful contraction will be produced. increase stroke volume |
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how would increase in sympathetic stim of heart effect end stystolic volume? |
sympathetic increases heart rate and force of contraction, therefor the lower the ESV will be, because stroke volume will push out more blood |
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joes end systoliv volume is 40ml and his end diastolic vol is 125ml, what is his stroke volume? |
stroke volume=EDV-ESV so 124-40=85ml |
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cardiac cycle is... |
comprises of the events in a complete heartbeat including contract/relax period of both atria and entricles. cycle begins with atria systole as they contract and push blood into ventricle. ends with atria and ventricles both passively filling with blood |
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sympathetic stim on heart? |
increases heart rate and force of contractions, |
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parasympathetic stim on heart? |
decreases heart rate and force of contractions |
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Types of arteries |
–Elasticarteries – conducting arteries –Musculararteries – distributing –Arterioles– small arterials |
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Veins |
carry blood to heart, small ones called venules |
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Capillaries |
blood moves from arterioles to capillaries where diffusion/exchange takes place between blood and interstitial fluid. from capillaries blood enters small venules which unite to form large veins to return blood to heart |
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capillary functions |
vital fx of cardiovasc system depends on events at capillary level-all chemical and gas exchange takes place across cap walls, cells rely on cap diffusion to obtain nutrients and oxygen and to remove metabolic waste |
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arteries and Veins |
-contain endothelium inner lining -layers of circular smooth muscles -elastc connective tissue fibers -structural connective tissue |
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compared to veins, arteries have... |
-relatively thick walls, -usually rippled due to inability to constrict -tunica media dominated by smooth and elastic fibers -carry blood under great pressure -are more resilient/less stretchable -resists arterial pressure generated by heart as it pumps blood to trunk and aorta -undergo change in diameter due to elasticity |
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veins are... |
-thin walls, -smooth endothelium -very little smooth muscle in tunica media -more collagen than elastic fibers -when not opposed by blood pressure, elastic fibers in arterial wall recoil, constricting lumen. tend to collapse. -typically contain valves (medium and venules) that prevent backflow to capillaries. |
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vasoconstriction |
primarily under control of sympathetic division of ANS, when stimulated arterial smooth muscles contract, constricting the artery |
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Vasodilation |
When smooth muscle relaxes, diameter of lumen increases, |
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affects of vasoconstriction/dilation |
1. affect afterload of heart 2. affect peripheral blood pressure 3. affect capillary blood flow |
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elastic arteries |
AKA conducting arteries carry large volumes of blood away from heart (pulmonary trunk, common carotic, subclavian, common iliac, etc.) |
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Venousreturn |
•movementof blood through veins to heart dependent on body movement to compress veins –Muscularcompression putspressure on veins and helps them move |
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constriction of veins |
•sympathetic stimulationofsmooth muscles in walls of veins can cause decrease in size of lumen |
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Totalblood volume is unevenly distributed |
– 30-35% inheart, arteries and capillaries – 65-70% invenous system |
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venous reserve/venoconstriction |
–Inresponse to blood loss, venoconstrictionoccurs, reducing amount of blood in venous system, increasing volume of bloodin arterial system and capillaries |
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Rateof blood flow through arteries, capillaries and veins determined by |
-pressure on blood –resistance toflow that the blood encounters |
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•Greaterpressure needed to push blood through systemic circuitthanpulmonary circuit because resistance is greater |
–Samevolume of blood per heart beat pushed through the two circuits –Leftventricle has thicker walls and generates more force than the right ventricle |
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Resistance |
the force opposing blood flow, •opposesthe movement of blood |
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•Bloodviscosity |
–Moreresistance if viscosity is higher –Lowerpercentage of plasma relative to cells increases viscosity, bc plasma is 92% water |
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5 general classes of blood vessels |
arteries, veins, capillaries, venules, and arterioles |
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why valves in veins but not arteries? |
arterial system has enough pressure to keep blood moving, in venous system pressure is too low to keep blood moving to heart -valves prevent backflow when venous pressure drops |
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Fenestrated capillaries |
located where fluid and small solutes move freely into and out of blood, including endocrine glands, choroid plexus of brain, absorptive areas of intestines, ad filtration areas of kidneys |
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•Forblood to flow, the pressure gradient must overcome total peripheral resistance |
peripheral resistance reflects a combination of vascular resistance, blood viscosity, and turbulence. |
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vascular resistance |
friction between blood and vessel walls -amount of friction depends on length and diameter of vessel. |
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Factorsinvolved in resistance |
•Bloodviscosity –Moreresistance if viscosity is higher –Lowerpercentage of plasma relative to cells increases viscosity •Vessellength–Lessresistance in pulmonary circuit than systemic circuit – less total numberof vessels •Vesseldiameter (R µ 1/r4) –Lessresistance in larger large diametervessels –Vasodilationand vasoconstriction change peripheral resistance |
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which of the following would not be a condition that would increase peripheral resistance? |
Dehydration would not increase resistance, it would decrease it because the blood is much less viscous during dehydration |
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(arterial) Systolicpressure |
•–blood forced into artery by ventricular contraction–~ 120 mmHg for “resting” heart |
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(arterial) Diastolicpressure |
•ventriclerelaxes–Pressuredoes not fall to zero because elastic & muscular wall of arteries putpressure on blood–~80 mm Hgfor “normal” arteries |
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Pulsepressure |
The difference betweensystolic and diastolic pressures |
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•Bloodpressure (arterial pressure) |
–Highestin arteries nearest heart–Approximately120/80 mm Hg |
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Capillarypressure |
–Arterialside ~ 35 mm–Venousside ~ 18 mm |
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•Venouspressure |
–Venules ~ 18 mm–VenaCavae ~ 2 mm |
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SystolicBP |
•bloodpressure in arteries when left ventricle is contracting |
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DiastolicBP |
bloodpressure remaining in arteries when left ventricle is in relaxation |
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hypotension |
•abnormallylow BP |
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Hypovolemia |
–dueto hemorrhage or dehydration–Overlyaggressive drug treatment for high blood pressure |
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hypertension |
•abnormallyhigh BP–Systolicgreater than 150 or diastolic greater than 90 at rest |
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–Hypervolemia |
fluid overload, is the medical condition where there is too much fluid in the blood. |
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–Vaso-constrictionin smooth muscles of blood vessels |
•Treatwith medications that reduce smooth muscle contraction–Plaqueformation reducing lumen size in blood vessels |
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•Hypertensionhas adverse effects on function of heart and blood vessels |
–Increasedworkload for the heart•increasedoxygen demand in myocardium can result in ischemia if coronary artery diseaseis present –Increasein arteriosclerosis –Aneurysmsin blood vessels |
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Aneurysm |
•bulgein weakened wall of an artery ruptured aneurysmcanlead to serious or fatal bleeding.If burst it can kill you |
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arteriosclerosis |
•thickeningof arterial walls–Focalcalcification – deposition of Ca+2salts |
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multiplesclerosis |
–formation of plaque |
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arterioles |
play most important role in regulating blood pressure and blood flow to a tissue |
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blood transported through venous system by means of... |
muscular contractions and respiratory pump |
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greatest effect of peripheral resistance? |
doubling the diameter of a vessel |
