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Stockton College Physiology, Cardiovascular System Chapter 14

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2 Types of pump in Cardiovascular system   -Chamber pump: heart rhythmic contraction -Lg veins in Human leg: blood pushed out vein by surrounding tissue pressure, veins have valves tht prevent backflow  
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How does blood flow from heart?   Blood flows from arteries on left side, thru capillaries in tissues, comes back thru right side of heart via veins thru vena cava  
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How does blood flow thru vessels?   Down pressure gradient from high pressure to low pressure  
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Hydrostatic Pressure   pressure exerted when fluid isn't moving (pressure in our cardio system-even though it's moving and should be "hydraulic pressure"  
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Order of Cardio vessels decreasing blood pressure   Aorta>Arteries>Arterioles>Capillaries>Venules>Veins>Venae cavae  
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Reason to get blood from vein instead of artery?   Blood pressure too high in arteries and much lower in veins  
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Driving Force   Pressure created in ventricles  
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Relationship between volume & pressure   Inverse relationship-as volume of vessel decreases, pressure increases (squeezing on water-filled balloon)  
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What does blood flow depend on?   Positive pressure gradient. Flow goes from high>low pressure. Flow depends on change in pressure. If pressure of 1 area equals pressure of another area, no flow occurs. NEED pressure change to induce flow!  
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Cardiovascular Resistance   Tendency of cardiovascular system to oppose blood flow. Resistance mainly determined by radius of tube. R has pos relationship w/ L & n(viscosity) and neg relationship w/ r  
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Relationship of Flow & Resistance   Inverse-As resistance incr, flow decr. F~Pressure/Resistance F~1/Resistance  
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Poiseuille's Equation   R~ 1/r(^4) R~ Ln/r(^4)  
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Impact of radius change on flow & resistance   -Flow inc 16 fold whn radius doubles -Sm change in radius caused Lg effect on resistance to blood flow  
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Vasoconstriction   decrease in blood vessel volume  
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Vasodilation   increase in blood vessel volume  
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Flow Rate   Volume of blood that passes one point in system per unit time (L/min, mL/min)  
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Velocity   -Distance fixed volume of blood travels in given period of time -velocity is faster in smaller vessel, but flow rate can be same in Lg/Sm vessel  
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Velocity Equation   V=flow rate/cross section area  
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How Cardiac muscles differ from Skeletal muscles   -Smaller size -More mitochondria -have intercalated discs to connect -T-tubules are larger for more efficiency -Smaller sarcoplasmic reticulum  
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2 Components of Intercalated Discs   -Desmosomes -Gap Junctions  
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Desmosomes   found in intercalated discs: transfer force from cell to cell  
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Gap Junctions   found in intercalated discs: transfer electrical signals rapidly from cell to cell  
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Mitochondria in Cardiac muscle   consume 70-80% of Oxygen delivered in blood (more than 2 times other cells in body) -reason reduced blood flow due to blockage of coronary artery can be deadly  
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Description of Myocardial Muscle Cells   -branched -single nucleus -attached to ea. other by intercalated discs  
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Heart's upward contraction   Spiral arrangement of muscles allows ventricular contraction to squeeze blood upward from apex(bottom) of heart  
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Myocardium   cardiac muscle of heart  
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Pericardium   sac surrounding heart, within sac is thin pericardial fluid tht lubes heart surface  
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What are the 2 types of cardiac muscle cells?   -contractile cells -autorhythmic cells  
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Contractile cells   cardiac muscle cells tht contract after autorhythmic cells start  
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Autorhythmic cells   pacemakers,synchronize contractile cells to coordinate a heart contraction -where action potentials originate -difference from contractile cells-smaller, no organized sarcomeres  
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Importance of Calcium in heart excitation-contraction   Cardiac muscle excitation-contraction coupling includes Calcium-induced Calcium release. -voltage gated calcium channels open in cell membrane of T-tubules & let calcium enter  
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How can cardiac muscle contraction be graded?   -single muscle fiber can start a graded contraction  
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What is force generated from cardiac cell-cell dependent on?   -Force generated dependent on # of crossbridges (which is determined by how much Ca2+ is bound to troponin, which depends on amt of Ca2+ tht enters cell  
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Role of epinephrine & norepinephrine   regulate amnt of calcium available for contraction  
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What is diff in action potential of cardiac contractile cells from nerve/skeletal muscle action potentials?   -cardiac has longer plateu due to opening of Ca2+ channels & closing of K+ channels -VERY important to prevent tetanus(state of continued muscular contraction) in heart -muscles must relax for ventricles to fill up  
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What is the Action potential sequence of events for cardiac contractile cells?   0-Na+ channels open 1-Na+ channels close 2-Ca2+ channels open; fast K+ channels close 3-Ca2+ channels close; slow K+ channels open 4-Resting Potential  
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What causes unstable membrane potential in autorhythmic cells?   the pacemaker potential-membrane potential never rests due to leaky funny channels (contain channels diff frm other excitable tissue)  
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Sympathetic vs. Parasympathetic Stimulation   -Sympathetic stim & epinephrine DEPOLARIZE autorhythmic cell & speed up depolarization rate, increasing heart rate -Parasympathetic stim w/ ACh HYPERPOLARIZES the membrane potential of autorhythmic cell & SLOWS depolarization, decreasing HR  
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How do depolarizations of autorhythmic cells spread to adjacent contractile cells to initiate heart contraction?   Through GAP JUNCTIONS -Electrical current leaves SA node to auto cells which sends via gap junctions in intercalated discs to contractile cells  
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SA Node   Sinoatrial Node-main pacemaker of heart (grp of autorhythmic cells), set heart's pace since they're the fastest  
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Internodal Pathway   non-contractile autorhythmic cells: connect SA node to AV node  
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Bundle of HIS   passes from AV (atrialventricular) node into septum and divides into right & left branches  
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What is the sequence of heart electrical conduction leading to muscle contraction (pump)?   1-SA node depolarizes 2-Rapid electric activity from SA to AV via Internodal pathway 3-Depolarization spreads slowly across atria/conduction slows thru AV node 4-Depolarization moves rapidly thry ventricular conducting system to heart apex 5-depolariz  
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What is complete heart block?   -When electrical signalling from atria to ventricles thru AV node is disrupted, resulting in ventricle contracting at diff rate than atria. Can insert pacemaker -  
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Electrocardiogram   Record of heart electrical activity due to NaCl being good electrical conductor. usually placed on skin thry Eithoven's Triangle tht encloses heart (both arms & left leg)  
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In ECG, why do downward deflections correspond to periods of depolarization?   Bc it represents multiple action potentials in heart  
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Cardiac Depolarization   Whn cell generates electrical impulse it causes ions to cross cell membrane & causes the action potential, also called depolarization. movement of ions across cell membrane thru Ca2+ channels causes contraction of the cardiac cells/muscle  
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Cardiac Repolarization   the return of the ions to their previous resting state, which corresponds with relaxation of the myocardial muscle  
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Normal Heart Rate Values/ Tachycardia= Brachycardia=   Norm HR= 70-100bpm Tachycardia=faster HR Brachycardia="brakes", slower HR  
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Fibrillation   myocardial cells contract in disorganized manner. Life threatening emergency bc can't get enough blood to brain (treated by electrical shock to heart)  
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Arrhythmia   electrical problems tht arises during generation/conduction of action potentials thru the heart  
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Long QT Syndrome (LQTS)   change in QT interval, can be Genetic or iatrogenic (caused by side effects of certain medications)  
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Diastole   (die/dead=relax) time during cardiac muscle relaxation  
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Systole   (sit up=contract)time during cardiac muscle contraction  
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What are the characteristics of the heart at rest?   -brief moment of relaxed atria & ventricles -atra filling w/ blood after ventricles completed contraction -As ventricles relax, valves open to let blood flow downward by gravity from atria to ventricles  
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Complete Cardiac Cycle Events 1-3   1-late diastole:all chambers relaxed & ventricles fill 2-Atrial systole: atrial contraction forces sm amt add't blood into ventricles 3-Isovolumetric ventricular contraction: pushes AV valves closed  
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Complete Cardiac Cycle Events 4-5   4-Ventricular ejection:as ventricular pressure rises & exceeds ateriole pressure, semilunar valves open and eject blood 5-Isovolumetric ventricular relaxation: as ventricles relax, pressure in ventricles falls&blood flows back thru semilunar valves/close  
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EDV   End Diastole Volume=max amt of blood in ventricles, ~135ml  
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ESV   End Systole Volume=minimum amt blood in ventricles, 1/2 blood volume remains, ~65ml  
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What creates heart sounds?   -1st sound "lub"=happens at isovolumic ventricular contraction from pushing AV valves closed -2nd sound "dub"= happens at isovolumic ventricular relaxation from closing of semilunar valves after pressure drop in atria & AV valves open  
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Wigger Diagram   summarizes events of cardiac contraction by combined chart of ECG, blood pressure, heart sounds, left ventricular volume throughout all the events  
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Stroke Volume   Amount of blood pumped by 1 ventricle during a contraction -70ml is average for humans -can incr up to 100ml during exercise  
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How to calculate stroke volume?   EDV-ESV=Stroke Volume (Blood vol b4 contraction)-(Blood vol after contraction)  
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What are heart attacks/strokes?   -Heart attack: blood flow is blocked to certain area of heart -Stroke: Lack of blood supply to brain, causing rapid loss of brain functions  
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Frank Starling Law of the Heart   -Shows relationship bw heart muscle stretch & force generated by heart -force increases w/ sarcomere length  
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Heart muscle stretch   determined by ventricular end-diastolic volume (ml), more blood=more force=more stretch  
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Heart muscle force   determined by stroke volume (ml) -muscle force incr w/ sarcomere length, so more blood entering heart= more forceful heart pumps=more stretch  
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What is end diastolic volume determined by?   Venous return: amt blood entering heart from veins  
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How does stretch increase in cardiac muscle?   When add't blood flows into heart, connects to EDV & stroke volume  
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Inotropic effect   -effect from chemical tht increases or decreases contraction force -ex-norepinephrine, epinephrine, digitalis  
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What is EDV (End Diastolic Volume) determined by?   Venous return tht is affected by: 1.skeletal muscle contraction 2. respirator pump: creates sub-atmospheric pressure in inferior vena cava & helps draw blood 3.sympathetic activity: decreases size of veins, thus more blood flows out of veins into hear  
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Cardiac Output   -Amount of blood pumped per ventricle per unit time (usually same for both ventricles) -During exercise CO can incr to 30-35ml/min -CO(cardiac output)=HR x SV (stroke volume) -Avg CO= 5040ml/min= 72 beats/min x 70ml/beat  
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How is heart rate controlled?   -heart normally under tonic contrl (dial to be turned) by the parasympathetic division -Reduce activity of parasym to incr HR to 90-100BPM -Above 100BPM, sympathetic input needed to incr HR -Both para & sympath influence HR by affecting conduction rate  
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