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Phys, Cardio chpt 14

Stockton College Physiology, Cardiovascular System Chapter 14

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
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
How does blood flow thru vessels? Down pressure gradient from high pressure to low pressure
Hydrostatic Pressure pressure exerted when fluid isn't moving (pressure in our cardio system-even though it's moving and should be "hydraulic pressure"
Order of Cardio vessels decreasing blood pressure Aorta>Arteries>Arterioles>Capillaries>Venules>Veins>Venae cavae
Reason to get blood from vein instead of artery? Blood pressure too high in arteries and much lower in veins
Driving Force Pressure created in ventricles
Relationship between volume & pressure Inverse relationship-as volume of vessel decreases, pressure increases (squeezing on water-filled balloon)
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!
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
Relationship of Flow & Resistance Inverse-As resistance incr, flow decr. F~Pressure/Resistance F~1/Resistance
Poiseuille's Equation R~ 1/r(^4) R~ Ln/r(^4)
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
Vasoconstriction decrease in blood vessel volume
Vasodilation increase in blood vessel volume
Flow Rate Volume of blood that passes one point in system per unit time (L/min, mL/min)
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
Velocity Equation V=flow rate/cross section area
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
2 Components of Intercalated Discs -Desmosomes -Gap Junctions
Desmosomes found in intercalated discs: transfer force from cell to cell
Gap Junctions found in intercalated discs: transfer electrical signals rapidly from cell to cell
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
Description of Myocardial Muscle Cells -branched -single nucleus -attached to ea. other by intercalated discs
Heart's upward contraction Spiral arrangement of muscles allows ventricular contraction to squeeze blood upward from apex(bottom) of heart
Myocardium cardiac muscle of heart
Pericardium sac surrounding heart, within sac is thin pericardial fluid tht lubes heart surface
What are the 2 types of cardiac muscle cells? -contractile cells -autorhythmic cells
Contractile cells cardiac muscle cells tht contract after autorhythmic cells start
Autorhythmic cells pacemakers,synchronize contractile cells to coordinate a heart contraction -where action potentials originate -difference from contractile cells-smaller, no organized sarcomeres
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
How can cardiac muscle contraction be graded? -single muscle fiber can start a graded contraction
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
Role of epinephrine & norepinephrine regulate amnt of calcium available for contraction
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
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
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)
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
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
SA Node Sinoatrial Node-main pacemaker of heart (grp of autorhythmic cells), set heart's pace since they're the fastest
Internodal Pathway non-contractile autorhythmic cells: connect SA node to AV node
Bundle of HIS passes from AV (atrialventricular) node into septum and divides into right & left branches
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
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 -
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)
In ECG, why do downward deflections correspond to periods of depolarization? Bc it represents multiple action potentials in heart
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
Cardiac Repolarization the return of the ions to their previous resting state, which corresponds with relaxation of the myocardial muscle
Normal Heart Rate Values/ Tachycardia= Brachycardia= Norm HR= 70-100bpm Tachycardia=faster HR Brachycardia="brakes", slower HR
Fibrillation myocardial cells contract in disorganized manner. Life threatening emergency bc can't get enough blood to brain (treated by electrical shock to heart)
Arrhythmia electrical problems tht arises during generation/conduction of action potentials thru the heart
Long QT Syndrome (LQTS) change in QT interval, can be Genetic or iatrogenic (caused by side effects of certain medications)
Diastole (die/dead=relax) time during cardiac muscle relaxation
Systole (sit up=contract)time during cardiac muscle contraction
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
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
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
EDV End Diastole Volume=max amt of blood in ventricles, ~135ml
ESV End Systole Volume=minimum amt blood in ventricles, 1/2 blood volume remains, ~65ml
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
Wigger Diagram summarizes events of cardiac contraction by combined chart of ECG, blood pressure, heart sounds, left ventricular volume throughout all the events
Stroke Volume Amount of blood pumped by 1 ventricle during a contraction -70ml is average for humans -can incr up to 100ml during exercise
How to calculate stroke volume? EDV-ESV=Stroke Volume (Blood vol b4 contraction)-(Blood vol after contraction)
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
Frank Starling Law of the Heart -Shows relationship bw heart muscle stretch & force generated by heart -force increases w/ sarcomere length
Heart muscle stretch determined by ventricular end-diastolic volume (ml), more blood=more force=more stretch
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
What is end diastolic volume determined by? Venous return: amt blood entering heart from veins
How does stretch increase in cardiac muscle? When add't blood flows into heart, connects to EDV & stroke volume
Inotropic effect -effect from chemical tht increases or decreases contraction force -ex-norepinephrine, epinephrine, digitalis
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
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
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
Created by: ericka3464



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