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Phys, Cardio chpt 14
Stockton College Physiology, Cardiovascular System Chapter 14
| Question | Answer |
|---|---|
| 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 |
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