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 |