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  • Frank starling law’s graphical representation is ventricle-function curve !! Also called the cardiac function curve… FS law has to do with preload (x-axis) and systole curve (costanzo) Berne; Frank-Starling Relationship The length-tension relationship for ventricular systole has already been described. This relationship now can be understood, using the parameters of stroke volume, ejection fraction, and cardiac output. The German physiologist Otto Frank first described the relationship between the pressure developed during systole in a frog ventricle and the volume present in the ventricle just prior to systole. Building on Frank's observations, the British physiologist Ernest Starling demonstrated, in an isolated dog heart, that the volume the ventricle ejected in systole was determined by the end-diastolic volume. Recall that the principle underlying this relationship is the length-tension relationship in cardiac muscle fibers. The Frank-Starling law of the heart, or the Frank-Starling relationship, is based on these landmark experiments. It states that the volume of blood ejected by the ventricle depends on the volume present in the ventricle at the end of diastole. The volume present at the end of diastole, in turn, depends on the volume returned to the heart, or the venous return. Therefore, stroke volume and cardiac output correlate directly with end-diastolic volume, which correlates with venous return. The Frank-Starling relationship governs normal ventricular function and ensures that the volume the heart ejects in systole equals the volume it receives in venous return. Recall from a previous discussion that, in the steady state, CO equals VR . It is the Frank-Starling law of the heart that underlies and ensures this equality. The Frank-Starling relationship is illustrated in Figure 4-21. Cardiac output and stroke volume are plotted as a function of ventricular end-diastolic volume or right atrial pressure. (Right atrial pressure may be substituted for end-diastolic volume since both parameters are related to venous return.) There is a curvilinear relationship between stroke volume or cardiac output and ventricular end-diastolic volume. As venous return increases, end-diastolic volume increases and, because of the length-tension relationship in the ventricles, stroke volume increases accordingly. In the physiologic range, the relationship between stroke volume and end-diastolic volume is nearly linear. Only when end-diastolic volume becomes very high does the curve start to bend: At these high levels, the ventricle reaches a limit and simply is not able to "keep up" with venous return. Also illustrated in Figure 4-21 are the effects of changing contractility on the Frank-Starling relationship. Agents that increase contractility have a positive inotropic effect (uppermost curve) . Positive inotropic agents (e.g., digoxin) produce increases in stroke volume and cardiac output for a given end-diastolic volume. The result is that a larger fraction of the end-diastolic volume is ejected per beat and there is an increase in ejection fraction. Agents that decrease contractility have a negative inotropic effect (lowermost curve) . Negative inotropic agents produce decreases in stroke volume and cardiac output for a given end-diastolic volume. The result is that a smaller fraction of the end-diastolic volume is ejected per beat and there is a decrease in ejection fraction. Physio (linda constanza): The upper curve is the relationship between ventricular pressure developed during systole and end-diastolic volume (or end-diastolic fiber length). This pressure development is an active mechanism. On the ascending limb of the curve, pressure increases steeply as fiber length increases, reflecting greater degrees of overlap of thick and thin filaments, greater cross-bridge formation and cycling, and greater tension developed. The curve eventually levels off when overlap is maximal. If end-diastolic volume were to increase further and the fibers were stretched to even longer lengths, overlap would decrease and the pressure would decrease (descending limb of the curve). In contrast to skeletal muscle, which operates over the entire length-tension curve (see Chapter 1 , Fig. 1-26), cardiac muscle normally operates only on the ascending limb of the curve. The reason for this difference is that cardiac muscle is much stiffer than skeletal muscle. Thus, cardiac muscle has high resting tension, and small increases in length produce large increases in resting tension. For this reason, cardiac muscle is "held" on the ascending limb of its length-tension curve, and it is difficult to lengthen cardiac muscle fibers beyond Lmax. For example, the "working length" of cardiac muscle fibers (the length at the end of diastole) is 1.9 μm (less than Lmax, which is 2.2 μm). This systolic pressure-volume (i.e., length-tension) relationship for the ventricle is the basis for the Frank-Starling relationship in the heart. Body_ID: P004127 The lower curve is the relationship between ventricular pressure and ventricular volume during diastole, when the heart is not contracting. As end-diastolic volume increases, ventricular pressure increases through passive mechanisms. The increasing pressure in the ventricle reflects the increasing tension of the muscle fibers as they are stretched to longer lengths. Body_ID: P004129 The terms "preload" and "afterload" can be applied to cardiac muscle just as they are applied to skeletal muscle. The preload for the left ventricle is left ventricular end-diastolic volume, or end-diastolic fiber length; that is, preload is the resting length from which the muscle contracts. The relationship between preload and developed tension or pressure, illustrated in the upper (systolic) curve in Figure 4-21, is based on the degree of overlap of thick and thin filaments. The afterload for the left ventricle is aortic pressure. The velocity of shortening of cardiac muscle is maximal when afterload is zero, and velocity of shortening decreases as afterload increases. (The relationship between the ventricular pressure developed and aortic pressure or afterload will be discussed more fully in the section on ventricular pressure-volume loops.)
  • Although this is for skeletal muscle, the same can be used for cardiac muscle (fab’s inference: since both muscle are the same in this respect) Reconciliatory concept plugin: this graph shows that as the sarcomere length increases beyond 2.25….the actual force generated by the muslce decreases…then y is that on the FS curve, increasing fiber length [along the diastole curve) shows increased pressure?? That is due to the fact that the non-contractile element of the muscle becomes stretched at these muscle lengths, raising the ‘overall’ tension, while contractile element becomes ‘flaccid’ (fab’s inference)
  • It is imp to understand that the voltmeter (or ECG) wil only record a deflection when a dipole exists Dipole in the context of this experiment is in B, direction is towards the +ve electrode, and in C , direction is away from +ve electrode. It is imp to understand that when we say ECG will exhibit a deflection only wen a state of particla de- or repolarization exists…we actually mean a dipole exists!!!
  • Top pic: atrial muscle Mean Electrical Vector Middle pic: generic showing movement of electrical vectors with respect to recording electrodes Lower pic: ventricular muscle Mean Electrical Vector
  • Upload 19 04-11

    1. 1. Regulation of Heart Pumping <ul><li>(1) INTRINSIC cardiac regulation of pumping in response to changes in volume of blood flowing into the heart ( Frank-Starling Law ) </li></ul><ul><li>(2) Control of heart rate and strength of heart pumping by ANS </li></ul>
    2. 2. Frank-Starling Law <ul><li>“ Volume of blood ejected by the ventricle depends on the volume present in the ventricle at the end of diastole” </li></ul><ul><li>Underlying principle </li></ul><ul><ul><li>Length-tension relationship in cardiac muscle fibers </li></ul></ul><ul><li>SV & CO correlate directly with EDV </li></ul><ul><li>EDV correlates with VR </li></ul><ul><li>CO = VR (FS Law ensures this) </li></ul><ul><li>Cardiac muscle normally operates only on the ascending limb of the systolic curve </li></ul>
    3. 3. Explanation of FS Law
    4. 4. Concept of Contractility <ul><li>Inherent cardiac M Ca++ based ability – INOTROPISM </li></ul><ul><ul><ul><li>Modified by ANS, catecholamines </li></ul></ul></ul><ul><li>Loading situations of the heart </li></ul><ul><ul><ul><li>Preload </li></ul></ul></ul><ul><ul><ul><ul><li>Stretch-induced enhancement in contraction </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>More overlapping of thick & thin filaments </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>More Ca ++ sensitivity of troponin C </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>More Ca ++ release from SR </li></ul></ul></ul></ul></ul><ul><ul><ul><li>After load </li></ul></ul></ul>
    5. 5. Heart Control by ANS <ul><li>Sympathetic </li></ul><ul><ul><ul><li>NE via action on Beta-1 receptors </li></ul></ul></ul><ul><ul><ul><ul><li>Positive CHRONOTROPIC </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Increased HR (increase Phase-4 depolarization) </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><li>Positive IONOTROPIC </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Increased force of contraction (increased inward Ca++ current during plateau + increases the ability of SR Ca++ pump) </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><li>Positive DROMOTROPIC </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Increased conduction velocity through AV node (increased inward Ca++ current) </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Decreased PR interval </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><li>Positive BATHMOTROPIC </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Increased excitability of myocardium </li></ul></ul></ul></ul></ul>
    6. 6. Heart Control by ANS <ul><li>Parasympathetic </li></ul><ul><ul><li>SA node, atria & AV node have supply, ventricles don’t! </li></ul></ul><ul><ul><li>Ach via muscarinic receptors </li></ul></ul><ul><ul><ul><li>Negative chronotropic </li></ul></ul></ul><ul><ul><ul><ul><ul><li>Decreasing phase-4 depolarizations </li></ul></ul></ul></ul></ul><ul><ul><ul><li>Negative dromotropic </li></ul></ul></ul><ul><ul><ul><li>Negative ionotropic </li></ul></ul></ul><ul><li>Vagal escape </li></ul>
    7. 7. Determinants of Performance of Heart as a Pump <ul><li>4 factors: </li></ul><ul><ul><ul><li>‘ Loading’ conditions of the cardiac muscle </li></ul></ul></ul><ul><ul><ul><li>(1) Preload , or the initial length to which the muscle is stretched prior to contraction </li></ul></ul></ul><ul><ul><ul><li>(2) Afterload , or all the forces against which cardiac muscle must contract to generate pressure and shorten </li></ul></ul></ul><ul><ul><ul><li>‘ Extrinsic’ factors </li></ul></ul></ul><ul><ul><ul><li>(3) Contractility , or inotropic state </li></ul></ul></ul><ul><ul><ul><li>(4) Inotropic effect of increased heart rate (beats/min) </li></ul></ul></ul>
    8. 9. S-A Nodal Action Potential <ul><ul><li>I ca L (long-lasting) </li></ul></ul><ul><ul><li>I ca T (transient) </li></ul></ul><ul><ul><li>Firing potential: </li></ul></ul><ul><ul><li>-40 mv </li></ul></ul><ul><ul><li>Hyperpolarization </li></ul></ul>
    9. 10. Cardiac Impulse <ul><li>Initiated in SA node </li></ul><ul><li>Spreads radially into atrial muscle mostly @ 0.3 m/sec </li></ul><ul><li>Atrial conduction is done via bands of fibres </li></ul><ul><ul><ul><li>Anterior </li></ul></ul></ul><ul><ul><ul><li>Middle </li></ul></ul></ul><ul><ul><ul><li>Posterior </li></ul></ul></ul><ul><li>Arrives at AV node after 0.03 sec </li></ul><ul><li>AV delay of 0.13 sec occurs </li></ul><ul><ul><ul><li>0.09 in bundle </li></ul></ul></ul><ul><ul><ul><li>0.04 in bundle of HIS </li></ul></ul></ul><ul><ul><ul><li>Reason for delay? </li></ul></ul></ul><ul><ul><ul><li>Benefit of delay? </li></ul></ul></ul><ul><li>Total delay at this point is 0.16 sec </li></ul>
    10. 11. Cardiac Impulse <ul><li>After AV node </li></ul><ul><ul><li>Velocity is maximum </li></ul></ul><ul><ul><li>Bundle of HIS – 1 m/sec </li></ul></ul><ul><ul><li>Purkinje system – 4 m/sec </li></ul></ul><ul><li>From the top of septum – via purkinje system – all of ventricle – 0.06 – 0.1 sec </li></ul><ul><li>Total duration: 0.22 sec </li></ul><ul><li>Parts that are last depolarized </li></ul><ul><ul><ul><li>Posterobasal portion of left ventricle </li></ul></ul></ul><ul><ul><ul><li>Pulmonary conus </li></ul></ul></ul><ul><ul><ul><li>Upper most part of septum </li></ul></ul></ul>
    11. 13. Normal ECG <ul><li>ECG is produced only when current flows through the heart and this occurs only when the heart is partially depolarized/polarized </li></ul>
    12. 14. Normal ECG <ul><li>P wave </li></ul><ul><ul><ul><li>Atria depolarize before contraction </li></ul></ul></ul><ul><ul><ul><li>0.08 - 0.10 sec </li></ul></ul></ul><ul><li>QRS complex </li></ul><ul><ul><ul><li>Ventricles depolarize before contraction </li></ul></ul></ul><ul><ul><ul><li>0.06 – 0.10 sec </li></ul></ul></ul><ul><li>T wave </li></ul><ul><ul><ul><li>Ventricles repolarize </li></ul></ul></ul><ul><ul><ul><li>Atrial T wave is obscured by QRS </li></ul></ul></ul><ul><ul><ul><li>Duration normally not taken </li></ul></ul></ul><ul><li>U wave </li></ul><ul><ul><ul><li>Inconstant finding </li></ul></ul></ul><ul><ul><ul><li>Slow repolarization of papillary muscles </li></ul></ul></ul>
    13. 15. Normal ECG <ul><li>PR interval – 0.16 sec </li></ul><ul><ul><ul><li>Time b/w beginning of P wave and beginning of QRS complex </li></ul></ul></ul><ul><ul><ul><ul><li>Interval between the beginning of electrical excitation of the atria and the beginning of excitation of the ventricles </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Prolonged: Vagal stimulation, AV block </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Shortened: Accelerated AV conduction, sympathetic stimulation </li></ul></ul></ul></ul></ul><ul><li>ST interval (QT minus QRS) – 0.32 sec </li></ul><ul><ul><ul><li>Ventricular repolarization </li></ul></ul></ul><ul><li>Q-T interval – 0.2-0.40 sec </li></ul><ul><ul><ul><li>Ventricular depolarization and ventricular repolarization </li></ul></ul></ul><ul><ul><ul><li>Corresponds to AP duration </li></ul></ul></ul><ul><ul><ul><ul><ul><li>Prolonged: ventricular extrasystole </li></ul></ul></ul></ul></ul>
    14. 16. Dipole <ul><li>The electric dipole consists of two equal and opposite charges, +q and –q , separated by a distance d </li></ul><ul><li>Dipole vector : </li></ul><ul><ul><ul><li>Vector whose magnitude is equal to the dipole moment [voltage] and that points from –ve charge to + one </li></ul></ul></ul><ul><li>Direction of dipole is from –ve towards +ve </li></ul>
    15. 17. <ul><li>A wave of depolarization heading toward the +ve electrode is recorded as a +ve voltage </li></ul><ul><ul><ul><li>Represents Atrial & Vent. Depol . </li></ul></ul></ul><ul><li>A wave of repolarization moving away from a +ve electrode produces a +ve voltage difference </li></ul><ul><ul><ul><li>T-wave (Vent. Repol.) </li></ul></ul></ul><ul><li>A wave of repolarization moving toward a +ve electrode produces a –ve voltage deflection </li></ul><ul><ul><ul><li>Atrial Repol. </li></ul></ul></ul>
    16. 18. Vectors and Mean Electrical Axis <ul><li>Individual waves of depol. – electrical vectors </li></ul><ul><li>Summation of electrical vectors at any instance – mean electrical vector </li></ul>