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Heart physiology
Heart physiology
Heart physiology
Heart physiology
Heart physiology
Heart physiology
Heart physiology
Heart physiology
Heart physiology
Heart physiology
Heart physiology
Heart physiology
Heart physiology
Heart physiology
Heart physiology
Heart physiology
Heart physiology
Heart physiology
Heart physiology
Heart physiology
Heart physiology
Heart physiology
Heart physiology
Heart physiology
Heart physiology
Heart physiology
Heart physiology
Heart physiology
Heart physiology
Heart physiology
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Heart physiology

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  • Skeletal vs cardiac muscle The striations in cardiac muscle are similar to those in skeletal muscle, and Z lines are present. Large numbers of elongated mitochondria are in close contact with the muscle fibrils. The muscle fibers branch and interdigitate, but each is a complete unit surrounded by a cell membrane. Where the end of one muscle fiber abuts on another, the membranes of both fibers parallel each other through an extensive series of folds. These areas, which always occur at Z lines, are called intercalated disks (Figure 5–15). They provide a strong union between fibers, maintaining cell-to-cell cohesion, so that the pull of one contractile cell can be transmitted along its axis to the next. Along the sides of the muscle fibers next to the disks, the cell membranes of adjacent fibers fuse for considerable distances, forming gap junctions. These junctions provide low-resistance bridges for the spread of excitation from one fiber to another. They permit cardiac muscle to function as if it were a syncytium, even though no protoplasmic bridges are present between cells. The T system in cardiac muscle is located at the Z lines rather than at the A–I junction , where it is located in mammalian skeletal muscle.
  • By convention, inward currents are downward on the graph (lower section), and outward currents are upward
  • Refractory Periods 0.25 - 0.3 sec (Absolute) Corresponds to plateau 0.05 sec (Relative)
  • Because phase 0 of myocyte action potentials is generated by activation of fast sodium channels, partial inactivation of these channels would decrease the upstroke velocity of phase 0 (decrease the slope of phase 0). Partial inactivation also would decrease the maximal degree of depolarization. These changes in phase 0 would reduce the conduction velocity within the ventricle. Blockade of fast sodium channels is the primary mechanism of action of Class I antiarrhythmic drugs such as quinidine and lidocaine .
  • Incisura – occurs due to closure of aortic valve
  • X descent: after c wave in JVP……y decent: after v wave in jvp The downward deflections of the wave are the "x"(the atrium relaxes and the tricuspid valve moves downward) and the "y" descent (filling of ventricle after tricuspid opening). ‘ a’ wave Increase due to atrial systole Tricuspid valve stenosis – large ‘a’ wave ‘ c’ wave An increase followed by a decrease in pressure during early phase of systole Upslope created by bulging of AV valve into atrium during ventricular contraction (+ transmission of carotid systolic arterial pulse to adjacent jugular vein) Subsequent decrease in pressure caused by descent of base of heart and atrial stretch Mitral/tricuspid regurgitation – large ‘c’ wave ‘ v’ wave Tricuspid valve stenosis increases resistance to filling of the right ventricle, which is indicated by an attenuation of the descending phase of the V wave.
  • FIGURE 4-3 Summary of normal pressures within the cardiac chambers and great vessels. The higher values for pressures (expressed in mm Hg) in the right ventricle ( RV ), left ventricle ( LV ), pulmonary artery ( PA ), and aorta ( A ) represent the peak pressures during ejection (systolic pressure), whereas the lower pressure values represent the end of diastole (ventricles) or the lowest pressure (diastolic pressure) found in the pulmonary artery and aorta.
  • Not relevant to undergrad courses (NRUC) Rhoedes: The isometric length–tension curve for isolated cardiac muscle. Cardiac muscle displays a parabolic active length-tension relationship similar to that of skeletal muscle but shows considerably more passive resistance to stretch at L0. Contanza Physiology: In addition to the degree of overlap of thick and thin filaments, there are two additional length-dependent mechanisms in cardiac muscle that alter the tension developed: Increasing muscle length increases the Ca2+-sensitivity of troponin C and increasing muscle length increases Ca2+ release from the sarcoplasmic reticulum.
  • Guyton: to determine external workoutput of the heart.. BRS: contrusted by combining systolic & diastolic pressure curves: Diastolic P curve: relationship between diastolic P and diastolic V in ventricle Systolic P curve: relationship between systolic P and systolic V in ventricle
  • Changes in following cause changed PV loops: A: Normal; B: Increased Preload; C: Increased afterload; D: increased contractility
  • 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)
  • Transcript

    • 1. Heart Physiology Department of Physiology SKZMDC
    • 2.  
    • 3.  
    • 4. Cardiac Muscle <ul><li>Cardiac Muscle </li></ul><ul><ul><ul><li>Atrial muscle </li></ul></ul></ul><ul><ul><ul><li>Ventricular muscle </li></ul></ul></ul><ul><ul><ul><li>Specialized excitatory & conductive muscle fibers </li></ul></ul></ul><ul><li>Cardiac Muscle as a Syncytium </li></ul><ul><ul><ul><li>Intercalated disc “communicating” junctions (gap junctions) - totally free diffusion of ions </li></ul></ul></ul><ul><ul><ul><li>Atrial syncytium </li></ul></ul></ul><ul><ul><ul><li>Ventricular syncytium </li></ul></ul></ul>
    • 5. Cardiac Muscle - Histology
    • 6.  
    • 7.  
    • 8. Cardiac Muscle Action Potential <ul><li>Depolarization </li></ul><ul><ul><ul><li>Fast Na + channels </li></ul></ul></ul><ul><li>Plateau </li></ul><ul><ul><ul><li>Slow Ca ++ channels </li></ul></ul></ul><ul><ul><ul><ul><li>Slow to open </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Slow to close </li></ul></ul></ul></ul><ul><ul><ul><li>After depol. cardiac muscle membrane permeability to K + decreases </li></ul></ul></ul><ul><ul><ul><li>Ca ++ thus pumped in – excitation-contraction coupling </li></ul></ul></ul><ul><li>Repolarization </li></ul><ul><ul><ul><li>Slow K + channels </li></ul></ul></ul><ul><li>Refractory Periods </li></ul><ul><ul><ul><li>0.25 - 0.3 sec (Absolute) </li></ul></ul></ul><ul><ul><ul><ul><li>Corresponds to plateau </li></ul></ul></ul></ul><ul><ul><ul><li>0.05 sec (Relative) </li></ul></ul></ul>
    • 9. AP Comparison
    • 10. Cardiac Muscle Action Potential
    • 11. Cardiac Muscle Action Potential
    • 12. Problem <ul><li>A drug is found to partially inactivate fast sodium channels. </li></ul><ul><li>Q: How would this drug alter the action potential in a ventricular myocyte? </li></ul><ul><li>Q: How would the drug alter conduction velocity within the ventricle? </li></ul>
    • 13. Cardiac Cycle <ul><li>Cardiac events occurring from beginning of one heartbeat to the beginning of the next beat </li></ul><ul><li>Each cycle – INITIATED by SA node </li></ul><ul><ul><ul><ul><li>Spontaneous generation of AP in SA node </li></ul></ul></ul></ul><ul><ul><ul><ul><li>AP travels through both atria </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Through A-V bundle into the ventricles </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>AV node delay (more than 0.1 second) </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Hence atria contract ahead of ventricles </li></ul></ul></ul></ul></ul><ul><li>Diastole and Systole </li></ul><ul><ul><ul><ul><li>Period of relaxation – Diastole </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Heart fills with blood </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><li>Period of contraction – Systole </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Ejection of blood </li></ul></ul></ul></ul></ul>
    • 14. Cardiac Cycle - Components <ul><li>ECG is the event marker </li></ul><ul><li>1. Atrial Systole </li></ul><ul><ul><ul><ul><li>Follows P wave (electric activation of atria) </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Contributes to ventricular filling </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Forms the ‘ a wave ’ in the venous pulse curve </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Ventricular filling by atrial systole – 4 th heart sound (not audible in normal adults) </li></ul></ul></ul></ul><ul><li>2. Isovolumetric contraction of Ventricle </li></ul><ul><ul><ul><ul><li>Occurs after QRS wave (electric activation of ventricles) </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Ventricular P raised above atrial P: </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>AV valves close ( 1 st heart sound ) </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Split in 1 st heart sound may occur (since mitral valve closes b/f tricuspid) </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><li>Ventricular P rises – NO CHANGE IN VOLUME </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Aortic valve is closed </li></ul></ul></ul></ul></ul>
    • 15. Cardiac Cycle - Components <ul><li>3. Rapid Ventricular Ejection </li></ul><ul><ul><ul><ul><li>Ventricular P reaches its max. </li></ul></ul></ul></ul><ul><ul><ul><ul><li>When it b/c greater than aortic P – aortic valve opens </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Rapid ejection of blood takes place </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><li>Ventricular volume decreases rapidly </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Atrial filling begins </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Onset of “T wave” (ventricular repolarization) – marks end of vent. contraction & ejection </li></ul></ul></ul></ul><ul><li>4. Reduced Ventricular Ejection </li></ul><ul><ul><ul><ul><li>Slower ejection of blood from ventricles </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Ventricle P decreases </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Aortic P decreases (runoff of blood from large arteries into smaller arteries) </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Atrial filling continues </li></ul></ul></ul></ul>
    • 16. Cardiac Cycle - Components <ul><li>5. Isovolumetric Ventricular Relaxation </li></ul><ul><ul><ul><ul><li>Ventricle replorization is complete (end of “T wave”) </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Aortic valve closes (followed by pulmonic valve) </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>2 nd heart sound </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Splitting occurs during inspiration </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><li>AV valves remain closed mostly during this phase </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Ventricle P drops rapidly </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Ventricle volume remains CONSTANT – all valves are closed </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Incisura </li></ul></ul></ul></ul><ul><ul><ul><ul><li>When ventricle P b/c < atrial P – mitral valve opens </li></ul></ul></ul></ul><ul><li>6. Rapid Ventricular Filling </li></ul><ul><ul><ul><ul><li>Post-mitral valve opening – rapid filling of ventricles occurs </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Aortic P continues to decrease – more run-off of blood </li></ul></ul></ul></ul><ul><ul><ul><ul><li>3 rd heart sound (due to rapid flow from atria to ventricles </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Normally heard in children </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Abnormal in adults </li></ul></ul></ul></ul></ul><ul><li>7. Reduced Ventricular Filling (Diastasis) </li></ul><ul><ul><ul><ul><li>Longest phase of cardiac cycle </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Ventricular filling slows down </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Diastasis time period depends on heart rate! </li></ul></ul></ul></ul>
    • 17.  
    • 18.  
    • 19. Cardiac Cycle <ul><li>End-diastolic volume (130 ml) </li></ul><ul><li>End-systolic volume (50 ml) </li></ul><ul><li>Stroke volume (70 to 90 ml - @ rest) </li></ul><ul><li>Ejection fraction </li></ul><ul><ul><ul><ul><li>% of end-diastolic ventricular volume that is ejected with each stroke </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Is about 65% </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Valuable index of ventricular function </li></ul></ul></ul></ul><ul><li>Preload </li></ul><ul><li>Afterload </li></ul>
    • 20. Cardiac Chamber Pressures
    • 21. Length (L) –Tension (T) Curve Isolated Cardiac Muscle
    • 22. Pressure (‘T’) – Volume (‘L’) Curve – Whole Heart <ul><li>PV loops: </li></ul><ul><ul><li>Depict cardiac cycle </li></ul></ul><ul><ul><li>Show effects of Preload, afterload & inotropic state on cardiac pumping ability (SV) </li></ul></ul>
    • 23.  
    • 24. 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>
    • 25. 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>
    • 26. Explanation of FS Law
    • 27. 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>
    • 28. 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>
    • 29. 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>
    • 30. 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>

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