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Heart
- 1. Heart Physiology Department of Physiology SKZMDC
- 5. Cardiac Muscle - Histology
- 10. Cardiac Muscle Action Potential
- 11. Cardiac Muscle Action Potential
- 22. Length (L) –Tension (T) Curve Isolated Cardiac Muscle
- 23. Length (L) –Tension (T) Curve – Skeletal M Fiber
- 29. Explanation of FS Law
- 53. Standard Limb Leads: Normal ECGs
- 63. AV BLOCKS - ECG
- 75. Atrial Flutter
- 81. Revision
Notas do Editor
- 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.
- Not relevant to undergrad courses (NRUC) This shows how the length-tension curve is generated bit by bit… This is an example of Isometeric M contraction Figure 8.18 A length-tension curve for skeletal muscle . Contractions are made at several resting lengths, and the resting (passive) and peak (total) forces for each twitch are transferred to the graph at the right. Subtraction of the passive curve from the total curve yields the active force curve. *Optimal length reflects Lo !!
- Not relevant to undergrad courses (NRUC) Comparison between cardiac and skeletal muscle length-tension curves…. A. The curve is generated (as mentioned previously) by stretching the fiber passively, taking the corresponding force generated [this is the resting/diastolic force] & then stimulating it [which will give the total force]…..subtracting the two gives us Active force/systolic. – {notice that beyond normal range: heart is less ‘accomodating’ to the increments in fiber length, hence the force (of resisting the increments) increases dramitically….which wud diminish the active force curve ! Hence during normal range of operation, resting force curve shows us how accomodating the heart is during its diastole + systolic curve almost increases in congruence!! {F-S Law}….beyond that the limits of the stretch of the fiber wud be achieved (i.e it wud be filled to max) which will result in increase in force (of resistance) [upward slant in resting curve] and downward slant in systolic B. note that in ‘normal range of operation’ [labelled as dark blue in upper & light greenish below] the cardiac muscle fiber curve is flatter – indicating the cardiac fibers are stiffer than skeletal muscle fibers - In this regard, however, it is important to realize that cardiac muscle is intrinsically stiffer than skeletal muscle and exhibits significant passive resistance to stretch at a length corresponding to Lo. As a result, cardiac muscle is constrained to contract from lengths < or = to Lo.
- 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 &quot;keep up&quot; 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 &quot;held&quot; on the ascending limb of its length-tension curve, and it is difficult to lengthen cardiac muscle fibers beyond Lmax. For example, the &quot;working length&quot; 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 &quot;preload&quot; and &quot;afterload&quot; 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!!!
- Previous experiment depicted a simplified model of single waves of depolarization & repolarization. In reality there is no single wave of electrical acitivity – rather electrical ‘waves’ go in many directions simultaneously.. Top pic: atrial muscle Mean Electrical Vector (MEV) *Middle pic: direction of MEV in relation to axis of recording electrodes determines the polarity & magnitude of recorded voltage. Lower pic: ventricular muscle Mean Electrical Vector
- Individual depol waves ( electrical vectors ) ------ (if summed) MEV ------- (if different MEVs are summed up in time) Mean electrical axis mean electrical axis of the normal ventricles is 59 degrees ( this axis can swing even in the normal heart from about 20 degrees to about 100 degrees. The causes of the normal variations are mainly anatomical differences in the Purkinje distribution system or in the musculature itself of different hearts). * a number of abnormal conditions of the heart can cause axis deviation beyond the normal limits, as follows: Change in the Position of the Heart in the Chest. If the heart itself is angulated to the left, the mean electrical axis of the heart also shifts to the left . Such shift occurs (1) at the end of deep expiration, (2) when a person lies down, because the abdominal contents press upward against the diaphragm, and (3) quite frequently in stocky, fat people whose diaphragms normally press upward against the heart all the time. Likewise, angulation of the heart to the right causes the mean electrical axis of the ventricles to shift to the right. This occurs (1) at the end of deep inspiration, (2) when a person stands up, and (3) normally in tall, lanky people whose hearts hang downward. Hypertrophy of One Ventricle. When one ventricle greatly hypertrophies, the axis of the heart shifts toward the hypertrophied ventricle for two reasons. First, a far greater quantity of muscle exists on the hypertrophied side of the heart than on the other side, and this allows excess generation of electrical potential on that side. Second, more time is required for the depolarization wave to travel through the hypertrophied ventricle than through the normal ventricle. Consequently, the normal ventricle becomes depolarized considerably in advance of the hypertrophied ventricle, and this causes a strong vector from the normal side of the heart toward the hypertrophied side, which remains strongly positively charged. Thus, the axis deviates toward the hypertrophied ventricle. Bundle Branch Block Causes Axis Deviation. Ordinarily, the lateral walls of the two ventricles depolarize at almost the same instant because both the left and the right bundle branches of the Purkinje system transmit the cardiac impulse to the two ventricular walls at almost the same instant. As a result, the potentials generated by the two ventricles (on the two opposite sides of the heart) almost neutralize each other. But if only one of the major bundle branches is blocked, the cardiac impulse spreads through the normal ventricle long before it spreads through the other. Therefore, depolarization of the two ventricles does not occur even nearly simultaneously, and the depolarization potentials do not neutralize each other.As a result, axis deviation occurs.
- Whether the limb leads are attached to the end of the limb (wrists and ankles) or at the origin of the limbs (shoulder and upper thigh) makes virtually no difference in the recording because the limb can be viewed as a wire conductor originating from a point on the trunk of the body. The electrode located on the right leg is used as a ground. *because the positive electrode is on the left arm.
- If the three limbs of Einthoven’s triangle (assumed to be equilateral) are broken apart, collapsed, and superimposed over the heart the positive electrode for lead I is defined as being at zero degrees relative to the heart (along the horizontal axis; see Figure 2-19). Similarly, the positive electrode for lead II is 60º relative to the heart, and the positive electrode for lead III is 120º relative to the heart, as shown in Figure 2-19. This new construction of the electrical axis is called the axial reference system . Although the designation of lead I as being 0º, lead II as being 60º, and so forth is arbitrary, it is the accepted convention. With this axial reference system, a wave of depolarization oriented at 60º produces the greatest positive deflection in lead II. A wave of depolarization oriented 90º relative to the heart produces equally positive deflections in both leads II and III. In the latter case, lead I shows no net deflection because the wave of depolarization is heading perpendicular to the 0º, or lead I, axis (see ECG rules). Three augmented limb leads exist in addition to the three bipolar limb leads described. Each of these leads has a single positive electrode that is referenced against a combination of the other limb electrodes. The positive electrodes for these augmented leads are located on the left arm (aVL), the right arm (aVR), and the left leg (aVF; the “F” stands for “ foot”). In practice, these are the same positive electrodes used for leads I, II, and III. (The ECG machine does the actual switching and rearranging of the electrode designations.) The axial reference system in Figure 2-20 shows that the aVL lead is at –30º relative to the lead I axis; aVR is at –150º, and aVF is at 90º. It is critical to learn which lead is associated with each axis. The three augmented leads, coupled with the three standard limb leads, constitute the six limb leads of the ECG. These leads record electrical activity along a single plane, the frontal plane relative to the heart. The direction of an electrical vector can be determined at any given instant using the axial reference system and these six leads. If a wave of depolarization is spreading from right to left along the 0º axis (heading toward 0º), lead I shows the greatest positive amplitude. Likewise, if the direction of the electrical vector for depolarization is directed downward (90º), aVF shows the greatest positive deflection.
- *remaining 2 leads The ECg MACHINE DOES THE ACTUAL SWITCHING The axial reference system in Figure 2-20 shows that the aVL lead is at –30º relative to the lead I axis; aVR is at –150º, and aVF is at 90º. It is critical to learn which lead is associated with each axis. The three augmented leads, coupled with the three standard limb leads, constitute the six limb leads of the ECG. These leads record electrical activity along a single plane, the frontal plane relative to the heart. The direction of an electrical vector can be determined at any given instant using the axial reference system and these six leads. If a wave of depolarization is spreading from right to left along the 0º axis (heading toward 0º), lead I shows the greatest positive amplitude. Likewise, if the direction of the electrical vector for depolarization is directed downward (90º), aVF shows the greatest positive deflection.
- 2:1 (2 atrial beats VS 1 ventricular beats)
- *during this interval, a normal SA nodal impulse was generated, producing a normal p wave which gets blurred with T wave of the premature beat…..this impulse fails to depolarize the ventricles cuz AV node and ventricles are still refractory from the premature beat, and hence cant be excited by this normal wave…hence no QRS wave either….compensatory pause!!........more pronounced in PVC than premature atrial contractions
- *because the cardiac impulse traveled backward into the atria at the same time that it traveled forward into the ventricles; this P wave slightly distorts the QRS-T complex, but the P wave itself cannot be discerned as such.
- Relative refractory period: 0.05 sec
- CoI: current of injury The 3 abnormalities are all linked to increased K+ efflux
- ST segment elevation or depression : remember that ischemia is associated with ST depression , while infarction is associated with ST elevation. Look for changes in two adjacent leads. Window effect: Q waves indicate that the infarcted area is dead, necrosed and electrically inert. Normally, ventricular wall activity interferes with the recording of Q wave – in case of infarction, there is no interference (window effect)
- A: normal ECG B: Hyperkalemia C: Hypokalemia
- From Concepts of CVS book in pdf