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Figure 3-1: (Plate 27) Electrical and mechanical events during the cardiac cycle. Shown are pressure curves of great vessels and cardiac chambers, valvular events, timing of heart sounds, LV volume curve, jugular venous pulse wave, and electrocardiogram (ECG). MC and TC, mitral and tricuspid valve closure; PO and AO, pulmonic and aortic valve opening; AC and PC, aortic and pulmonic valve closure; TO and MO, tricuspid and mitral valve opening.

Figure 3-2: Mitral flow recorded with a Doppler probe in the mitral annulus and simultaneous LA (LAP) and LV (LVP) pressures in a dog. Note initial gradient immediately after LV pressure crosses LA pressure. As shown here, when recorded with high-fidelity manometers, this is typically followed by a brief reversal of the gradient and then, following the slow-filling phase, by atrial contraction and a second increase in the gradient. Note rapid, early transmitral mitral flow (E wave) and smaller contribution of atrial contraction (A wave). The record also reveals a middiastolic increase in flow (L wave) that is occasionally observed. (From Yellin EL, Nikolic SD. Diastolic suction and the dynamics of LV filling. In: Gaasch WH, LeWinter MM, eds. LV Diastolic Dysfunction and Heart Failure. Philadelphia: Lea & Febiger, 1994:92. Reproduced with permission of the publisher.)

Figure 3-3: Schematic diagram of the major cellular components involved in contraction of the myocyte (see text). (Modified from Katz AM. Physiology ofthe Heart, 2d ed. New York: Raven, 1992. Reprinted with permission of the publisher.) Figure 3-4: Phases of cellular AP and major associated currents in ventricular myocyte. Initial phase zero spike (not labeled) and overshoot (1) is caused by rapid inward Na current, the plateau phase (2) by slow inward Ca current through L-type Ca channels, and repolarization (phase 3) by outward K current. Phase 4 resting potential (Na efflux, K influx) is maintained by the Na-K-ATPase. Na-Ca exchanger is mainly responsible for Ca extrusion. In specialized conduction system tissue, there is spontaneous depolarization during phase 4 until the voltage resulting in opening of the Na channel is reached. Figure 3-5: Schematic of Ca-induced Ca release from SR resulting in a Ca "spark." Opening of sarcolemmal (SL) L-type Ca channel results in movement of a relatively small amount of Ca ions into the cell. The latter causes opening of a number of nearby RyR channels (Ca release unit) with local release of a large amount of Ca ions from the SR and appearance of a "spark," as bioluminescent dye responds to change in local Ca concentration. (From Williams.8 Reproduced with permission of the publisher.) Figure 3-6: Intracellular Ca transient obtained with the bioluminescent dye Indo-1 is shown in the middle of this figure. It reflects the average instantaneous intracellular Ca ion concentration. The L-type Ca channel current modified by voltage clamping is shown in the top panel, and myocyte shortening is shown in the bottom panel. Note the voltage dependence of the Ca current and the parallel changes in both the Ca transient and shortening. (From Williams.8 Reproduced with permission of the publisher.) Figure 3-7: (Top) Electronmicrograph of sarcomere. (Bottom) Schematic (see text). (From Woledge et al.58 Reproduced with permission of the publisher.)

Figure 3-8: (Plate 28) Cartoon of sarcomeric proteins (titin not shown). (From Spirito P, Seidman CE, McKenna WJ, Maron BJ. The management of hypertrophic cardiomyopathy. New Eng J Med 1997; 336:775. Reprinted with permission of the publisher.)

Figure 3-9: Cartoon of the thin filament with actin and regulatory proteins, Tm and Tn complex, showing conformational differences between inactive state (diastole) and activation (systole). C, COOH terminus; N, NH2 terminus. (From Solaro and Rarick.48 Reproduced with permission from the publisher.)

Figure 3-10: Relation between log Ca concentration (pCa) and isometric tension in detergent-treated ("skinned") strips of mouse cardiac muscle. R403Q indicates a transgenic animal with a mutation causing hypertrophic cardiomyopathy; control is wild type. Skinning results in loss of integrity of the sarcolemma and all intracellular membranes, leaving sarcomeric proteins intact. In skinned strip, the ionic milieu of the contractile proteins can be manipulated and their behavior studied in isolation from the excitation and ECC systems. Note very steep relation between isometric tension and pCa between relaxing (pCa >7) and fully activating Ca concentrations (pCa 5) in both strips. The relation is shifted to the left in R403Q mice. (From Blanchard E, Seidman C, Seidman JG, et al. Altered crossbridge kinetics in the 0(MHC403/+ mouse model of familial hypertrophic cardiomyopathy. Circ Res 1999; 84:475. Reprinted with permission of the publisher.)

Figure 3-11: Schematic of the mechanical interaction between the myosin head (triangular structure) and actin located on the thin filament. Letter z denotes the distance moved by the thick filament as a result of rotation of the head region (see text). (From Woledge et al.58 Reproduced with permission of the publisher.)

Figure 3-12: (Left) Force (P) versus velocity (V) relation for two muscles with differing contractile performance. Velocity normalized to maximum unloaded value (Vmax) and force to maximum isometric value (P0). (Right) Normalized force versus power (force x velocity) for same muscles. Power is maximal at midrange force values. (Modified from Woledge et al.58 Reproduced with permission of the publisher.)

Figure 3-13: Schematic of relation between sarcomere length and developed tension (or force). Note fall in tension at lengths below approximately 2.2 Mm. At very long sarcomere lengths, thick-thin filament overlap is reduced, resulting in descending limb of relation (not observed in ventricle). (Modified from Braunwald E, Ross J Jr, Sonnenblick EH, eds. Mechanisms of Contraction ofthe Normal and Failing Heart. Boston, Little, Brown, 1976:77.)

Figure 3-14: Example of average relation between developed force and stimulation frequency in strips of human myocardium obtained by epicardial biopsy from a group of patients undergoing coronary bypass surgery, all with normal LV contraction patterns. Note the marked increase in force as contraction frequency increases from typical basal level of 60 per minute to a value of 170 to 180 per minute, at which force is maximal (see text).

Figure 3-15: Three-dimensional architecture of LV, illustrating spiraling bundles of myofibers (see text). (From Streeter.102 Reprinted with permission of the publisher.) Figure 3-16: LV function curves relating SV to ED pressure (see text). A. Normal function. B,C. Augmented and depressed contractility, respectively, as occur with increases or decreases in adrenergic stimulation. Because ED pressure is plotted, identical shifts could be observed with altered diastolic compliance.

Figure 3-17: Schematic illustrating concept of preload and afterload during isotonic contraction. (Left) Linear muscle is depicted as consisting of contractile element (CE) (i.e., thick and thin filaments) and spring in series (SE). (Right) Shortening and force are depicted. A. Muscle is at rest, with one end tethered and the other connected to a weight (P). P is supported, however, so that muscle is only subjected to a fraction of weight (or load). This relatively small load is the preload, which stretches the muscle to the initial, resting length. B. Muscle begins to contract. In order to shorten, it must lift the entire weight P, which is the afterload. Initially, force increases but is insufficient to lift the weight. During this period, the CE shortens and reciprocally lengthens the SE, while total muscle length remains constant. Eventually, the developed force just exceeds the afterload, and the muscle begins to shorten (C). Once shortening begins, force is constant and essentially equal to the afterload. In an isometric contraction, the muscle cannot lift the load and therefore does not shorten (although the CE shortens and SE lengthens by the same amount).

Figure 3-18: Relation between EF and circumferential stress (with 95 percent confidence intervals) in human subjects with normal ventricular function (control, filled squares) and mitral regurgitation (MR, open circles) (see text). Some MR patients fall below confidence intervals. (From Starling et al.115 Reproduced with permission of publisher.) Figure 3-19: Schematic of elastance concept (see text). A. Series of variably loaded pressure-volume loops. Filled circles connected by straight lines occur at same time t during contraction. Emax is line connecting points at ES. B. Elastance E(t) increases at each time t during contraction until it reaches maximal value at ES. Increased contractility increases slope at any time t, including ES (Emax); vice versa for decreased contractility. C,D. The concept that the ventricle behaves like a spring of increasing stiffness (increased slope of elastance relations) during contraction. (From Suga H, Takaki M, Matsubara H, Goto Y. Energy costs of PVA and Emax: Constancy and variability. In: LeWinter MM, Suga H, Watkins MW, eds. Cardiac Energetics: From Emax to Pressure-Volume Area. Boston, Kluwer, 1996:2. Reprinted with permission of publisher.) Figure 3-20: (Top) Schematic of VO2-PVA concept (see text). In ejecting contraction, PVA = EW + PE; in isovolumic contraction, PVA = PE only. (Bottom) Correlation of PVA with VO2. (From Goto et al.128 Reproduced with permission of publisher.) Figure 3-21: Determinants of relation between LV diastolic pressure and volume during filling. Solid line, LV pressure during isovolumic relaxation, filling, and isovolumic contraction; dashed line, positive and negative portions of passive pressure-volume relation. Ves, ES volume; V> equilibrium volume or zero pressure intercept of passive pressure-volume relation (which is not same as dead volume of ESPVR); Ved, ED volume. (From Gilbert JC, Glantz SA. Determinants of LV filling and of the diastolic pressure-volume relation. Circ Res 1989; 64:828. Reproduced with permission of publisher.)

Figure 3-22: (Left) EDPVR in two ventricles with differing passive diastolic properties. Chamber stiffness is dP/dV at any point on the EDPVR. Chamber compliance is its inverse. Stiffer chamber (left) has steeper overall slope. (Right) Same data plotted as pressure versus chamber stiffness. Because of exponential nature of EDPVR, result is a straight line. Its slope (kc) is a chamber-stiffness constant that characterizes the overall slope of the EDPVR. (From Gaasch.157 Reprinted with the permission of the publisher.) Figure 3-23: Relations between total cross-sectional area of the vascular bed (cm2), velocity of blood flow (cm/s), and blood pressure (mmHg) in various vessels in systemic circulation. (From Marieb EN. Human Anatomy and Physiology. Redwood City, CA: Benjamin/Cummings; 1989:629. Reproduced with permission of the publisher.)

s Figure 3-24: Illustration of principle of resistance elements arranged in series versus parallel. (Top) If the driving pressurer (DP) across each series resistance is 3 mmHg, and flow (Q) is 1 mL/min, each resistance (R) would be DP/Q, or 3 mmHg/mL per minute, and total resistance (Rt) would be 9 mmHg/mL per minute. (Bottom) In parallel resistances, if driving pressure (DP) is 3 mmHg, and flow (Q) is 1 mL/min, total resistance is 1/R1 + 1/R2 + 1/R3, or 1 mmHg/mL per minute. When three resistances are in parallel, total resistance is only one-ninth that with resistances in series, so it would take a DP of only 1 mmHg to produce a 1 mL/min flow. (From Smith JJ, Kampine JP. Circulatory Physiology: The Essentials. Baltimore: Williams & Wilkins, 1990:20. Reprinted with permission of the publisher.)

s Figure 3-25: Regional blood flow at rest (shaded areas) and at maximal dilatation (stippled areas) per organ and per 100 g tissue, illustrating the concept of arterial/arteriolar vasodilator reserve. (From Mellander S, Johansson B. Control of resistance, exchange and capacitance functions in the peripheral circulation. Pharmacol Rev 1968; 20:117. Reprinted with permission of the publisher.)

' Figure 3-26: Schematic diagram of integrated response of metabolic, myogenic and flow-mediated regulation of coronary vascular resistance and flow during increase in metabolic demand. Plus sign indicates vasodilatory feed-forward steps in response to initial increase in demand. Minus sign indicates negative-feedback processes that limit vasodilation. Events marked by lines ("Production of Metabolites") occur as a reaction to metabolic or vascular changes. Bolded items are metabolic or vasoactive adjustments. (From Muller et al.200 Reprinted with permission of the publisher.)

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