KUMAR_5 - Systoie ' n. s ‘a‘m- H33 £ ($21. Tim Ma v,...

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Unformatted text preview: Systoie ' n. s ‘a‘m- H33 £ ($21. Tim Ma v, r.» m; M ,6": u 5 1 “w. «HA. Diastele ' Cardiac Cycie , ‘ Fimzr‘eifwz ' Semiimar Semifuna: waives npmevi V ~vafivea cioged AV vaéves ; AV wives; ciased {3}" Swmie: Pemd a”: Qsawéumix: Cantmatizm. W' him: a? {b} Sysreée: 53m 0? Egaeiicn. Canéismetfi ventricuiaz ceiyxéraufim gauges; mg m: mamas 2:: WM 2 £5; flee , swim:sz pajamas: him;in G?" we: ventfimm, figuring; 91 wazriwiaf 32,93 323, The semiiunar rem/sea v- , causéwg mfiimar vawés 'impen. wag classed in the prefix) wasted a L V 3% Ea: ’ Semtéumr waves alva yam aimed _ AV Mimi; ‘ NJ waives; ‘ _ ' _ dosed waned ' * ' ‘ ‘3: Wm; The aim (mama? and {a} magma: 9mm :6 R/létaxaiian. Bimd' fimég back mam fife (Mama vensz causes {ms smrémnaf vaives‘m mm, which is; {he beginning 0? vars-323mm" dimioke. Sen‘fiéunar _ vafvea nosed -' AV vaéwes opened m; magma: Paasive Vanfricular filing T932 AV vaiwamwn V -. _ I am fined flaws "mm the relaxad vanzrimas, amounemg has» - ' mum: of ma vamficulm fining, ' " ' * I-xwfi‘vfiwzmmt cmmmmzmwz Liin m-Hixt " r ,7. The cardiac cyésm “ 5911:9291?" Diastole v, » :‘ Pawn? $396106 vi 99m? 0? 'E‘ass'we mm Time pgrisdfi: iwwiumic momma: issevawmic vemfxculm venir‘ecum; , cmfi’acmn ; - .3'aéaxafiag filling Wing Semifixmar waives; 7 E M , ‘i - mi Syatcéiz: i E i 1 mwwrew 3 i i 1 “'é a G x .z: :33 E E3 U! C) ‘2‘} {$3 15 ca 9 Dias‘iafic gregaxm ‘WLQWWJ ‘ ., , :ezsim {mm Hg} 51‘»! 33mg 1% ‘4?“ L. AV waives VV/opzm 3.», immuw. :3" 5:? mew Enrjdéafitoiic Enmiéaswéis: _ “wiume ‘ ‘ ’ I _ ‘ _ y‘ 1 ' évomme 125*»; . y . ' ‘ g i a L I ‘ s /—-~" 3 i ' E 73-; E g 3' "5’ i H , '9 QC) m i 5 SE 31 - é g 3. g M u 2 5‘3“ '3“ é. - E i ' r E a 2 V i E Y Emzimyssir'ilic - E , v ‘: Enfl-ayfiifiizc i _ ‘ r’vcafiume I , , mme ,‘ i 5 ' s g “1 I { ii V L g? g "E g " ' ’ _ s ' - *1 ' B ' x E E hazafl 33m ham ; , ‘ 3 193mm { 7mg: heart '5‘ E E snund ' sowd ’ t V 5mm 23 3 a ‘ ‘ . - , g . - L, § NE E I ( 2 § ,, _ ,Wii .fi W M. M ....... .mwim M} .Eventsifiawmagflmmglthe Card‘bac h v » wmhfaw finnzzs’znyhfii’faaifi‘gx anms fiflfii‘S * r c,&§\sm§:rmwrm,, : ‘ FIGURE 4—24. The cardiac cycle. The mechanical and electrical events that occur during one cycle are shown A, Atrial systole: B, iso- volutnetric ventricular contrac- tion; C, rapid ventricular ejection; 1). reduced ventricular ejection; E, isovolumetric ventricular relax- ation; F, rapid ventricular filling; G, reduced ventricular filling (cli- astasis). CHAPTER 4 CARDlOVASEUtAR PHvsmtucv l Aortic valve closes -‘-~+. Aortic pressure Left ventricular pressure Venous pulse 133 134 PHi’SIDiOGY TABLE 4—5. Events of the Cardiac Cycle Phase of Cardiac Cycle* Major Events Electrocardiogram Valves Heart Sounds Atrial systole (A) f Atria contract P wave — Fourth heart sound ‘ Final phase of ventricular PR interval f filling lsovolumetric ventricular Ventricles contract QRS Mitral valve closes First heart sound contraction (B) Ventricular pressure \ increases 3 Ventricular volume is i constant (all valves are closed) Rapid ventricular ejection (C) Ventricles contract ST segment Aortic valve opens ~— Ventricular pressure increases and reaches maximum Ventricles eject blood into arteries Ventricular volume decreases Aortic pressure increases and reaches maximum Reduced ventricular ejection (D) arteries (slower rate) Ventricular volume reaches minimum Aortic pressure starts to fall as blood runs off into arteries Ventricles relaxed — ’ Ventricular pressure decreases : Ventricular volume is i constant i lsovolumetrlc ventricular relaxation (E) Ventricles eject blood into T wave Aortic valve closes Second heart sound ) l a i 5 l Ventricles relaxed — Ventricles fill passively with blood from atria Ventricular volume increases Ventricular pressure low and constant Rapid ventricular filling (F) Mitral valve opens ! Third heart sound Ventricles relaxed 3 _ Final phase of ventricular filling Reduced ventricular filling or ‘ diastasis (G) i__'_ * Lettered phases of cardiac Cycle. correspond to phases in Figu e 4—24 increase in atrial pressure is reflected back to the veins, it appears on the venous pulse record as the a wave. The left ventricle is relaxed during this ’ phase and, because the mitral valve (AV) is open, the ventricle is filling with blood from the atrium, even prior to atrial systole. Atrial systole causes a further increase in ventricular volume as blood is actively ejected from the left atrium to the left ven— tricle through the open mitral valve. The corre- sponding “blip” in left ventricular pressure reflects this additional volume added to the ventricle from atrial systole. The fourth heart sound (S4) is not audible in normal adults, although it may be heard in ventricular hypertrophy, where ventricular com- pliance is decreased and forceful ventricular filling produces a sound. lsovolumetric Ventricular Contraction (B) lsovolumetric ventricular contraction begins during the QRS complex, which represents the elec— trical activation of the ventricles. When the left ven— tricle contracts, left ventricular pressure begins to increase. As soon as left ventricular pressure ex- ceeds left atrial pressure, the mitral valve closes. (In the right heart, the tricuspid valve closes.) Clo— sure of the AV valves produces the first heart sound (51), which may be split because the mitral valve closes slightly before the tricuspid valve. Ventricular pressure increases dramatically during this phase, but ventricular volume remains constant since all valves are closed (the aortic valve has remained closed from the previous cycle). H4 PHYSIOLOGY Sinoatrial node Atrioventricular node Bundle of His (common bundle) Right bundle branch Right ventricle Left bundle branch Left ventricle Purkinje fibers FIGURE 4—11. Schematic diagram showing the sequence of activation of the myocardium. The cardiac action potential is initiated in the sinoatrial node and spreads throughout the myocardium, as shown by the arrows. flow to occur, the cell membrane must be permeable to that ion. Depolarization causes the membrane potential to become less negative. Depolarization oc— curs when there is net movement of positive charge into the cell, which is called an inward current. Hyperpolan‘zation causes the membrane potential to become more negative, and it occurs when there is net movement of positive charge out of the cell, which is called an outward current. 7. Two basic mechanisms can produce a change in membrane potential. In one mechanism, there is a change in the electrochemical gradient for a permeant ion, which changes the equilibrium potential for that ion. The permeant ion then will flow into or out of the cell in an attempt to reestab- lish electrochemical equilibrium, and this current flow will alter the membrane potential. For example, consider the effect of decreasing the extracellular K“ concentration on the resting membrane potential of a myocardial cell. The equilibrium potential, cal culated by the Nernst equation, will become more negative. K+ ions will then flow out of the cell, down the now, larger electrochemical gradient, and drive the resting membrane potential toward the new, more negative, equilibrium pctential. in the other mechanism, there is a change in conductance to an ion. For example, the resting permeability of ventricular cells to Na+ is quite low, and Nat contributes minimally to the resting mem- brane potential. However, during the upstroke of the action potential, Na“ conductance dramatically increases, Na+ flows into the cell down its electro— chemical gradient, and the membrane potential is briefly driven toward the Na+ equilibrium potential (depolarization). Action Potentials of Ventricle, Atria, and the Purkinie System The ionic basis for the action potentials in the ventricles, atria, and Purkinje system is identical. The action potential in these tissues shares the fol- lowing characteristics Cl" able 4—2). 0 Long duration. In each of these tissues, the action potential is of long duration. Action po— tential duration varies from 150 msec in the atria, to 250 msec in ventricles, to 300 msec in Purkinie fibers. These durations can be com— pared with the very brief duration of the action potential in nerve and skeletal muscle (1—2 msec). Recall that the duration of the action CHAPTER 4 CARDIOVAstUtAR PHYSIOLOGY 115 TABLE 4—2. Comparison of Action Potentials in Cardiac Tissues W Action Potential Duration Phase 4 Cardiac Tissue (msec) Upstroke Plateau Depolarization Sinoatrial node 150 Inward Ca“ current None Inward Na* current (1,) T—type Ca2+ channels Normal pacemaker Atrium 150 Inward Na+ current Inward Ca2+ current None (slow inward current) L—type Ca“ channels Ventricle 250 Inward Na+ current inward Ca“ current None (slow inward current) L—type Caz" channels Purkinje fibers 300 Inward Na‘ current Inward Ca2+ current Latent pacemaker (slow inward current) L—type Ca“ channels WWW potential also determines the duration of the refractory periods: The longer the action poten- tial, the longer the cell is refractory to firing another action potential. Thus, atrial, ventricu- lar, and Purkinje cells have long refractory peri- ods compared with other excitable tissues. 0 Stable resting membrane potential. The cells of the atria, ventricles, and Purkinje system ex- hibit a stable resting membrane potential. (AV nodal fibers and Purkinje fibers can develop unstable resting membrane potentials and, un- der special conditions, they can become the heart’s pacemaker, as discussed in the section on latent pacemakers.) o Plateau. The action potential in cells of the atria, ventricles, and Purkinje system is Charac- terized by a plateau. The plateau is a sustained period of depolarization, which accounts for the long duration of the action potential and, conse- quently, the long refractory periods. Figure 4—12 illustrates the action potential in a ventricular muscle fiber and an atrial muscle fiber. An action potential in a Purkinje fiber (not shown) would look similar to that in the ventricular fiber, but it would have a slightly longer duration. The phases of the action potential are described below and correspond to the numbered phases shown in Figure 4—12A and 4-128. Some of this information also is summarized in Table 4—2. 1. Phase 0, upstroke. In ventricular, atrial, and Purkinje fibers, the action potential begins with a rapid depolarization, called the upstroke. As in nerve and skeletal muscle, the upstroke is caused by a transient increase in Nai conductance (gm), produced by depolarization-induced opening of acti— vation gates on the Na+ channels. When gNa in- creases, there is an inward Na+ current (influx of Na"‘ into the cell), which drives the membrane po— tential toward the Na+ equilibrium potential of +65 mV. The membrane potential does not quite reach the Na "‘ equilibrium potential because, as in nerve, the inactivation gates on the Nat channels close in response to depolarization (albeit more slowly than the activation gates open). Thus, the Na‘r channels open briefly and then close. At the peak of the 5C,,‘EV‘Sinoatrialinode,if;-‘: r FIGURE 4—12. Cardiac action potentials in the ventricle, atrium, and sinoatrial node. The numbers correspond to the phases of the action potentials. Carotid presém‘éceptofs I Common carotid artery Cerebmm , I i Aortic Hypothalamus ‘ pressurec Cardiac Center Medufla S-A node Parasympathetic vagus nerve Spinal cord 533mg I, Sympathetic 9 acceierator nerve , Sympathetic: trunk I H I flats 30mm! , Fig .A e 18.24 . Hose JmnWJx i’rxsma'zns-zr ~31); muskzgz»; fly: ex: #3 w?!) xm (2. 951m Pumfims~ ...
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This note was uploaded on 11/22/2011 for the course DIAG 2725 taught by Professor Williamkessel during the Winter '11 term at Life Chiropractic College West.

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KUMAR_5 - Systoie ' n. s ‘a‘m- H33 £ ($21. Tim Ma v,...

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