Cardiovasculaire Physiologie Concepts: PDF

06/11/2024 II. La fonc*on cardiaque 1 Le cycle cardiaque: événements électriques (l’électrocardiogramme, ECG) Ø Les courants électriques générés e...

06/11/2024 II. La fonc*on cardiaque 1 Le cycle cardiaque: événements électriques (l’électrocardiogramme, ECG) Ø Les courants électriques générés et transmis à travers le cœur se propagent dans tout le corps et peuvent être détectés à l’aide d’un électrocardiographe. Ø ECG: enregistrement graphique de l'acFvité cardiaque composée de tous les poten*els d’ac*on générés par les cellules nodales et contracFles à un instant donné. Ø On place des électrodes à des endroits spécifiques de la surface du corps: Sur chaque bras et chaque jambe Six électrodes sont placées à des emplacements définis sur la poitrine. Ø On mesure les différences de poten*el entre les électrodes sélecFonnées pour produire des tracés ECG caractérisFques. 2 1  26 CARDIOVASCULAR PHYSIOLOGY CONCEPTS 06/11/2024 THE ELECTROCARDIOGRAM ECG Tracing As cardiac cells depolarize and repolarize, The ECG is a crucial diagnostic tool in clini- electrical currents spread throughout the cal practice. It is especially useful in diagnos- body because the tissues surrounding the ing rhythm disturbances, changes in electrical heart are able to conduct electrical currents conduction, and myocardial ischemia and generated by the heart. When these electri- infarction. The remaining sections of this cal currents are measured by an array of elec- chapter describe how the ECG is generated trodes placed at specific locations on the body and how it can be used to examine changes in surface, the recorded tracing is called an ECG cardiac electrical activity. Ø Onde P, complexe QRS et onde T représentent respecFvement la dépolarisaFon auriculaire, la dépolarisaFon ventriculaire et la R repolarisaFon ventriculaire. 704 Intervalle Ø UNIT PR: of 4 Maintenance temps the Bodynécessaire à l'onde de dépolarisaFon SA node R pour The T wave, caused by ventricular repolari traverser les oreillePes et le nœud lasts about 0.16 s. Repolarization is slower than T so the T wave is more spread out and has a l P AV. P T (height) than the QRS complex. Because atria takes place during the period of ventricular exc Ø Intervalle QT: période Q de representing atrial repolarization is normally S Q S dépolarisaFon large QRS complex being recorded at the same 1 Atrialet repolarisaFon depolarization, initiated by The P-R interval is the time (about 0.16 s) the SA node, causes the P wave. PR ST ventriculaire ning of atrial excitation to the beginning of ve AV node R tion. If the Q wave is visible (which is often QT Ø Segment ST: période isoélectrique, marks the beginning of ventricular excitation, son this interval is sometimes called the P-Q in 0 0.2 0.4 0.6 0.8 tout le ventricule P est dépolarisé. T interval includes atrial depolarization (and con Time (sec) as the passage of the depolarization wave throug FIGURE 2.13 Components of the ECG trace. An enlargement of one of the repeating waveform units Q S conduction system. in the rhythm strip shows the P wave, QRS complex, and T wave, which represent atrial depolarization, During the S-T segment of the ECG, when t ventricular depolarization, and ventricular repolarization, respectively. The PR interval represents the time 2 With atrial depolarization complete, required for the depolarization wave to transverse the atria and the AV node; the QT interval represents 3 tials of the ventricular myocytes are in their pla the impulse is delayed at the AV node. the period of ventricular depolarization and repolarization; and the ST segment is the isoelectric period when the entire ventricle is depolarized. Each small square is 1 mm. entire ventricular myocardium is depolarized. R val, lasting about 0.38 s, is the period from t ventricular depolarization through ventricular Figure 18.17 relates the parts of an ECG to P T Klabunde_Chap02.indd 26 6/11/2011 10:28:41 AM depolarization and repolarization in the heart. Q S HOMEOSTATIC C 3 Ventricular depolarization begins at IMBALANCE 18.5 704 UNIT 4 Maintenance of the Body apex, causing the QRS complex. Atrial In a healthy heart, the size, duration, and timing repolarization occurs. waves tend to be consistent. Changes in the patt SA node R The T wave, caused by ventricular repolarization, R typically the ECG may reveal a diseased or damaged he lasts about 0.16 s. Repolarization is slower than depolarization, with the heart’s conduction system (Figure 18.1 so the T wave is more spread out and has a lower amplitude T an enlarged R wave hints of enlarged ventricles, P (height) than the QRS complex. Because P atrial repolarization T that is elevated or depressed indicates cardiac takes place during the period of ventricular excitation, the wave prolonged Q-T interval reveals a repolarization Q representing atrial repolarization is normallyQ obscured by the S increases the risk of ventricular arrhythmias. ✚ large QRS complex being recorded at the same Stime. 1 Atrial depolarization, initiated by 4 Ventricular depolarization is complete. The P-R interval is the time (about 0.16 s) from the begin- Check Your Understanding the SA node, causes the P wave. ning of atrial excitation to the beginning of ventricular R excita- 10. Cardiac muscle cannot go into tetany. Why? AV node R tion. If the Q wave is visible (which is often not the case), it marks 18 the beginning of ventricular excitation, and for this rea- 11. Which part of the intrinsic conduction system d ventricular myocardial cells? In which direction son this interval is sometimes called thePP-Q interval. TheT P-R T depolarization wave travel across the ventricles P interval includes atrial depolarization (and contraction) as well 12. Describe the electrical event in the heart that o as the passage of the depolarization wave through Q the rest of the of the following: (a) the QRS wave of the ECG; Q S conduction system. S the ECG; (c) the P-R interval of the ECG. 5 Ventricular repolarization begins at During the S-T segment of theapex, ECG, whenthe causing theTaction wave. poten- 2 With atrial depolarization complete, 13. MAKING connections Below are drawings of thr tials of the ventricular myocytes are in their plateau phases, the action potentials. Two of these occur in the hea the impulse is delayed at the AV node. entire ventricular myocardium is depolarized.R The Q-T inter- occurs in skeletal muscle (as you learned in Cha R val, lasting about 0.38 s, is the period from the beginning of ventricular depolarization through ventricular repolarization. Figure 18.17 relates the parts of an ECG P to the sequence T of P T mV mV m depolarization and repolarization in the heart. Q Q S S HOMEOSTATIC C L I N I C A isL 6 Ventricular repolarization Time Time 3 Ventricular depolarization begins at IMBALANCEcomplete. 18.5 (a) (b) (c apex, causing the QRS complex. Atrial repolarization occurs. In a healthy heart, the size, duration, Depolarization and timing of the deflection Repolarization Which one comes from a contractile cardiac mu waves tend to be consistent. Changes in the pattern or timing of skeletal muscle cell? A cardiac pacemaker cell? R the ECG may 18.17 reveal The a diseased or damaged heart or problems Figure sequence of depolarization and 4 state which ion is responsible for the depolariza with the heart’s conduction repolarization of thesystem heart (related Figure to the).deflection 18.18 For example, waves which ion is responsible for the repolarization p T an enlarged of an R ECGwave hints of enlarged ventricles, an S-T segment tracing. For answers, see Ans P that is elevated or depressed indicates cardiac ischemia, and a prolonged Q-T interval reveals a repolarization abnormality that Q S increases the risk of ventricular arrhythmias. ✚ 4 Ventricular depolarization is complete. Check Your Understanding R 10. Cardiac muscle cannot go into704tetany. M18_MARI6971_10_SE_CH18_683-717.indd Why? 18 11. Which part of the intrinsic conduction system directly excites ventricular myocardial cells? In which direction does the 2 P T depolarization wave travel across the ventricles? 12. Describe the electrical event in the heart that occurs during each Q of the following: (a) the QRS wave of the ECG; (b) the T wave of S 5 Ventricular repolarization begins at the ECG; (c) the P-R interval of the ECG. apex, causing the T wave. 13. MAKING connections Below are drawings of three different action potentials. Two of these occur in the heart, and one  06/11/2024 Le cycle cardiaque: événements mécaniques Ø Le cœur se contracte (systole) forçant le sang à sorFr de ses chambres, puis se détend (diastole) permePant à ses chambres de se remplir de sang. Ø Un cycle cardiaque comprend tous les événements associés au flux sanguin dans le cœur au cours d'un baKement cardiaque complet = systole + diastole auriculaires suivies de systole + diastole ventriculaires. Ø Durée 0,8 s = 0,1 s systole auriculaire + 0,3 s systole ventriculaire + 0,4 s relaxaFon Ø L'auscultaFon du thorax révèle 2 sons à chaque baPement: Premier son: les valves AV se ferment (début de la systole ventriculaire) Deuxième son: les valves sigmoÏdes se ferment (début de la diastole ventriculaire). 5 1. Remplissage ventriculaire Ø Le sang revenant de la circulaFon circule passivement à travers les oreillePes. Ø Valvules AV ouvertes et valvules aorFque et pulmonaire fermées. Ø 80% du remplissage ventriculaire se produit passivement. Ø Les oreilleKes se contractent et propulsent le sang résiduel (20%) vers les ventricules. Ø VTD volume télédiastolique = volume maximum de sang contenu dans les ventricules. Ø Les oreilleKes se relâchent pendant le reste du cycle. 6 3  06/11/2024 2a. Systole ventriculaire: contrac*on isovolumétrique Ø Les ventricules commencent à se contracter fermant les valvules AV. Ø La pression ventriculaire augmente. Ø Les ventricules sont des chambres complètement fermées (volume sanguin constant). 7 2b. Systole ventriculaire: éjec*on ventriculaire Ø La pression ventriculaire conFnue d'augmenter. Ø Lorsqu'elle dépasse la pression dans les artères, les valves sigmoïdes sont ouvertes de force. Ø Le sang afflue vers l'aorte et le tronc pulmonaire. 8 4  06/11/2024 3. Relaxa*on isovolumétrique Ø Les ventricules se relâchent. Ø VTS volume télésystolique = volume de sang restant dans les chambres. Ø Le sang de l'aorte et du tronc pulmonaire retourne vers le cœur, fermant les valvules sigmoïdes. Ø Les ventricules sont de nouveau des chambres fermées (volume sanguin constant). 9 Diagramme de Wiggers ouverture incisure valve aorFque fermeture valve aorFque fermeture valve mitrale VTD ouverture VS valve mitrale VTS 10 5  06/11/2024 Rela*on pression-volume ventriculaire: courbe (boucle) pression-volume Aortic Aortic Valve Valve 100 Opening Closing Débit cardiaque (DC) au repos LV Mitral Pressure Valve Mitral Closing (mmHg) Valve Opening QuanFté de sang pompée par le 0 VTD EDV cœur en 1 min = efficacité de la LV 100 Volume VTS ESV pompe cardiaque (ml) 0 a b c d a 200 Volume d’éjec*on systolique relaFon ESPVR pression-volume Aortic télésystolique VS = VTD – VTS = 130 – 60 = 70 mL Valve Aortic Closing Valve LV c Opening Pressure 100 DC = fréquence (72 baP/min) x VS (mmHg) d Mitral Mitral VS SV Valve (70 mL/baP) = 5040 mL/min Valve Closing Opening b a EDPVR 0 relaFon pression-volume télédiastolique 0 100 200 VTS ESV VTD EDV LV Volume (ml) 11 Facteurs influençant le volume d’éjec*on systolique Klabunde_Chap04.indd 68 6/10/2011 10:49:39 PM 12 6  06/11/2024 1. Effets de la précharge sur le volume d’éjec*on systolique 70Précharge = éFrement des CARDIOVASCULAR myocytesCONCEPTS PHYSIOLOGY cardiaques avant la contracFon, proporFonnel à la compliance de la chambre cardiaque. by the compliance of the ventricle, in which is, the ventricle becomes less compliant or compliance is defined as the ratio of a change “stiffer” at higher volumes. in volume divided by a change in pressure. Nor- Ventricular compliance is determined by Compliance = rapport entre mally, compliance curves are plotted with vol- Compliance the physical properties of the =tissues Capacité avec mak- ume on thedeY-axis un changement volumeandetpressure on the X-axis, ing up the ventricular wallune laquelle andchambre the state of so that the compliance is the slope of the ventricular relaxation. For example, in ven- le changement de pression cardiaque se dilate lorsqu'elle line at any given pressure (i.e., the slope of tricular hypertrophy, the increased muscle correspondante the tangent(slope = at a particular point on the line). thickness decreasesest theremplie d'un volume ventricular compli-de pente). For the ventricle, however, it is common to sang. ance; therefore, ventricular end-diastolic plot pressure versus volume (Fig. 4.5) and pressure is higher for any given EDV. This as volume increases Paroi to refer to this pressure–volume relationship is shown in Figure 4-5, in which the filling fine as the filling curve for the ventricle. Plotted curve of the hypertrophied ventricle shifts in this manner, the slope of the tangent at a upward and to the left. From a different per- given point on the curve is the reciprocal of spective, for a given end-diastolic pressure, the compliance. Therefore, the steeper the a less compliant ventricle will have a smaller slope of the pressure–volume relationship, EDV (i.e., filling will be decreased). If ven- the lower the compliance. This means that tricular relaxation (lusitropy) is impaired, Paroi as the ventricle becomes “stiffer” when the slope occurs in some forms of diastolic ventricular épaisse of the passive filling curve is greater; there- failure (see Chapter 9), the functional ven- fore, compliance and stiffness are reciprocally tricular compliance will be reduced. This will related. impair ventricular filling and increase end- 13 The relationship between pressure and diastolic pressure. If the ventricle becomes volume is nonlinear in the ventricle (as in chronically dilated, as occurs in other forms most biological tissues); therefore, compli- of heart failure, the filling curve shifts down- ance decreases with increasing pressure or ward and to the right. This enables a dilated volume. When pressure and volume are plot- heart to have a greater EDV without causing a ted as in Figure 4.5, we find that the slope large increase in end-diastolic pressure. of the filling curve (the EDPVR described in The length of a sarcomere prior to contrac- Fig. 4.4) increases at higher volumes; that tion, which represents its preload, depends on Courbes de compliance (ou de remplissage) ventriculaire gauche 100 AugmentaFon de l'épaisseur musculaire Decreased LV Compliance Pressure (e.g., hypertrophy) (mmHg) 50 Increased Compliance Normal (e.g., dilation) Pression (EDP) télédiastolique 0 0 100 200 300 VTS (EDV) LV Volume (ml) FIGURE 4.5 Left ventricular compliance (or filling) curves. The slope of the tangent of the passive pres- sure–volume curve Ø at a1/compliance = pentethe given volume represents dereciprocal la tangente of thede la courbe ventricular compliance. The slope of the normal compliance curve is increased by a decrease in ventricular compliance (e.g., ventricular hypertrophy), whereaspression-volume. the slope of the compliance curve is reduced by an increase in ventricular compli- ance (e.g., ventricular dilation). Decreased compliance increases the end-diastolic pressure (EDP) at a given end-diastolic volume (EDV), whereas increased compliance decreases EDP at a given EDV. LV, left ventricle. Ø RelaFon pression-volume non linéaire è ventricule moins souple ("plus rigide") à des volumes plus élevés. 14 Klabunde_Chap04.indd 70 6/10/2011 10:49:40 PM 7  example, a stiff, hypertrophied ventricle may solution. One end of the muscle is attached have an elevated end-diastolic pressure with to a force transducer to measure tension, and a reduced EDV owing to the reduced compli- the other end is attached to an immovable ance. Because the EDV is reduced, the sar- support rod (Fig. 4.6, left side). The end that comere length will be reduced despite the is attached to the force transducer is mov- increase in end-diastolic pressure. As another able so that the initial length (preload) of example, a larger than normal EDV may not the muscle can be fixed at a desired length. be associated with an increase in sarcomere length if the ventricle is chronically dilated The muscle is then electrically stimulated to contract; however, the length is not permit- 06/11/2024 and structurally remodeled such that new ted to change and therefore the contraction sarcomeres have been added in series, thus is isometric. maintaining normal individual sarcomere If the muscle is stimulated to contract lengths. at a relatively short initial length (low preload), a characteristic increase in tension Effects of Preload on Tension (termed “active” tension) will occur, last- Development (Length–Tension ing about 200 milliseconds (Fig. 4.6, right side, curve a). By stretching the muscle to Effets de la précharge sur le développement de la tension Relationship) a longer initial length, the passive tension We have seen how ventricular EDV, which will be increased prior to stimulation. The CHAPTER 4 CARDIAC FUNCTIO is determined by Barre ventricular mobileend-diastolic pour ajuster laamount of passive tension depends on the longueur musculaire iniFale Increased Increased Resting Preload Tension Length c Preload Resting For curve c Transducer Stimulate Increased 72 CARDIOVASCULAR PHYSIOLOGY CONCEPTS Length Preload Tension b Active Bande elastic isolée modulus (“stiffness”) of the tissue. deelastic The muscle Muscle L !L modulus of a tissue is related to Total Tension Total B dL/dt the ability of a tissue to resist deformation; a cardiaque DL Length therefore, the higher the elastic modulus, Passive Muscle DL Tension the “stiffer” the tissue. When the muscle is stimulated at theTige increased Fixed immobile preload, there Time A will be a larger increase in active tension (curve FIGURE b)4.6than had occurred Effects of increased at the preloadlower on tension development by an isolated strip of cardiac muscle. Passive Les augmentaFons The left side preload. If shows the preload de muscle how précharge is again length entraînent and increased, tension are measuredune augmentaFon cdeTension in vitro. The bottom lathe of tension muscle stripacFve. Resting CARDIOVASCULAR Tension isthere fixed will to anbe acFve immovable bar=that rod, whereas a further increase in active tension totale Load the top - tension of the muscle passive is connected a b to a tension transducer and Length 72 atension PHYSIOLOGY movable CONCEPTS(curve c).can be used Therefore, toincreases adjust initial in muscle length (L). The right side shows how increased Contrac preload preload(initial lead tolength) increases both tension. passive and active (developed) tension. The greater the preload, the an increase in active Leng elastic modulus (“stiffness”) of the Not greater tissue. the active tension generated by the muscle. only is the magnitude of active tension Total Active A B The elastic modulus of a tissue is related to increased, but also the rate of active tension Tension Tension the ability of a tissue to resist deformation; Time Tension therefore, the higher the elastic modulus, development (i.e., the maximal slope with respect is to time of the tension curve during Tension the “stiffer” the tissue. When the muscle stimulated at the increased preload,contraction). there The duration of contraction will be a larger increase in active tension FIGURE 4.8 Effects of c increased initial muscle length (increased preload) on muscle shorte and the time-to-peak tension, however, are (curve b) than had occurred at the lower not changed. Passive (isotonic contractions). b The left panel shows a muscle lifting a load (afterload) at two differen preload. If the preload Klabunde_Chap04.indd is again increased, 71 c lengths (A and B). The right panel shows6/10/2011 10:49:41 PM how increasing the preload leads to increased short If the results shown in Figure b 4.6 areTension plot- there will be a further increase in active a a and increased velocity of shortening (dL/dt; change in length with respect to time). The musc tension (curve c). Therefore, increases ted as in tension versus initial length (preload), a length–tension diagram is generated preload lead to an increase in active tension. to the same minimal length when preload is increased. Not only is the magnitude of active tension (Fig. 4.7). In the top panel, the passiveActive ten- Length 15 increased, but also the rate of active tension Tension sion curve is the tension that is generated Tension development (i.e., the maximal slope with FIGURE 4.7 Length–tension relationship for respect to time of the tension curve as duringthe muscle is stretched prior to contrac- cardiac muscle undergoing isometric contraction. contraction). The duration of contraction tion. Points a, b, and c on the passive curve The top panel shows that increasing the preload and the time-to-peak tension, however, correspond to the passive tensions and ini- are c length from points a to c increases the passive b a, b, and c in tension. Furthermore, increasing the preload not changed. tial preload lengths for curves If the results shown in Figure 4.6 are plot- isolated increases muscles, the total cancontraction tension during be applied as to the whole ric ventricular pressure developm Figure 4.6 prior to acontraction. The total ted as tension versus initial length (preload), tension curve represents the maximal tension heart. By substituting ventricular shown by arrows a, b, and c, which correspond to active tension changes depicted by curves a, b, volume for during ventricular contraction, a length–tension diagram is generated (Fig. 4.7). In the top panel, the passive that ten-occurs during contraction Lengthat different length and c in Figureand ventricular 4.6. The pressure length of the arrow active tension, which is the difference between is the for tension, to what is observed with a sing sion curve is the tension that is generated initial preloads. FIGUREThe total tensionrelationship curve isforthe as the muscle is stretched prior to contrac- cardiac 4.7 Length–tension muscle undergoing thetotallength–tension the and passive tensions. The relationship bottom panel becomes a muscle (see Fig. 4.7). This can sum of the passive tension andisometric contraction. the additional shows that the active tension increases to a tion. Points a, b, and c on the passive curve correspond to the passive tensions and ini- tension The top panel shows that increasing the preload generated length from during points a tocontraction c increases the (active passive pressure–volume maximum relationship value as preload increases. for the ven- experimentally in the ventricle b tial preload lengths for curves a, b, and tension). c in tension. The Furthermore, active tension, increasingtherefore, the preload is increases the total tension during contraction as tricle. This can be done because a quantita- the aorta during ventricular co Figure 4.6 prior to contraction. Thethe difference total shown by between arrows a, b,theandtotal and c, which passiveto correspond Effets de l'augmenta*on du volume ventriculaire (précharge) tension curve represents the maximal tension that occurs during contraction at different active tension changes depicted by curves a, b, tension curves; it is plotted separately in the and c in Figure 4.6. The length of the arrow is the tive relationship exists between tension and different ventricular volumes and bottom panel initial preloads. The total tension curve is the of Figure active tension, which 4-7. The active is the difference ten- between pressure (i.e., with noand changebetween in length). length Cardiac and volume the peak systolic pressure gener sur le développement de la pression ventriculaire. the total and passive tensions. The bottom panel muscle fibers, however, normally shorten sion diagram demonstrates that as preload sum of the passive tension and the additional tension generated during contraction increases, (active shows that the active tension increases to a there value maximum is asanpreload increase increases. in active that they when is determined by the contract (i.e., undergo geometry of the isotonic ventricle under this isovolumetri tension). The active tension, therefore, tension is up to a maximal limit. The maxi- ventricle. IfFigure contractions). a strip of4.9 shows cardiac musclethatin as ventricu- The peak systolic pressure curve i the difference between the total and passivemal active tension in cardiac muscle corre- vitro is set at a given preload length and stim- tension curves; it is plotted separately in the lar EDV increases, an increase in isovolumet- to the ESPVR shown in Figure 72 CARDIOVASCULAR PHYSIOLOGY CONCEPTS bottom panel of Figure 4-7. The active ten- sponds to(i.e., a sarcomere length of about 2.2 with no change in length). Cardiac ulated to contract, RelaFon pression-volume it will shorten and then this is the maximal pressure that sion diagram demonstrates that as preload µm. Because muscleof the passive fibers, however,mechanical normally prop- shorten return to its resting preload length (Fig. 4.8). increases, there is an increase in erties active of cardiac myocytes, theirundergo lengthisotonic sel- If the initial preload is increased and the mus- elastic modulus (“stiffness”) of the tissue. when they contract (i.e., erated by the ventricle at a given tension up to a maximal limit. Thedom maxi-exceeds 2.2 µm Ifatamaximal contractions). Total strip of cardiac muscle in cle stimulated again, it will ordinarily shorten ventricular Peak-Systolic The elastic modulus of a tissuemal is related to in cardiac muscleEDVs. active tension corre- vitro is set at a given preload length and stim- to the same minimal Tension length, albeit at a higher volume. the ability of a tissue to resist deformation; sponds to a sarcomere length of about 2.2 ulated to contract, it will shorten and then velocity of shortening. Pressure This discussion return to itsdescribed howlength changes in What mechanisms are Ventricular µm. Because of the passive mechanical prop- resting preload (Fig. 4.8). Pressure therefore, the higher the elastic modulus, preload The length–tension relationship, although erties of cardiac myocytes, their length sel- affect the force If the initial preloadgenerated is increasedby andcardiac the mus- for the increase in force gene Tension the “stiffer” the tissue. When the dommuscle is µm at maximal ventricular exceeds 2.2 muscle ficle bers duringagain, stimulated isometric contractions it will ordinarily shorten usually used to describe the contraction ofDeveloped stimulated at the increased preload, EDVs. there to the same minimal length, albeit at a higher c Pressure increased preload in the heart? will be a larger increase in active Thistension discussion described how changes in velocity of shortening. preload affect the force generated by cardiac (curve b) than had occurred at the lower The length–tension relationship, although b it was thought that changes in muscle fibers during isometric contractions usually used to describe Passive the contraction of preload. If the preload is again increased, c Tension a End-Diastolic sion caused by altered preload there will be a further increase in active a b Pressure explained by the overlap of acti tension (curve c). Therefore, increases in Klabunde_Chap04.indd 72 6/10/2011 10:49:41 PM sin and therefore by a change in preload lead to an increase in active tension. Length Ventricular Volume Not only is the magnitude of active 72 Klabunde_Chap04.indd tension Active 6/10/2011 10:49:41 PM of actin and myosin cross brid increased, but also the rate of active tension Tension FIGURE 4.9 Effects of increasing ventricular (see Chapter 3). However, unl Tension development (i.e., the maximal slope with respect to time of the tension curve during volume (preload) on ventricular pressure develop- muscle that can operate under contraction). The duration of contraction ment. Increasing ventricular volume from a to c c and then stimulating the ventricle to contract range of sarcomere lengths (1.3 and the time-to-peak tension, however, are not changed. b isovolumetrically increases the developed pressure the intact heart under physiol If the results shown in Figure 4.6 are plot- a and the peak-systolic pressure. tions operates within a narrow ted as tension versus initial length (preload), 16 a length–tension diagram is generated (Fig. 4.7). In the top panel, the passive ten- Length sion curve is the tension that is generated FIGURE 4.7 Length–tension relationship for as the muscle is stretched prior to contrac- cardiac muscle undergoing isometric contraction. tion. Points a, b, and c on the passive curve The top panel shows that increasing the preload correspond to the passive tensions and ini- length from points a to c increases the passive tension. Furthermore, increasing the preload tial preload lengths for curves a, b, and c in increases the total tension during contraction as Klabunde_Chap04.indd 73 Figure 4.6 prior to contraction. The total shown by arrows a, b, and c, which correspond to tension curve represents the maximal tension active tension changes depicted by curves a, b, and c in Figure 4.6. The length of the arrow is the that occurs during contraction at different initial preloads. The total tension curve is the active tension, which is the difference between the total and passive tensions. The bottom panel 8 sum of the passive tension and the additional shows that the active tension increases to a tension generated during contraction (active maximum value as preload increases. tension). The active tension, therefore, is the difference between the total and passive tension curves; it is plotted separately in the bottom panel of Figure 4-7. The active ten- (i.e., with no change in length). Cardiac sion diagram demonstrates that a