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Note thestaircase-like increase in the force of contraction when frequency (heartrate) is increased. Because this effect is not dependent on changes inresting fiber length, contractility (inotropism) is increased.sympathetic nerves, which release norepinephrine. Norepinephrine, through binding to β-adrenergic receptors (β1),produces elevation of intracellular free Ca2+ levels, resulting inincreased contractility of the heart. This is a true increase ininotropism or contractility, because it is independent of anychange in preload. Release of epinephrine by the adrenalmedulla may also produce greater contractility of the heart,although levels of circulating epinephrine rarely reach levelsthat significantly affect inotropic activity.
The parasympathetic nervous system has only limited effects on contractilityof human ventricles. Clinically, a number of drugs are usedto promote inotropism in heart failure patients, includingdigitalis, dopamine, and dobutamine. Although the basiccardiac function curve simply describes the effects of preloadon cardiac output or stroke volume, the slope of this curve isa measure of inotropism. With sympathetic stimulation, theslope is steeper, indicating enhanced contractility.Treppe, also known as the staircase effect, is an intrinsicmechanism for regulation of stroke volume. When cardiaccontractions are infrequent, force of contraction is reduced;as heart rate increases, force of contraction is elevated(Fig.
11.4). Because these changes occur independently ofchanges in preload, they reflect a change in contractility. Theincreased contractility at higher heart rates is associated withelevated free intracellular Ca2+ in myocardial fibers.During a baroreceptor-mediated response to a fall in arterialpressure (see Fig. 11.2), many mechanisms contribute to thechange in cardiac output. Sympathetic activation elevatesheart rate, as discussed previously, but unless mechanisms areavailable for maintaining or elevating stroke volume simulta-The Cardiac Pumpneously, elevation of heart rate is not an effective mechanismfor raising cardiac output, because filling time for the heart isreduced. By raising contractility of the heart, sympathetic activation enhances stroke volume as well, and, simultaneously,sympathetic constriction of the systemic venous system elevates preload of the heart, allowing the Frank-Starling relationship to further augment stroke volume and cardiacoutput.119VmVelocity of shorteningIncreased preloadASSESSMENT OF CARDIAC FUNCTIONForce–Velocity CurvesAAfterloadVmIncreased contractilityVelocity of shorteningAssessment of cardiac function and, in particular, inotropismis important both clinically, in heart failure patients, andexperimentally.
In addition to analysis of the cardiac functioncurve and its slope, analysis of the force–velocity relationshipin cardiac muscle illustrates the effects of preload and alteredcontractility on cardiac function (Fig. 11.5). Experimentally,force–velocity curves are usually constructed by measuringvelocity of contraction of isolated segments of cardiac muscleagainst various afterloads. When velocity of contraction isplotted against afterload, an inverse relationship is revealed:when the force of contraction is higher (i.e., when the musclecontracts against higher afterload), velocity of shortening isreduced. Maximum force of contraction occurs at zero velocity, that is, during an isometric contraction.
On the otherhand, velocity is highest (Vm) at zero afterload. Changes inpreload produce a family of curves, all with the same y-intercept (the same maximum velocity of contraction at zero afterload). These curves are another manifestation of theFrank-Starling relationship: greater preload generally resultsin greater force of contraction, and thus velocity of contraction, although Vm is unchanged. Vm is a measure of thecontractile state of the tissue, representing the maximalrate at which actin and myosin filaments can interact toproduce contraction. In contrast to the effects of changes inpreload, positive inotropic influences such as sympatheticstimulation change Vm. The force–velocity curve is shiftedupward and to the right, with an increase in the maximal forcethat can be developed by the muscle (during an isometriccontraction, at the x-intercept) and an increase in Vm (at they-intercept).
An increase in Vm is indicative of a positiveinotropic effect.BAfterloadFigure 11.5 Force–Velocity Relationship in Cardiac MuscleForce–velocity curves depict the effect of afterload on velocity of contraction of cardiac muscle. A, When the force of contraction is higher(i.e., when the muscle contracts against higher afterload), velocity ofshortening is reduced. Velocity is highest (Vm) at zero afterload.
Increasedpreload shifts the curve upward, but Vm, a measure of contractility, isunchanged. B, Positive inotropic influences such as sympathetic stimulation change Vm. The force–velocity curve is shifted upward.beat. The shape and the area within this loop are affected bychanges in preload, afterload, and contractility.Pressure–Volume RelationshipEjection FractionThe ventricular pressure–volume loop is a continuous measurement of ventricular volume against ventricular pressureduring the cardiac cycle (Fig. 11.6). During the period of isovolumetric contraction, volume is constant, but pressure risesrapidly. During the ejection phase of the cycle, volume falls,while pressure remains high. Subsequently, during isovolumetric relaxation, volume is constant and pressure fallsrapidly.
This cycle is then repeated over and over, with eachA simple and useful measurement for assessment of myocardial function is the ejection fraction. Ejection fraction is theratio of stroke volume to end-diastolic volume. In a healthyperson at rest, this should be greater than 50%. If a positiveinotropic drug is administered, ejection fraction will rise; inmyocardial ischemia or heart failure, ejection fraction isdiminished. Ejection fraction can be estimated noninvasivelyby echocardiography.120Cardiovascular PhysiologyCLINICAL CORRELATEEchocardiographyEchocardiography is a technique in which inaudible, highfrequency sound is transmitted through the thorax (transthoracicechocardiography) or esophageal wall (transesophageal echocardiography) into the heart. The echoes of the ultrasound, reflectedat the interfaces of tissue and fluid, are recorded to produce agraphic image of the heart.
In standard echocardiography, theresulting echocardiogram is a two-dimensional image of a slice ofthe heart. In Doppler echocardiography, the use of continuouswave Doppler ultrasound allows assessment of the velocity ofblood flow within the heart. Using these techniques, it is possibleto determine size and structure of valves and chambers; todetermine ejection fraction and other parameters; and to detectabnormal wall motion, valvular regurgitation (leakage) or narrowing, bacterial growths (vegetation) within the heart, and otherpathologies.Transducer Positions in Echocardiographic ExaminationParasternal positionLong-axis planeNormal long-axis view during systoleShort-axis planeLeft parasternal position allows views in longand short-axis planes.
Tilting transducer allowsmultiple sections.Apical positionNormal short-axis view at mitral valve levelLong-axis planeTwo-chamber plane90⬚Normal apical long-axis view45⬚Transverse (four-chamber, five-chamber) planeApical studies imaged from point of maximal impulsetoward base. Four-chamber plane passes throughatrioventricular valves; upward tilt gives five-chamberplane. Counterclockwise rotation of 45⬚ givestwo-chamber plane.
90⬚ rotation gives long-axis plane.Normal apical four-chamber viewThe Cardiac Pump121120100ClosePressure(mm Hg)Aorticvalve OpenStrokevolume40neOp200Mitralvalve Close15050Ventricular volume (mL)Preload( venous return)Afterload( arterial pressure)Cardiac outputContractilityCardiac output12012010010080806060Strokevolume4020200Strokevolume4050100015050100150Cardiac output1201008060Strokevolume4020050100150Figure 11.6 Ventricular Pressure–Volume Loop A continuous plot of ventricular volume and ventricular pressure during the cardiac cycle yields a closed loop. Following the red arrows from the bottomleft of the top graph, during diastole, filling of the ventricle occurs with little change in pressure; during isovolumetric contraction, volume is constant, but pressure rises rapidly. During the ejection phase of the cycle,volume falls, while pressure remains high. During isovolumetric relaxation, volume is constant and pressurefalls rapidly, to the starting point on the diagram.
Changes in preload, afterload, and contractility affectstroke volume as illustrated.VASCULAR FUNCTION AND CARDIAC OUTPUTRegulation of cardiac output depends not only on adjustmentof heart rate and stroke volume, but also on regulation of thefunction of veins and venous return.
Venous return is definedas the flow returning to one side of the heart. Thus, sincecardiac output is defined as flow from one ventricle, thenormal value for venous return will be identical to cardiacoutput when averaged over time. If cardiac output is 5 L/min,venous return will also be 5 L/min. Matching of cardiac outputand venous return is an important aspect of cardiovascularfunction.Just as cardiac output is affected by various factors, sois venous return. Flow from the capillaries to the rightatrium occurs despite a small pressure gradient. Because this122Cardiovascular Physiologypressure gradient is small, venous return is affected by factorsthat are often different from those affecting the arterialsystem.Cardiac output and venous return can be conceptualizedas two sides of the same coin, cardiac output being theflow from one side of the heart and venous return being theflow back to one side of the heart.
Measured over time, cardiacoutput and venous return must be equal, since cardiac outputis completely dependent upon return of blood to the heart(venous return). A change in one of these parameters willproduce an equivalent change in the other.Venous Compliance and Gravitational EffectsAn important factor affecting veins is compliance (the changein volume associated with a change in pressure). Complianceof veins is approximately 20-fold greater than that of arteries.Thus, when a person stands from a recumbent position, bloodpools in the lower extremities as veins distend due to thehydrostatic pressure associated with the column of bloodbetween the lower extremities and the right atrium.
Cardiacoutput is transiently reduced upon standing as pooling occurs.To prevent orthostatic hypotension (decrease in blood pressure upon standing) and to restore venous return under theseconditions, the most important compensatory mechanism isthe baroreceptor reflex (see Fig. 11.2). Increased sympatheticoutflow results not only in constriction of the arteries andaugmentation of rate and contractile force of the heart, butalso constricts veins, reducing the pooling effects of gravity.Veins, in fact, act as a reservoir of blood, which can be mobilized by sympathetic nervous system activation and venoconstriction, to increase venous return and, thus, cardiac output.This is an important mechanism in maintaining cardiacoutput during volume depletion as well.
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