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During ejection of blood, the aortic and pulmonic valves are open; they prevent backflow to the ventriclesduring cardiac filling. Valvular opening and closing areaccomplished by passive responses of the valves to pressuregradients.The four-chambered heart of mammals and birds is anevolutionary adaptation to prevent mixing of oxygenated blood returning to the heart from the lungs with deoxygenated blood returning from the systemic circulation.
Theefficiency of the series circulation created by this adaptation isconsistent with the high metabolic rate and warm-bloodednature of these species. Some reptiles also have four-chamberedhearts. Amphibians have a dual circulation with a threechambered heart; the muscular ventricle is not separated intotwo pumps. In contrast to the dual circulation made possibleby four chambers, fish have a single circulation and a twochambered heart.CONDUCTION SYSTEM OF THE HEARTEffective ejection of blood from the heart requires coordinated contraction and relaxation of the chambers. At rest,this cycle occurs approximately 70 times per minute, andto accomplish this, the sinoatrial (SA) node acts as thepacemaker, initiating the depolarization of the heart.98Cardiovascular PhysiologyDepolarization spreads from the SA node across the atria,depolarizing atrial muscle and initiating atrial contraction(Fig.
8.3). The atrioventricular (AV) node is the only pathwayfor spread of the depolarization to the ventricle. Electricalconduction through the AV node is slow, allowing atrial con-■CLINICAL CORRELATECardiac Structural Changes in DiseaseThe normal structure of the heart may be altered in valvulardisease, systemic or pulmonary hypertension, heart failure, andother diseases. Common pathologies affecting cardiac structureinclude the following:■traction to accomplish the final filling of the ventricles. Next,depolarization reaches the bundle of His, and depolarizationproceeds rapidly through the left and right bundle branchesto the Purkinje fibers and ventricular muscle, producingventricular contraction.■Aortic stenosis (narrowing of the aortic valve): Left ventricularhypertrophy occurs in response to the greater work performedby the ventricle.Mitral incompetence: Left atrial dilation may develop as a resultof the elevation of left atrial pressure and volume caused bymitral regurgitation (leakage of blood back into the atriumfrom the left ventricle).Pulmonary hypertension: Right ventricular hypertrophy mayoccur in response to the chronically increased work of the rightventricle.Mitral insufficiency: Mitral valve viewed from below;marked shortening of posterior cusp, with only slightcommissural fusion, and little fusion and shorteningof chordae tendineaeIn time,left ventricledilates toaccommodateincreasedvolume.Shortened,thickenedmitral cuspsCardiac Structural Changes in Mitral Regurgitation Incompetence of the mitral valve results inregurgitation of blood into the left atrium during systole.
Chronic mitral regurgitation results in left atrialenlargement and left ventricular dilation.Left atrialenlargementdue to mitralregurgitationOverview of the Heart and CirculationA. Volume distributionB. Distribution of vascular resistanceVeins(64%)Small arteriesand arterioles(47%)Brain:Q = 13%VO2 = 21%Lungs (9%)Capillaries(27%)Largearteries(19%)Capillaries (5%)Small arteriesand arteriolesHeart in diastole (7%)(8%)Large arteries (7%)Pulmonaryartery pressure:25/10 mm Hg(mean pressure15 mm Hg)Veins(7%)LungsLARALVRVAortic pressure: 120/80 mm Hg(mean pressure95 mm Hg)Coronarycirculation:Q = 4%VO2 = 11%Liver and gastrointestinal tract:Q = 24%VO2 = 23%Low-pressuresystem(reservoir function)Skeletalmuscle:Q = 21%VO2 = 27%High-pressuresystem(supply function)Kidney:Q = 20%VO2 = 7%Skin and other organsQ = 18%VO2 = 11%.Figure 8.1 General Scheme of the Circulation .
The distribution of flow Q to various organs aspercentage of cardiac output and the utilization of oxygen V O2 relative to total O2 consumption are illustrated.The pie charts show distribution of blood volume throughout the system (A) and the distribution of vascularresistance as a percentage of total resistance (B).
The greatest volume of blood in the cardiovascular systemis in the systemic veins. The greatest resistance to flow occurs in small arteries and arterioles. All values inthe figure are those observed at rest; these are adjusted to meet changes in physiological requirements, forexample during exercise.99Mitral valveMitral valvePulmonarytrunkOrifices of coronary arteriesL. pulmonaryveinsL.
atriumR. pulmonaryveinAscending aortaAscending aortaR. atriumAortic valveAortic valveOutflow topulmonary trunkSuperiorvena cavaR. ventricleAtrioventricularseptumPapillarymuscle (cut)R. atriumL. ventricleTricuspid valveR. ventriclePapillary musclesInterventricularseptumL. ventriclePlane of sectionFigure 8.2 Structure of the Heart The muscular left ventricle pumps blood into the high-pressure systemic circulation, and the less muscularright ventricle pumps blood into the lower pressure pulmonary circulation. The mitral and tricuspid valves prevent backflow of blood into the atria,while the aortic and pulmonic valves prevent regurgitation of blood from the aorta and pulmonary artery to the ventricles.AortaA. Right sideAtrioventricular septumSuperior vena cavaPulmonary valveAtrioventricular (AV) nodeSA nodeCommon AV bundle (His)Internodal tractsFigure 8.3Purkinje fibers“Bypass” fibersConduction System ofthe Heart Contraction of cardiac muscleis initiated by electrical depolarization.
Thepacemaker for this electrical activity is in thesinoatrial (SA) node. Impulses travel fromthe SA node through internodal conductingpathways to the atrioventricular (AV) node,and then spread through the His-Purkinjesystem of the ventricle. The bypass fibersand Kent bundle are not normally part of theconducting system but may play a role inpathologic states.Right bundle branchAccessory bundleof KentInferior vena cavaAnnulus of tricuspid valveAortaB.
Left sideAtrioventricular septumAortic valvePulmonary trunkSuperior vena cavaLeft bundle branchAnterior papillarymusclePurkinje fibersR. pulmonaryveinsMitral valve (cut away)Interventricular septumPosterior papillarymuscle101CHAPTER9Cardiac ElectrophysiologyCells of the heart, like other excitable cells, have the ability togenerate action potentials. These action potentials and theirconduction throughout the heart are the basis of the rhythmiccontraction and relaxation of the heart; the conduction ofaction potentials in the heart is recorded on the surface of thebody as the electrocardiogram.■■CARDIAC ACTION POTENTIALSIn a normal heart, the pacemaker activity of the sinoatrial(SA) node produces a resting heart rate of approximately 70beats per minute.
The SA node is a group of specialized, noncontractile cardiomyocytes in the wall of the right atrium,adjacent to the opening of the superior vena cava. The restingmembrane potential of SA node cells is initially around−60 mV, but the cells undergo gradual, spontaneous depolarization, due to an inward current, if, mainly carried by Na+;an inward Ca2+ current, iCa; and reduced activity of an outwardK+ current. The diastolic depolarization resulting from theinward currents is responsible for the pacemaker activity ofthe SA node cells. Once threshold is reached, the upstroke ofthe action potential occurs, due to opening of T-type and Ltype Ca2+ channels (Fig. 9.1). Repolarization is caused byincreased conductance of K+ and closing of Ca2+ channels,completing the pacemaker cycle.
Action potentials of atrioventricular (AV) node cells, found in the atrial septum at thejunction of the atria and ventricles, are similar to those in theSA node, although the pacemaker activity of these cells isslower, overridden in normally functioning hearts by SA pacemaker activity.In contrast to SA and AV nodal cells, depolarization of othercardiac cells is largely dependent on Na+ influx rather thanCa2+ influx. Action potentials of ventricular and atrial myocytes and cells of the His-Purkinje system are characterized byfive distinct phases (see Fig.
9.1):■Phase 4 (the resting membrane potential): The restingmembrane potential of these cells is mainly a functionof K+ efflux and is close to the Nernst potential for K+.During phase 4, ion concentrations that were altered bythe previous action potential are restored to restinglevels by the Na+/K+-ATPase and a Na+/Ca2+ exchanger,as well as an ATP-dependent Ca2+ pump.■■Phase 0 (upstroke of the action potential): Rapid depolarization occurs when the cells reach threshold and fastchannels for Na+ open. This is accompanied by reducedconductance of the inwardly rectified K+ current (iK1).The rapid upstroke results in rapid spread of depolarization through most of the conducting system of the heart.Phase 1 (rapid repolarization to the plateau): This phaseis caused by inactivation of Na+ channels and openingof voltage-sensitive K+ channels, producing a transientoutward K+ current (iTO).Phase 2 (the plateau): The membrane remains depolarized during the plateau due to opening of voltagesensitive, slow L-type Ca2+ channels and inward currentof Ca2+.
Simultaneously, an outward K+ current occursthrough a voltage-dependent K+ channel (delayed rectifier K+ channel).Phase 3 (repolarization): Gradual inactivation of theL-type Ca2+ channels leads eventually to activation of K+channels, causing rapid repolarization, substantially dueto an inwardly rectified K+ current (iK1).The plateau of the action potential is functionally important,because it normally prevents premature depolarization ofcardiac cells and associated arrhythmias. There is an effectiverefractory period, beginning with phase 1 and extendingthrough the plateau and much of phase 3, during whichanother action potential cannot be generated. This is followedby the relative refractory period, which lasts until the restingmembrane potential is fully restored; during this period, it ismore difficult to elicit another action potential than in aresting cell.During the conduction of the wave of depolarization of theheart, forward propagation occurs as a result of the localChronotropic, dromotropic, and inotropic effects arethose that alter heart rate, conduction velocity, and myocardial contractility, respectively.
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