1、第八版南京医科大学生理学系 戈应滨朱大年 王庭槐44个腔室2 心房2 心室隔断(Septum)房间隔 室间隔基底部心尖部房室瓣=AV valves右侧=三尖瓣左侧=二尖瓣乳头肌及腱索防止瓣膜外翻半月瓣（Semilunar valves）主动脉瓣肺动脉瓣顺压力梯度房室瓣开放 心房压 心室压 半月瓣开放心室压 主（肺）动脉压肺循环（Pulmonary circuit）右心血管由心脏到肺脏，再由肺脏到心脏体循环（Systemic circuit）左心血管由心脏到组织，再由组织到心脏心脏的一次收缩和舒张成年人安静时的心率约为成年人安静时的心率约为75 75 次次/min/min，心动周期为，心动周期为
2、0.8 s0.8 s。心房收缩期占心房收缩期占0.1 s0.1 s，舒张期为，舒张期为0.7 s0.7 s。心室收缩期持续心室收缩期持续0.3 s0.3 s后，转为心室舒张期，约为后，转为心室舒张期，约为0.5 s0.5 s。心房收缩期心房收缩期心房舒张期心房舒张期心室舒张期心室舒张期心室收缩期心室收缩期心室充盈 动脉压 心室压房室瓣开放全心舒张心房收缩心室等容收缩心室收缩 压力增加房室瓣和半月瓣关闭心室内没有血液进出心室射血心室压 动脉压 半月瓣开放心室等容舒张心室舒张 压力降低房室瓣及半月瓣关闭没有血液进出心室声音是由于瓣膜关闭时血液发生湍流第一心音=低音调，时间长房室瓣关闭第二心音=高音
3、调，时间短半月瓣关闭EDV=舒张末期容积=心室舒张末期的血量ESV=收缩末期容积=心室收缩末期的血量SV=每博输出量=每个心动周期心室射出的血量SV=EDV-ESV每博输出量（Stroke Volume）=EDV ESV=130 mL 60 mL=70 mL每次心跳的射血量占心室舒张末期容积的比例射血分数（Ejection Fraction）=每博输出量（SV）/心室舒张末期容积（EDV）=70 mL/130 mL=0.54每分钟一侧心室射出的血量心输出量=SV x 心率（HR）平均射血量=5.5 升u 静息状态下心率为75次/min，搏出量70ml。心输出量为5L左右。强体力劳动时，心率可达
4、180200次/min，搏出量可增加到150ml左右，心输出量可达30L,是静息状态下的。u 训练有素的运动员：8倍以上。调节心率和每博输出量外源性调节和内源性调节外源性 神经和体液 内源性 自身调节基本因素心室肌收缩能力（Ventricular contractility）舒张末期容积（End-diastolic volume）后负荷（Afterload）回心血量增加心室肌收缩力增强每博输出量增加Length=EDVTension=SVEDV增加 心肌纤维拉长接近最适初长度肌张力增加每博输出量增加心室舒张末期压力=前负荷充盈时间动脉压中心静脉压后负荷=心室射血时的动脉压心肌细胞膜的生物电活动
5、是引起和控制心肌收缩的始因素心肌细胞膜的生物电活动是引起和控制心肌收缩的始因素 正离子内流或负离子外流形成的电流去极化正离子外流或负离子内流形成的电流复极化或超极化物理学名词，电流易向一个方向流动，而不易向反方向流动超极化通透性去极化通透性Five phasesPhase 0 increased permeability to sodiumPhase 1 decreased permeability to sodiumPhase 2 increased permeability to calcium,decreased permeability to potassiumPhase 3 incr
6、eased permeability to potassium,decreased permeability to calcium Phase 4 resting membrane potentialLong duration of action potential=250-300 msec(only 1-2 msec in skeletal muscle)Autorhythmic cells have pacemaker potentialsSpontaneous depolarizations caused by closing K+channels and opening 2 types
7、 of channelsTwo channels that open:If channels:Na+&K+,net depolarizationCa2+channels:further depolarizationDepolarize to thresholdOpen fast Ca2+channels-action potentialRepolarization Open K+channels 静息电位绝对值或阈电位上移。激活、失活和备用3种状态。激活和失活状态时，无论受多强大的刺激，通道都不能被再次激活而产生动作电位。effective refractory periodrelative
8、refractory periodsupranormal periodobsolute refractory period因为心肌细胞的有效不应期特别长，时间上 正常心脏按窦房结的起搏信号兴奋和收缩，如在有效不应期之后心室或心房受到人工或病理性的额外刺激，产生一次正常节律以外的收缩premature systole。紧接期前收缩之后的窦性兴奋常落在期前兴奋的有效不应期内，不能引起心脏兴奋和收缩，形成一次“脱失”，直到下次窦房结兴奋传来，才引起心房和心室的兴奋和收缩。因而期前收缩之后有一段较长的舒张期compensatory period。Autorhythmic cells that prov
9、ide pathway to spread excitation through the heartPacemaker cellsSpontaneously depolarizing membrane potentials to generate action potentialsCoordinate and provide rhythm to heartbeatConduction fibers Rapidly conduct action potentials initiated by pacemaker cells to myocardiumConduction velocity=4 m
10、eters/secondOrdinary muscle fibers,CV=0.4 meter/secondSinoatrial nodePacemaker of the heartAtrioventricular nodeInternodal pathwaysBundle of HisPurkinje fibersAtria contract first followed by ventriclesCoordination due to presence of gap junctions and conduction pathwaysIntercalated disksJunctions b
11、etween adjacent myocardial cellsDesmosomes to resist mechanical stressGap junctions for electrical couplingInteratrial PathwaySA Node right atrium left atriumRapid Simultaneous contraction right and left atriaInternodal PathwaySA Node AV NodeAV Node TransmissionOnly pathway from atria to ventriclesS
12、low conduction-AV Nodal Delay=0.1 secAtria contract before ventriclesVentricular ExcitationDown Bundle of HisUp Purkinje FibersPurkinje Fibers contact ventricle contractile cellsVentricle contracts from apex up (pacemaker)Fastest depolarizing cells drive all other cells(they are linked together by g
13、ap junctions)=pacemaker=sets pace for entire heart LocationFiring Rate at Rest SA Node 70-80 APs/min AV Node40-60 APs/min Bundle of His20-40 APs/min Purkinje Fibers20-40 APs/minProperties similar to skeletal muscleT tubulesSarcoplasmic reticulum calciumTroponin-tropomyosin regulationProperties simil
14、ar to smooth muscleGap junctionsExtracellular calcium1.Depolarization of cardiac contractile cell to threshold via gap junction2.Opening of calcium channels in plasma membrane3.AP travels down T tubulesRemove calcium from cytosol Ca2+ATPase in sarcoplasmic reticulumCa2+ATPase in plasma membraneNa+-C
15、a2+exchanger in plasma membraneTroponin and tropomyosin return to position covering myosin binding sites on actinNon-invasive techniqueUsed to test for clinical abnormalities in conduction of electrical activity in the heartExternal measure of electrical activity of the heartBody=conductor Currents
16、in body can spread to surface(ECG,EMG,EEG)Distance&litude of spread depends on size of potentials and synchronicity of potentials from other cellsHeart electrical activity-synchronizedLead I:LA(+)and RA(-)Lead II:LL(+)and RA(-)Lead III:LL(+)and LA(-)P wave atrial depolarizationQRS complexvent.dep
17、olarizationT wave vent.repolarizationPQ segment AV nodal delayQT segmentventricular systoleTQ intervalventricular diastoleVentricular action potential recorded from a single contractile cell in the ventricle.ECG surface recording of the summed electrical activity of all cells“Sinus rhythm”=rhythm ge
18、nerated by SA nodeAbnormal Heart Rates:Tachycardia-fastBradycardia-slowSlowed/diminished conduction through AV node occurs in varying degrees1st degree block=slowed conduction through AV nodeIncreases PQ segmentIncreases delay between atrial and ventricular contractionSlowed,sometimes stopped conduc
19、tion through AV node2nd degree block:Lose 1-to-1 relationship between P wave and QRS complexLose 1-to-1 relationship between atrial and ventricular contraction3rd degree block:P wave independent of QRS complexAtrial and ventricular contractions are independentLoss of conduction through AV nodeExtra
20、contractionPAC=premature atrial contractionPVC=premature ventricular contractionLoss of coordination of electrical activityAtrial fibrillation-weaknessVentricular fibrillation-death within minutesArteries carry blood away from heartMicrocirculationArteriolesCapillaries site of exchangeVenulesVeins r
21、eturn blood to heartEndothelial cells line inner layer of all blood vesselsOther components of blood vessel walls can include:Smooth muscleFibrous connective tissueCollagenElastic connective tissueElastinRapid transport pathwayLarge diameter-little resistanceWalls contain elastic and fibrous tissueU
22、nder high pressureStorage site for pressureThick elastic arterial wallsLow complianceExpand as blood enters arteries during systoleRecoil during diastoleMeasure of how the pressure of a vessel will change with a change in volume Low compliance(arteries)Small increase in blood volume causes a large i
23、ncrease in pressureHigh complianceLarge increase in blood volume required to produce large increase in pressureLess than 0.1 mm diameterLittle elastinSmooth muscle regulates radiusFigure 15.10Circulatory system=closed systemPressure=force exerted by bloodFlow occurs from high pressure to low pressur
24、eFlow=D DP/RPressure gradients drive flow from high pressure to low pressureFlow due to pressure gradients=bulk flowHeart creates pressure gradient for bulk flow of bloodA gradient must exist throughout circulatory system to maintain blood flowPressure gradient=driving force=40 mm HgFlow=20 mL/minPr
25、essure gradient=driving force=0 mm HgNo flow because no driving forcePressure gradient=driving force=40 mm HgFlow=20 mL/min(same as 15.1a)Pressure gradient=pressure in aorta minus pressure in vena cava just before it empties into right atriumPressure in aorta=mean arterial pressure(MAP)=90 mm HgPres
26、sure in vena cava=central venous pressure(CVP)=0 mm HgPressure gradient=MAP CVP=90 0=90 mm HgPressure gradient=pressure in pulmonary arteries minus pressure in pulmonary veinsPulmonary arterial pressure=15 mm HgPulmonary venous pressure=0 mm HgPressure gradient=15 0=15 mm HgPressure gradient in syst
27、emic circuit much greater than for pulmonary circuitFlow through both circuits equalFlow=DP/RResistance through pulmonary circuit much less than through systemic circuitRadius of vesselIn arterioles(and small arteries)-can regulate radiusLength of vesselViscosity of fluid=Blood viscosity dependent o
28、n amount of RBCs and proteins R=8 L r4Flow =D DP/R=D DP r4 8 L Regulation of radius of arterioles(and small arteries)Vasoconstriction decrease radius increase resistanceVasodilation increase radius decrease resistancePulmonary circuit less resistance than systemiclower pressure gradient required for
29、 blood flowCombined resistance of all blood vessels within the systemic circuitResistance across a network of blood vessels depends on resistance of all vesselsFlow through network varies with resistanceVasoconstriction in network increase resistance decrease flowVasodilation in network decrease res
30、istance increase flow Flow=cardiac output=CO DP=mean arterial pressure=MAP R=total peripheral resistance=TPRFlow=D DP/RCO=MAP/TPRRegulation of blood flow to organs based on needRegulated by varying resistanceOrgan blood flow=MAP/organ resistanceDriving force across all organs=MAPFlow varies due to d
31、ifferences in resistanceBlood flow changes when resistance changesVascular resistance regulated through changes in radius of arterioles Depends on contractile state of smooth muscle in walls of the vesselLocal factors regulate radius to regulate blood flowIncreased blood flow in response to increase
32、d metabolic activityChanges associated with increased metabolic activity generally cause vasodilationCarbon dioxidePotassium Hydrogen ionsChanges associated with decreased metabolic activity generally cause vasoconstrictionOxygenSteady stateIncreased metabolic rateVasodilation to increase blood flow
33、Increased blood flow provides oxygen,removes carbon dioxideIncreased blood flow in response to a previous reduction in blood flowBlockage of blood flow to tissueMetabolites increase and oxygen decreasesVasodilationRelease blockageIncreased blood flow due to low resistanceMetabolites removed,oxygen d
34、eliveredPressure in the aortaVaries with cardiac cycleSystolic blood pressure=maximum pressureDue to ejection of blood into aortaDiastolic blood pressure=minimum pressureNot zero due to elastic recoilPulse Pressure=SBP DBPMean Arterial Pressure=MAP=(SBP+2DBP)/3Measured BP=SP/DP=110/70 Pulse Pressure
35、=SP DP=110-70=40 mm HgMAP=(SP+(2 x DP)/3=(110+140)/3=83.3 mm HgNo SoundSoundsNo Flow:No Sound13.3 16.0 kPa (100120 mmHg)8.0 10.6 kPa (6080 mmHg)4.0 5.3 kPa (30 40 mmHg)18.6/12.0 KPa(140/90 mmHg)AbsorptionNet filtration=3 L/dayLymphatic system picks up excess filtrate and returns it to circulationSta
36、nding on feet increases hydrostatic pressureInjuriesCapillaries damaged and leak fluid&proteinsHistamine increases capillary permeability to proteinsLiver diseaseDecrease in plasma proteinsKidney diseaseIncrease blood volume,and thus blood pressureDecrease in plasma proteinsHeart diseasePulmonary ed
37、emaSystem of vessels,nodes,and organs.Vessels involved in returning excess filtrate to circulationVessels form open system starting at capillariesAlso part of immune systemLymph moves from capillaries to veinsLymphatic veins drain into thoracic duct which empties into right atriumMovement of lymph t
38、hrough lymphatic veins same as the regular veinsContain macrophagesFilter lymph flowing through the nodeMean arterial pressure determined by:Heart rateStroke volumeTotal peripheral resistanceMAP=CO x TPRCO=HR x SVMAP=HR x SV x TPRMAP regulated through control of the heart(CO)and arterioles&veins(TPR
39、)Neural controlHormonal controlMAP=driving force for blood flowF=DP/RRegulating MAP critical to normal functionMAP normal HypertensionStress on heart and walls of blood vesselsShort-term regulation seconds to minutesRegulate cardiac output and total peripheral resistanceInvolves heart and blood vess
40、elsPrimarily neural controlLong-term regulation minutes to daysRegulate blood volumeInvolves kidneysPrimarily hormonal controlMedulla oblongataIntegration center for blood pressure regulationInputArterial baroreceptorsLow pressure baroreceptorsChemoreceptorsProprioceptorsHigher brain centersOutputSy
41、mpathetic nervous systemParasympathetic nervous systemParasympathetic input to:SA node(decrease HR)AV nodeSympathetic input to:SA node(increase HR)AV nodeVentricular myocardium(increase contractility)Arterioles(increase resistance)Veins(increase venomotor tone)Norepinephrinea adrenergic receptorsPho
42、sphatidyl inositol triphosphate systemVasoconstrictionBoth a and b2 adrenergic receptorsNorepinephrine binds to a receptorsVasoconstrictionEpinephrine binds to a and b2 receptorsVasoconstriction at a receptorsVasodilation at b2 receptorsEpinephrine has greater affinity for b2 receptorsNorepinephrine
43、b2 adrenergic receptorscAMP systemVasodilationConcentration dependentLower concentrations binds b2VasodilationHigher concentrations binds a and b2Vasodilation in skeletal and cardiac muscle vascular bedsDecrease TPR Decrease blood pressureVasoconstriction in most vascular bedsMaintain/increase TPR M
44、aintain blood pressureDominant effect usually vasoconstrictionReleased from adrenal medulla on sympathetic activationNegative feedback loopsDetector=baroreceptorsIntegration Center=cardiovascular centers in the brainstemControllers=autonomic nervous systemEffectors=heart and blood vesselsBarorecepto
45、rs=stretch receptorsArterial baroreceptors High pressure baroreceptorsSinoaortic baroreceptorsLocationCarotid sinusAortic archNegative feedback loop to maintain blood pressure at normal levelDetectors=baroreceptorsAfferents=visceral afferentsIntegration center=cardiovascular control centerEfferents=
46、autonomic nervous systemEffectors=heart,arterioles,veinsHemorrhage decrease in blood volumeDecrease in mean arterial pressureFollowing hemorrhage:Baroreceptor reflex Increase in sympathetic activityDecrease in parasympathetic activityResult Reflex compensationBrain vasculature not subject to extrins
47、ic controlsBaroreceptor reflex quickly compensates for changes in blood pressureIt does not correct problemLong-term regulation occurs through renal regulation of blood volumeEpinephrine VasopressinAngiotensin IIReleased by adrenal medulla in response to sympathetic activityIncreases mean arterial p
48、ressureActs on heartIncreases HRIncreases SVActs on smooth muscle of arteriolesIncreases TPRActs on smooth muscle of veinsIncreases venomotor toneVasoconstrictorsIncrease TPRIncrease MAPLow pressure baroreceptors=volume receptorsLocationWalls of large systemic veinsWalls of the atriaDecrease in blood volume activates receptors triggering responses that act in parallel with baroreceptor reflex
