Presentation is loading. Please wait.

Presentation is loading. Please wait.

Chapter 4 BLOOD CIRCULATION. Key points in this unit: 1.the action potential of the ventricular muscle and the action potential of the pacemaker cells.

Similar presentations


Presentation on theme: "Chapter 4 BLOOD CIRCULATION. Key points in this unit: 1.the action potential of the ventricular muscle and the action potential of the pacemaker cells."— Presentation transcript:

1 Chapter 4 BLOOD CIRCULATION

2 Key points in this unit: 1.the action potential of the ventricular muscle and the action potential of the pacemaker cells. 2.electrophysiological properties of cardiac muscle.

3 1.Physiology of the heart Function of heart Pumping Endocrine atrial natriuretic peptide(ANP, 心房钠尿肽 ) brain natriuretic peptide(BNP, 脑钠尿肽 )

4 General process of excitation and contraction of cardiac muscle Initiation of action potential in sinoatrial node Conduction of action potential along specialized conductive system Excitation-contraction coupling Muscle contraction

5 +30 -55 0 -70 阈电位 静息电位 时间( ms ) 后电位 0 2 4 6 8 10 12 神经或骨骼肌 AP 心室肌 AP

6 1.1 Action potentials in cardiac muscle

7 Two major types of cardiac muscle: Working cardiac muscle cell: atrial and ventricular muscle cells Specialized excitatory and conductive muscle: sinoatrial (SA) node, Purkinje fiber non-autorhythmic cardiac cell autorhythmic cardiac cell

8 1.1.1 AP of ventricular muscleAP Phase 0: rapid depolarization -90mV - +30mV Phase1: early phase of rapid repolarization +30mV - +10mV Phase2: the plateau or slow phase of repolarization +10 - 0mV Phase3: late phase of rapid repolarization 0mV - 90mV Phase4: resting phase -90mV

9 Mechanism Phase 0: Na + influx Phase 1: K + outflux Phase 2: K + outflux, Ca 2+ and Na + influx Phase 3: K + outflux Phase 4: Na + - K + pump Ca 2+ pump Na + - Ca 2 exchanger Na + K +, Ca 2+, Na + K+K+ K+K+

10 Phase2 needs 100-150ms. the main cause of long duration of cardiac action potential. the main characteristic which differs from the action potential in nervous fiber or skeletal muscle.

11 working cells phase4 autorhythmic cells phase4 stable spontaneous depolarization resting potential maximal repolarization potential

12 1.1.2 AP of Purkinje cellPurkinje cell quite similar to that of working cells except spontaneous depolarization during phase 4. Phase 4: I f (inward current, caused by Na + influx) increases outward current ( caused by K + outflux) decreases gradually. IfIf 内向电流

13 1.1.3 AP of the P cell of SA nodeP cell of SA node Phase 0: Ca 2+ influx Phase 3: K + outflux Phase 4: fast spontaneous depolarization 4 0 3 I K decreases I f increases I Ca-T I Ca IKIK I K, I f, I Ca Slow response cell

14 outflow of K + < inflow of Na + outflow of K + inflow of Na +

15 2. Electrophysiological Characteristics of cardiac muscle 2.1 ExcitabilityExcitability

16 2.1.1 Factors affecting excitabilityFactors oLevel of RP ↓ :→ excitability ↓ oLevel of TP:↑→ excitability ↓ oStates of sodium channel: resting state: excitability is normal activated state: Na + diffuse in inactivated state: excitability is zero

17 2.1.2 Excitability changes:Excitability changes oEffective refractory period (ERP ): Any strong stimulus fails to elicit an AP. Cause: The sodium channels are at inactivated state and so the excitability is zero. ERP is nearly 100-250ms. Significance: the heart can not be tetanized. the heart can eject and fill continually. ARP:phase0---phase3 -55mV ERP LRP:phase0---phase3 -60mV ERP

18 oRelative refractory period phase3 -60-- -80mV Effective stimulus is suprathreshold stimulus. Cause: the most sodium channels are at resting state but their opening ability are not good as normal, so the excitability is lower than normal.

19 oSupranormal period phase3 -80-- -90mV subthreshold stimulus can elicit an AP. Cause: the sodium channels are at resting state and the distance between the resting potential and the threshold potential is nearer, so the excitability is better than normal.

20 2.1.3 Extrasystole and compensatory pause ① extrasystole ( 期前收缩) premature systole ② compensatory pause (代偿间歇) After ERP, a stimulus can evoke a extrasystole. compensatory pause: a S-A node AP meets the ERP of extrasystole. ① ② ERP

21 2. 2 Autorhythmicity the ability that the cardiac muscle can generate an action potential by itself. Index: frequency of AP SA node AV node left,right bundle branch terminal Purkinje cells (beats/min) 50 100 40 25

22 Natural pacemaker: the pacemaker which can control the activity of the heart under normal condition.(SA node)node Latent pacemaker: the pacemaker which doesn’t show its autorhythmicity under normal condition. (other rhythmic regions of the heart) Ectopic pacemaker: from latent pacemaker ① autorhythmicity of latent pacemaker increases ② autorhythmicity of SA node decreases ③ severe conduction block

23 WhyWhy can SA node be natural pacemaker? ① Preoccupation ( 抢先抑制 ): SA node autorhythmicity is much higher than latent pacemakers and elicit excitations before they finish phase 4. ② Overdrive suppression ( 超速抑制 ): The higher rate pacemaker suppresses the autorhythmicity of the lower rate pacemakers

24 FactorsFactors affecting Autorhythmicity oVelocity of spontaneous depolarization: ↑(b to a)→autorhythmicity oThreshold potential: (TP2 to TP1)→ autorhythmicity ↑ oMaximum repolarization potential (d to a)→ autorhythmicity ↑

25 2.3 Conductivity 2.3.1Specialized conducting system SA node preferential pathway ( 优势通路 ) AV node AV bundle right and left bundle branch terminal Purkinje fibers

26 0.1s synchronization contraction 传导最慢 纤维最小, 缝 隙连接少, 慢反应细胞

27 2.3.2 Factors affecting conduction velocityFactors Rate and amplitude of phase0 depolarization: local current↑→ conduction↑ rate and number of Na + or Ca 2+ influx level of resting potential concentration and potential gradient of Na +, Ca 2+ Structure of cardiac muscle: diameter↑→ local current↑→conduction↑ number of intercalated disc (gap junction)gap junction Excitability of the adjacent region: ↑→conduction ↑

28 2.3.3 Spread of cardiac impulseSpread

29

30

31 Electrocardiogram (ECG) With an electrocardiogragh, electrical activity of the heart can be recorded from the surface of the body. When a large number of cells are simultaneously depolarizing or repolarizing, large voltages are observed on ECG.

32

33 Normal ECG

34 P wave : depolarization of the atria. PQ(PR) interval: from the onset of atrial excitation to the onset of Q QRS complex: depolarization of the ventricles. S-T segment : from the end of QRS complex to the onset of T wave (plateau) T wave : repolarization of the ventricles. Q-T interval : from the onset of QRS complex to the end of the T wave. (AP duration)

35 +30 -55 0 -70 a bc d 阈电位 静息电位 时间( ms ) 反极化 e f 2 4 6 8 10 12 14

36 Cardiac muscle as a syncytium


Download ppt "Chapter 4 BLOOD CIRCULATION. Key points in this unit: 1.the action potential of the ventricular muscle and the action potential of the pacemaker cells."

Similar presentations


Ads by Google