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心脏功能 —— 概述 夏 强, PhD 浙江大学基础医学系. 学习目标 学生在学完本部分后,能够: 描述心动周期与心脏传导系统 标示和解释正常心电图 描述心脏搏动调节机制 描述引起心脏病发作的原因或条件.

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Presentation on theme: "心脏功能 —— 概述 夏 强, PhD 浙江大学基础医学系. 学习目标 学生在学完本部分后,能够: 描述心动周期与心脏传导系统 标示和解释正常心电图 描述心脏搏动调节机制 描述引起心脏病发作的原因或条件."— Presentation transcript:

1 心脏功能 —— 概述 夏 强, PhD 浙江大学基础医学系

2 学习目标 学生在学完本部分后,能够: 描述心动周期与心脏传导系统 标示和解释正常心电图 描述心脏搏动调节机制 描述引起心脏病发作的原因或条件

3 The sinoatrial node is the heart’s pacemaker because it initiates each wave of excitation with atrial contraction. The Bundle of His and other parts of the conducting system deliver the excitation to the apex of the heart so that ventricular contraction occurs in an upward sweep. Sequence of cardiac excitation

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

5 Transmembrane potentials recorded in different heart regions

6 Transmembrane potential of ventricular cells and its ionic mechanisms Resting Potential: -90 mV Action Potential Phase 0: Depolarization Phase 1: Early phase of rapid repolarization Phase 2: Plateau (平台期) Phase 3: Late phase of rapid repolarization Phase 4: Resting phase


8 Transmembrane potential of autorhythmic cells and its ionic mechanisms

9 During which phase of the ventricular action potential is the membrane potential closest to the K+ equilibrium potential? (A) Phase 0 (B) Phase 1 (C) Phase 2 (D) Phase 3 (E) Phase 4

10 Electrocardiogram (ECG) (心电图) The electrocardiogram (ECG) measures changes in skin electrical voltage/potential caused by electrical currents generated by the heart

11 The standard 12 lead ECG Einthoven’s Triangle Limb leads (Bipolar) (I, II, III) Augmented limb leads (Unipolar) (aVR, aVL, aVF) Chest leads (Unipolar) (V1, V2, V3, V4, V5, V6) I II III aVRaVL aVF V1 V2 V3 V4 V5 V6 Willem Einthoven: Dutch physiologist. He won a 1924 Nobel Prize for his contributions to electrocardiography.

12 Normal ECG 0.04 sec ECG interpretation Measurements Rhythm analysis Conduction analysis Waveform description Comparison with previous ECG (if any)

13 P wave: the sequential depolarization of the right and left atria QRS complex: right and left ventricular depolarization ST-T wave: ventricular repolarization U wave: origin for this wave is not clear - but probably represents "afterdepolarizations" in the ventricles

14 PR interval: time interval from onset of atrial depolarization (P wave) to onset of ventricular depolarization (QRS complex) QT interval: duration of ventricular depolarization and repolarization ST segment: the time period between the end of the QRS complex and the beginning of the T wave, during which each myocyte is in the plateau phase (phase 2) of the action potential

15 Normal Partial block Complete block

16 Q-T interval recorded on an ECG primarily corresponds to: A Ventricular repolarization B Ventricular depolarization plus ventricular repolarization C Ventricular depolarization and atrial repolarization D Atrial depolarization and conduction through AV node E Purkinje fibers repolarization

17 Excitability Autorhythmicity Conductivity Contractility Electrophysiological properties (电生理特性) Mechanical property (机械特性) Physiological properties of cardiac cells

18  Factors affecting excitability –Resting potential –Threshold potential –Status of Na + or Ca 2+ channels  Excitability (兴奋性)

19 Hyperkalemia (高钾血症) The QRS complexes may widen so that they merge with the T waves, resulting in a “sine wave” appearance. The ST segments disappear when the serum potassium level reaches 6 mEq/L and the T waves typically become tall and peaked at this same range. The P waves begin to flatten out and widen when a patient‘s serum potassium level reaches about 6.5 mEq/L; this effect tends to disappear when levels reach 7-9 mEq/L. Sinus arrest may occur when the serum potassium level reaches about 7.5 mEq/L, and cardiac standstill or ventricular fibrillation may occur when serum levels reach 10 to 12 mEq/L.

20  Autorhythmicity (自律性) SA node100 times/min AV node 50 times/min Bundle of His 40 times/min Purkinje fibers 25 times/min

21 Factors Affecting Autorhythmicity  Maximal repolarization potential  Threshold potential  The rate of phase 4 spontaneous depolarization

22  Conductivity (传导性) SA nodeAtriaA-V node 0.05 m/s0.4 m/s0.02~0.05 m/s His bundlePurkinje fiber Ventricle 1.2~2.0 m/s2.0~4.0 m/s1.0 m/s Atrioventricular delay (房室延搁) : Asynchronization of atrial and ventricular depolarization to provide adequate cardiac output

23 Factors Affecting Conductivity  Structural factors Diameter of cardiac cells Gap junctions at Intercalated disk  Physiological factors The velocity and amplitude of phase 0 depolarization Excitability of adjacent region

24 You see a 55-year-old, white female for a routine check-up. On the ECG you see a prolonged PQ interval suggesting a first-degree atrioventricular block. What is the primary pacemaker of the heart? A Sinoatrial node B Atrioventricular node C Atrioventricular bundle D Right and left bundle branches E Purkinje fibers

25 The mechanism that couples excitation – an action potential in the plasma membrane of the muscle cell – and contraction of heart muscle Excitation-Contraction Coupling In Cardiac Muscle 兴奋 - 收缩偶联

26 Passage of an action potential along the transverse tubule opens nearby voltage-gated calcium channels, the “ryanodine receptor,” located on the sarcoplasmic reticulum, and calcium ions released into the cytosol bind to troponin. The calcium-troponin complex “pulls” tropomyosin off the myosin- binding site of actin, thus allowing the binding of the cross-bridge, followed by its flexing to slide the actin filament. Excitation-contraction coupling in skeletal muscle

27 Calcium ions regulate the contraction of cardiac muscle: the entry of extracellular calcium ions causes the release of calcium from the sarcoplasmic reticulum (calcium-induced calcium release [ 钙诱导的钙释放 ]), the source of about 95% of the calcium in the cytosol. Excitation-contraction coupling in cardiac muscle

28 Cardiac cycle (心动周期) The cardiac events that occur from beginning of one heartbeat to the beginning of the next are called the cardiac cycle Pressure (压力) Volume (容积) Valves (瓣膜) Blood flow (血流)

29 Systole: ventricles contracting Diastole: ventricles relaxed

30 Summary of events in the left atrium, left ventricle, and aorta during the cardiac cycle

31 Pressure changes in the right heart during a contraction cycle.

32 Evaluation of Heart Pumping 1.Stroke volume (SV) (搏出量) : volume of blood pumped per beat SV = EDV – ESV EDV: end-diastolic volume (舒张末期容积) ESV: end-systolic volume (收缩末期容积) ~70ml (60~80ml)

33 2. Ejection fraction (EF) (射血分数) EF=(SV/EDV) x 100% 55~65%

34 3. Cardiac output (CO) (心输出量) : the total volume of blood pumped by each ventricle per minute CO=SV x heart rate (HR) 5 L/min (4.5~6.0 L/min)

35 4. Cardiac index (CI) (心指 数) : cardiac output per square meter of body surface area 3.0~ 3.5 L/minm 2

36 5. Cardiac reserve (心力储备) : the maximum percentage that the cardiac output can increase above the normal level In the normal young adult the cardiac reserve is 300 to 400 percent Achieved by an increase in either stroke volume (SV) or heart rate (HR) or both

37 Regulation of heart pumping

38 Ventricular function curve (Frank-Starling curve)

39  Afterload has very little effect on the normal ventricle  However, as systolic failure develops even small increases in afterload have significant effects on compromised ventricular systolic function  Conversely, small reductions in afterload in a failing ventricle can have significant beneficial effects on impaired contractility Congestive heart failure (CHF)

40 Factors regulating contractility

41 To increase SV, increase: end-diastolic volume, norepinephrine delivery from sympathetic neurons, and epinephrine delivery from the adrenal medulla. To increase HR, increase: norepinephrine delivery from sympathetic neurons, and epinephrine delivery from adrenal medulla (reduce parasympathetic). It is not possible, under normal circumstances, to increase one but not the other of these determinants of cardiac output.



44 The End.

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