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1、Cardiovascular Physiology (心血管生理学) 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 Passage of an action potential along the transverse tubule opens nearby voltage-gat

2、ed 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 fle

3、xing to slide the actin filament. Excitation-contraction coupling in skeletal muscle 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 钙诱导的钙释放钙诱导的钙释放), the so

4、urce of about 95% of the calcium in the cytosol. Excitation-contraction coupling in cardiac muscle Click here to play the Cardiac EC Coupling Flash Animation 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 Pr

5、essure Volume Valves Blood flow What happens in the heart during each cardiac cycle? Systole: ventricles contracting Diastole: ventricles relaxed Click here to play the Mechanical Events of the Cardiac Cycle Flash Animation Mechanical Events of the Cardiac Cycle Summary of events in the left atrium,

6、 left ventricle, and aorta during the cardiac cycle Pressure changes in the right heart during a contraction cycle. Atriaprimer pump Ventriclesmajor source of power Role of atria and ventricles during each cardiac cycle Heart Sounds 1st sound soft low-pitched lub associated with closure of the AV va

7、lves Marks the onset of systole 2nd sound louder dup associated with closure of the PA and aortic valves Occurs at the onset of diastole Chest surface areas for auscultation of normal heart sounds Four traditional value areas Aortic space: 2RIS Pulmonic valve: 2LIS Tricuspid valve: 4ICS LLSB Mitral

8、valve: Apex RIS-right intercostal space LISleft intercostal space ICS-intercostal space LLSB-left lower sternal border Phonocardiogram(心音图) Heart valve defects causing turbulent blood flow and murmurs Acute rheumatic fever Mitral stenosis - Accentuated first sound Mitral stenosis Presystolic murmur

9、Mitral regurgitation - systolic murmur Aortic insufficiency - Loud systolic ejection murmur, third sound 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 (6080ml) heart enlargem

10、ent Stroke volume for evaluating different patients? 2. Ejection fraction (EF)(射血分数) EF=(SV/EDV) x 100% 5565% 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 (4.56.0 L/min) What parameters for comparison of people in differe

11、nt size? 4. Cardiac index (CI)(心指数) : cardiac output per square meter of body surface area 3.0 3.5 L/minm2 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 i

12、ncrease in either stroke volume (SV) or heart rate (HR) or both Measurement of Cardiac Function Echocardiography Cardiac angiography Coronary Angiography from a 56-year-old man presented with unstable angina and acute pulmonary edema Rerkpattanapipat P, et al. Circulation. 1999;99:2965 Regulation of

13、 heart pumping Regulation of stroke volume 1. Preload Frank-Starling mechanism Preload(前负荷) of ventricles: end-diastolic volume (EDV) end-diastolic pressure (EDP) Frank-Starling mechanism (Intrinsic regulation or heterometric regulation) (内在调节,或,异长调节) The fundamental principle of cardiac behavior wh

14、ich states that the force of contraction of the cardiac muscle is proportional to its initial length Significance: Precise regulation of SV To increase the hearts stroke volume: fill it more fully with blood. The increased stretch of the ventricle will align its actin and myosin in a more optimal pa

15、ttern of overlap. Control of stroke volume Frank-Starling mechanism Ventricular function curve (Frank-Starling curve) Ventricular function curve (Frank-Starling curve) Factors affecting preload (EDV) (1) Venous return Filling time Venous return rate Compliance (2) Residual blood in ventricles after

16、ejection 2. Afterload(后负荷)(Usually measured as arterial pressure) pAfterload has very little effect on the normal ventricle pHowever, as systolic failure develops even small increases in afterload have significant effects on compromised ventricular systolic function pConversely, small reductions in

17、afterload in a failing ventricle can have significant beneficial effects on impaired contractility Congestive heart failure (CHF) 3. Myocardial contractility (Inotropic state) (心肌收缩性变力状态) Homometric regulation (等长调节) To further increase the stroke volume: fill it more fully with blood AND deliver sy

18、mpathetic signals (norepinephrine and epinephrine); it will also relax more rapidly, allowing more time to refill. Sympathetic signals (norepinephrine and epinephrine) cause a stronger and more rapid contraction and a more rapid relaxation. Factors regulating contractility HRCO (CO = SV x HR) HRCont

19、ractility (Treppe effect) HR diastolic filling time Regulation of heart rate 40180 /min,HRCO 180 /min,or 40/min,CO Control of heart rate To speed up the heart rate: deliver the sympathetic hormone, epinephrine, and/or release more sympathetic neurotransmitter (norepinephrine), and/or reduce release

20、of parasympathetic neurotransmitter (acetylcholine). T, ions, metabolites, other hormones Staircase phenomenon (Treppe effect , Force- frequency relationship) Increase in rate of contraction (heart rate) causes increase in contractility To increase SV, increase: end-diastolic volume, norepinephrine

21、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 bu

22、t not the other of these determinants of cardiac output. Case A 70-year-old man was admitted to the hospital with shortness of breath, severe fatigue and weakness, abdominal distension, and swelling of ankles. At night he requires four pillows and often wakes up because of acute air hunger. His hist

23、ory revealed episodes of angina pectoris and a progressive shortness of breath with exertion for several years. On examination the chief abnormalities were slight cyanosis (bluish cast to the skin), distension of the neck veins, rapid respirations (20/min), rales (crackling sounds) at the lung bases bilaterally, an enlarged heart with slight tachycardia (110 beats/min) and a diastolic gallop rhythm (sounds like galloping horse),

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