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Transcript
Heart Anatomy and Cardiac Muscle Cell Structure Chapter 12 Figure 12.1: Location of the Heart Aorta Vena Cava Pulmonary Trunk RA RV Right Coronary Artery Fig 12.2: The Heart Figure 12.3: VentricularMusculature Figure 12.4: A-V Valves Figure 12.5. Aortic & Pulmonary Valves Figure 12.6: Pulmonary vein SA NODE Vena Cava L R AORTA AV NODE AV Bundle & Purkinje Fibers PULMONARY ARTERY Fig 12.8 Blood Flow Systemic Capillaries --> Veins-->Vena Cava --> Right Atrium --> Right Ventricle Pulmonary Artery --> Pulmonary Capillaries --> Pulmonary Vein Left Atrium --> Left Ventricle --> Aorta --> Arteries --->Systemic Capillaries Cardiac cell structure Small discrete cells Intercalated disks with desmosomes Gap junctions = syncytium Many mitochondria Sr and t tubules Striated Figure 12.7: Cardiac Muscle Cells Fig 12.8: Cardiac Conduction System Electrical Activity of the Heart Fig 12.10: Pacemaker Cell Ion channels in pacemaker cells: see page 381 • • Slow initial depolarization caused by closing of K+ channels Next funny channels open – Allow Na to enter causing depolarization – Only open briefly + • This depolarization opens two types of Ca++ channels -T - type channels open briefly before inactivating - L - type channels then open finishing depolarization Note Differences in Conduction Velocity Due to Rates of Depolarization! RECTIFICATION Minimized efflux of K+ during AP plateau because of decreased K+ conductance at this positive Vm See Fig 12.10 !!!! Duration for complete contraction of the ‘pump’ Long AP with long refractory period to prevent fibrillation ACh or PARASYMP. ON SA NODE Vm mV - 60 Inc. P K Dec. P Ca ACh See Fig 12.10 !!!! SA NODE: NE or EPI Vm mV - 60 + P Na and P Ca and - P K SYMPATHETIC STIMULATION See Fig 12.10 !!!! VENTRICULAR ACTION POTENTIAL Vm in mV 0 -80 F O R C E 0 0.1 0.2 SECONDS 0.3 Fig 12.12: Einthoven’s Triangle and the ECG: Figure 12.13 ECG R T P Q S M U S C L E F O R C E POTENTIAL ISOMETRIC FOR CE AFTERLOAD ISOTON IC SHORTENING Systole ISOMETRIC R ELAXATION ISOMETRIC C ON TR ACTION Diastole MUSCLE LENGTH Terminology End Systolic Volume (ESV in ml) End Diastolic Volume (EDV in ml)) Stroke Volume (SV in ml/beat) SV = EDV - ESV Heart Rate (in beats/min) SV (ml/beat) Cardiac Output (CO in ml/min) CO = HR x SV Starling’s Law of the Heart Increased EDV or myocardial fiber length results in increased SV or increased strength of contraction. Basis for Starling’s Law: P = 2T/r where P = pressure in ventricle or aorta at ejection T = myocardial tension required to generate that tension r = radius of ventricle at beginning of systole P = 2T/r Which ventricle must develop more tension or contractile force, a fuller, larger EDV or a smaller EDV? M U S C L E F O R C E POTENTIAL ISOMETRIC FOR CE ISOTON IC SHORTENING ISOMETRIC R ELAXATION AFTERLOAD ISOMETRIC C ON TR ACTION Filling MUSCLE LENGTH Sympathetic response 1 receptors on nodes and atrial and ventricular muscle cells Increases rate Increases ca++ released per beat via cyclic amp 1 receptor activation G protein adenylate cyclase --> cyclic AMP Activates cAMP-dependent protein kinase Phosphorylates an SR protein, phospholamban myocardial SR takes up and releases more Ca++ per beat result = more cross bridges = more tension As heart rate increases, filling time decreases DIGITALIS DECREASE HR BUT INCREASE STRENGTH Vagus nerve •Parasympathetic fibers •Baroreceptors from aortic arch •Stretch receptors from lungs Parasympathetic nerves Right vagus to SA node Left vagus to AV node and bundle Decreases rate No DIRECT influence on strength 12 0 10 0 LEFT HEART 80 b 60 VENTRICULAR Press ure 40 AORTIC Press ure c a - mitral closes b - aortic opens c - aortic closes d - mitral opens ATRIAL Press ure 20 a d 0 150 100 Ventricular Volume in mls 50 T IME: 0 0.1 sec 0.2 0.3 R E C G S O U N D S P P T Q 4 S 1 2 3