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Diterbitkan olehRidwan Darmadi Telah diubah "9 tahun yang lalu
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Physiology of Cardiac Muscle and Electrical Activity of the Heart
Denny Agustiningsih Denny Agustiningsih
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How the heart pump blood?
Denny Agustiningsih
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Cardiac muscle Denny Agustiningsih
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Two Types of Cardiac Muscle Cells
Ordinary: make up 95%- 99% of all heart muscle cells. Also called worker cells or contractile cells Biochemically similar to red skeletal muscle Slow to fatigue Specialized: make up remaining 1%-5% Also called autorhythmic or automatic cells Responsible for initiation and/or transportation of electrical impulses through the heart pacemaker potential Denny Agustiningsih
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Atrioventricular Node
CONDUCTION SYSTEM Sinoatrial Node Atrioventricular Node Denny Agustiningsih
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Electrical Conduction
SA node - 75 bpm Sets the pace of the heartbeat AV node - 50 bpm Delays the transmission of action potentials Purkinje fibers - 30 bpm Can act as pacemakers under some conditions
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Membrane Potential (mV)
-40 -60 K Ca ++ in K + out symphathetic Threshold Potential Ca (T-type) Depolarization Spontaneous Na parasymphathetic Time (msec) Denny Agustiningsih
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HEART RATE Normally : 60-100 bpm > 100 bpm : tachycardia
< 60 bpm : bradycardia Denny Agustiningsih
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The HR can be increased about 3 times in exercise
Resting heart rate is about beats/min (lower in athletes because they have large stroke volumes) The HR can be increased about 3 times in exercise Above about 200 beats/min the heart would not have time to fill properly therefore nature limits the rate Rate is controlled by the autonomic nervous system Denny Agustiningsih
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Extrinsic Influences Autonomic nervous system Hormonal influences
Ionic influences Temperature influences Denny Agustiningsih
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Control of Heart by ANS Sympathetic innervation-
+ heart rate + strength of contraction + conduction velocity Parasympathetic innervation - heart rate - strength of contraction - conduction velocity Denny Agustiningsih
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Autonomic nervous system modulates the frequency of depolarization of pacemaker
Sympathetic stimulation (neurotransmitter = NE ); binds to b1 receptors on the SA nodal membranes Parasympathetic stimulation (neurotransmitter = ACh ); binds to muscarinic receptors on nodal membranes; increases conductivity of K+ and decreases conductivity of Ca2+ How do these neurotransmitters get these results?
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Major Hormonal Influences
NE/E Thyroid hormones + inotropic + chronotropic also causes an increase in CO by BMR Estrogen/ Testosteron Denny Agustiningsih
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Ionic influences Effect of elevated [K+]ECF
dilation and flaccidity of cardiac muscle at concentrations 2-3 X normal (8-12 meq/l) Effect of elevated [Ca++] ECF spastic contraction Denny Agustiningsih
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Effect of body temperature
Elevated body temperature HR increases about 10 beats for every degree F elevation in body temperature Contractile strength will increase temporarily but prolonged fever can decrease contractile strength due to exhaustion of metabolic systems Decreased body temperature decreased HR and strength Denny Agustiningsih
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Direct Stretch on SA node
Stretch on the SA node will increase Ca++ and/or Na+ permeability which will increase heart rate Denny Agustiningsih
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Terminology Chronotropic (+ increases) (- decreases) Dromotropic
Anything that affects heart rate Dromotropic Anything that affects conduction velocity Inotropic Anything that affects strength of contraction eg. Caffeine would be a + chronotropic agent (increases heart rate) Denny Agustiningsih
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Ca, K mV +20 -90 K out K out ∞ Ca in (L-Type) plateau Na in
K out ∞ Ca in (L-Type) plateau Ca, K Na in Denny Agustiningsih
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AP of Contractile Cardiac cells
Action potentials of cardiac contractile cells exhibit prolonged positive phase (plateau) accompanied by prolonged period of contraction Ensures adequate ejection time Plateau primarily due to activation of slow L-type Ca2+ channels
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Refractory period
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Action Potential Skeletal Cardiac
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Mechanism of Cardiac Muscle Excitation, Contraction & Relaxation
Kalsium yg menginduksi pelepasan kalsium Hanya mengetuk pintu Pengeluaran kalsium salah satu caranya Na, Ca exchanger Denny Agustiningsih
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REFRACTORY PERIOD mV +20 -90 Relative Refractory period 1 2 3
2 membrane potential 3 Period of Supranormal excitability Absolute Refractory period 4 400 100 200 300 Time (msec) Denny Agustiningsih
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Modulation of Contraction
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RECORDING Denny Agustiningsih
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The Body as a Conductor This is a graphical representation of the geometry and electrical current flow in a model of the human thorax. The model was created from MRI images taken of an actual patient. Shown are segments of the body surface, the heart, and lungs. The colored loops represent the flow of electric current through the thorax for a single instant of time, computed from voltages recorded from the surface of the heart during open chest surgery.
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The Modern ECG Machine
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ECG examines how depolarization events occur in the heart
If a wavefront of depolarization travels towards the electrode attached to the + input terminal of the ECG amplifier and away from the electrode attached to the - terminal, a positive deflection will result. If the waveform travels away from the + terminal lead towards the - terminal, a negative going deflection will be seen. If the waveform is travelling in a direction perpendicular to the line joining the sites where the two leads are placed, no deflection or a biphasic deflection will be produced.
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R T P Q S Serabut purkinje – ventrikel Nodus SA – atrium
Atrium (ototnya lebih sedikit) Klw siklusnya atrium - atrial cyte Sirkulasi-peredaran darah Siklus-kontraksi dan relaksasi P Q R S T Denny Agustiningsih
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R T P Q S Denny Agustiningsih
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P Q R S T 1 sec 0.5 Sec Denny Agustiningsih
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ECG Complexes
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ECG Complexes Kontraksi – sistol Ventrike kaknan-memoma darah ke paru
Ventrikel kiri-memompa darah keseluruh jantung Pintu masuk – katub yang menghubgungkan dengan atrium (valam atrioventricualr) Pintu keluar kiri - aorta Pintu keluar kanan – katub pulmu\onal Tujuan awal kontraksi untuk membuka pintu keluar (aorta)
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ECG Description ECG description amplitude (voltage) width (duration)
recorded in mm positive or negative or biphasic width (duration)
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ECG in Perspective ECG recording of electrical activity not the mechanical function ECG does not depict abnormalities ECG does not record all the heart’s electrical activity
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Excitation-Contraction Coupling in Cardiac Contractile Cells
Ca2+ entry through L-type channels in T tubules triggers larger release of Ca2+ from sarcoplasmic reticulum Ca2+ induced Ca2+ release leads to cross-bridge cycling and contraction
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Frank-Starling Law Preload, or degree of stretch, of cardiac muscle cells before they contract is the critical factor controlling stroke volume
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Extrinsic Factors Influencing SV
Contractility is the increase in contractile strength, independent of stretch and EDV Increase in contractility comes from Increased sympathetic stimuli Hormones - epinephrine and thyroxine Ca2+ and some drugs Intra- and extracellular ion concentrations must be maintained for normal heart function
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Modulation of Cardiac Contractions
Figure 14-30
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Reflex Control of Heart Rate
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Regulation of Cardiac Output
Figure 18.23
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Depolarisasi mendahului kontraksi Repolarisasi mendahului relaksasi
Kontraksi jantung tidak melalui otak Listrik-otot atrium-kontraksi--ketika sampai di ventrikel-ventrike berkontraksi Gap junction Kontraksi otot jantung-otot pekerja Otot pekerja memiliki aktin & myosin Mendapat rangsang sehingga ion Repolarisasi = fase istrahat Kontraksi & relaksasi-aktin & myosin Sebagian kalsium pergi ke aktin & myosin untuk berikatan dengan troponin C, sebagian ke retikulum sarkoplasma Retikulum sarkoplasma-tempat penyimpanan ion calsium (ada pintu yang disebut , hanya terbuka untuk kalsium)-masuk ke sitosol Denny Agustiningsih
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