Chapter_9_Cardiac_Conduction_Systems__1_slide_per_page

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Chapter 9: The Cardiac Conduction System depolarization initiates contraction by a process called excitation-contraction coupling action potential is transmitted to all myocytes triggers release of Ca2+ from the sarcoplasmic reticulum contraction : initiated when Ca2+ binds to troponin C leads to uncovering myosin binding sites on actin Leads to formation of cross-linkages between actin & myosin Leads to sliding of thin on thick filaments resulting in shortening relaxation : Ca2+ pumped back into sarcoplasmic reticulum Ca2+ released from troponin actin and myosin cease to interact The parts of the heart normally beat in an orderly sequence: 1) contraction of the atria ( atrial systole ) 2) contraction of the ventricle ( ventricular systole ) 3) during diastole, the ventricles are relaxed BE501 T. K. Hsiai, MD, PhD, FACC Objectives
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Heart is an obligate aerobic organ • At resting pulse rate, the heart consumes approximately 8-15 ml/O 2 /100g tissue . • The brain consumes approximately 3 ml/O 2 /100g tissue • During vigorous exercise, the heart consumes approximately 70 ml/O 2 /100 g tissue • Mammalian heart muscle cannot produce enough energy under anaerobic conditions to maintain essential cellular processes.
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The nerve impulse . In the resting neuron, the interior of the axon membrane is negatively charged with respect to the exterior ( A ). As the action potential passes ( B ), the polarity is reversed. Then the outflow of K + ions quickly restores normal polarity ( C ). At the instant pictured in the diagram, the moving spot, which has traced these changes on the oscilloscope as the impulse swept past the intracellular electrode, is at position C .
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The cardiac action potential is produced through changes in membrane ion permeabilities. The cardiac cells tend to stay depolarized for a longer period of time, thus forming a plateau in the action potential (phase 2). This change in the shape of the cardiac action potential is due to calcium ions. The initial depolarization observed is due to an increase of Na+ permeability of the membrane through quickly opened Na+ channels. -90 mV Æ resting state Equilibrium potential of Na + Æ electrostatic=chemical forces Equilibrium potential of K + Action potential of muscle (fast) Rapid inward Na + Outward K +
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Atrial and ventricular myocytes (fast response) Rapid depolarization Increased sodium permeability (I Na inward current) Brief repolarization Due to transient outward current of potassium ions (I to ) Plateau phase A delicate balance between small inward and outward currents: Outward current mediated by activation of Potassium conducting ionic channel (I k ) Inward current by slow calcium current (I Ca ) Repolarization to the resting state. -slow inward Ca++ current -outward K+ current (I KI ) - Sodium-potassium pump (I p ) ERP RRP Diastolic portion of the action potential No spontaneous diastolic depolarization occurs due to the activation of K current (the inward rectifier, I KI ) Tetrodoxin Na/K channel inhibitors Premature action potential
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Fast Responses
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