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Specialized excitatory and conductive system of the heart Automatic electrical rhythmicity of sinus fibers Mechanism of sinus nodal rhythmicity iK: delayed rectifier current slow voltage-gated K+ channels (activated by depolarization) if: funny current Voltage-gated Na+ channels activated at hyperpolarization beyond -50 mV iCa2+: L-type Ca2+ channel activated at Em higher than 55 mV Transmission of cardiac impulse through atria and internodal pathways Ends of SA nodal fibers connect (gap junctions) direclty with: 1. Surrounding atrial muscle fibers (0.3 m/s) 2. Conduction fibers (1 m/s): Anterior interatrial band Anterior, lateral and posterior internodal pathways Atrioventricular node The only pathway of cardiac impulse entry into ventriculi. Delays the impuls transmission – slow conduction. transmission in only one direction. Transmission of cardiac impulse in ventriculi Fast transmission through Purkinje fibers (1.5-4 m/s). Subendocardial position of left and right bundle branch. Penetration of their branches to 1/3 thickness of LV. Then, connection with cardiac muscle fibers and slower conduction (0.3-0.5 m/s). Sinus node- cardiac pacemaker Discharge rates: SA node: 70-80 /min AV node: 40-60 /min Purkinje fibers: 15-40 /min Abnormal “ectopic” pacemakers increased discharge rate most often in AV-node and Purkinje fibers. Or, blockage in A-V transmission. Stokes-Adams syndrome sudden A-V bundle block synkope Control of heart rhythmicity and impulse conduction Regulation by autonomic nervous system: Parasympathetic innervation Sinus node, AV-node, lesser atria, ventriculi no supresseion of sinus node rhythmicity slows down conduction through AV-node (can cause complete AV-block – ventricular escape) mechanism: hyperpolarization (-65 to-75 mV) Sympathetic innervation whole heart (conduction and contractile fibers) β1-receptors: increase permeability to Ca2+ and Na+ Modulation of pacemaker rhythmicity