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Understanding Cardiac Physiology: Heart's Electrical & Contractile Mechanisms - Prof. Char, Study notes of Biology

An in-depth exploration of the cardiac myocyte, focusing on the sliding filament mechanism, calcium release, and the role of the sarcoplasmic reticulum. Additionally, it covers the conduction pathways, action potentials, and pacemaker activity. The document also discusses electrocardiography and its significance in measuring heart function.

Typology: Study notes

2011/2012

Uploaded on 09/22/2012

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Download Understanding Cardiac Physiology: Heart's Electrical & Contractile Mechanisms - Prof. Char and more Study notes Biology in PDF only on Docsity! 19 September 28 MC 2 short answer Cardiac Myocyte Sliding filament mechanism T tubules extend from sarcolemma and permit extracellular ions and fluid to diffuse near intracellular structures Sarcoplasmic reticulum stores substantial amounts of Ca++ which is released when ryanodine receptors are stimulated by extracellular Ca++ which flow through L type voltage sensitive dihydropyridine receptors Calcium induced calcium release Ryanodine receptors – activated by calcium, initiate calcium release Intercalated discs allow low resistance for charge to flow from cell to cell Ca++ enters cytoplasm via VG L-type Ca++ channels which interact with ryanodine receptors on SPR (“trigger calcium”). Calcium induced calcium release. Ca++ released from sequestered Ca++ Tropomyosin is associated with three regulatory proteins: TN-T, TN-C, and TN-I Ca++ binds to TN-C which in presence of ATP changes conformation of troponin Myosin and actin cross-bridge when myosin binding sites exposed on actin SERCA-resequesters Ca++ via phosphorylation of phospholamban (SERCA = SPEndoreticulum CaATPase) Calsequestrin is the primary calcium storage protein in the SR. It binds to approximately 50 Ca++ ions per molecule during diastole which prevents Ca++ precipitation. Ca++ releases from TN-C and inhibition of binding sites occurs → relaxation ATP needed for contraction and relaxation (lusitropy) Conduction Pathways SA node → atrial muscle → AV node → bundle of His → right and left bundle branches → Purkinje fibers → ventricular muscle Delay at AV node Most of end-diastolic volume reaches the ventricles due to the pressure difference rather than atrial contraction SA node generates fastest signal (60/min) Generation gets slower farther down the chain SA node, while functional, overrides the others SA node does not have resting membrane potential Action Potential Conduction IAB = (VA – VB) / RAB IAB – current between cells A and B V – voltage R – resistance Depolarizing current or + charges Current flows from depolarized to hyperpolarized within cell Ion causing rapid upswing of action potential Ventricular muscle – sodium
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