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Lecture 5

Lecture 5.docx

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University of Otago
Regis Lamberts

Electrical Properties of Cardiac Tissue Objectives:  Explain the generation and conduction of the AP in the heart  Explain how the action potentials are generated in the nodal cells and myocardial cells  State the difference between nodal and ventricular action potentials  Understand the basic concepts of the ECG  Explain some of the important clinical issues associated that can be diagnosed using an ECG Nodal Tissue: (SA node and AV node- structurally very similar)  Forms 1% of all cardiac cells  Contains small round cells with little or no contractile proteins  Specialised for the generation and conduction of action potentials in the atria  Gap junctions present Conduction of the Cardiac Action Potential:  Action potentials spontaneously generated in the SA node  AP can travel from cell to cell via gap junctions- organised along preferential pathways, determined by location of intercalated discs  Main conduction pathways comprise groups of specialised cells  To get to the ventricles, AP has to pass through AV ring ( via AV node) Generation and Conduction of the AP:  SA node generates AP at about 100-110/min (HR under parasympathetic control- regulates normal heart rate)  AP conducted through atrial muscle at circa0.5m/s  AP conducted slowly through AC node at 0.05m/s- in order for the depolarisation and contraction of the atria to occur before the ventricles contract  AP conducted rapidly through the bundle of His, bundle branches and Purkinje Fibres at 5.0m/s to the ventricular myocardium where it spreads at 0.5m/s  This allows fairly synchronous depolarisation and contraction of all regions of the ventricles  The rapidly conduction system comprises modified myocardial cells called Purkinje Fibres. Basis of Resting and Action Potentials:  The RMP of nodal cells and myocardial cells depends on the high resting permeability to K (Pk)  Pk is lower in nodal cells than myocardial cells and the RMP is less negative  The RMP of SA Nodal cells is unstable Pacemaker Cells:  Pk gradually reduces, and this, combined with an increasing permeability to Na (PNa) and Ca (PCa) causes a gradual decrease in RMP  This slow depolarisation is called the pacemaker potential  At threshold voltage, other Ca channels open and a relatively ‘slow’ AP occurs  A similar AP occurs in nodal cells  Other cells may spontaneously depolarise- >ectopic pacemakers/arrhythmias Action Potentials in the Sinoatrial (SA) Node: Ventricular Cells:  Pk is higher and hence RMP is more negative  Depolarisation phase of AP is due to the opening of voltage-gated Na channels  Long-lasting, slow Ca channel compared to fast channels in SA node- plateau in ventricular action  Ventricular opening of Na channel = depolarisation  SA nodal cells opening of Ca channels = depolarisation  Ventricular cells more permeable to K – more stable than SA nodal cells  Number of transient Ca channels in ventricular action- ventricular Ca channel opens for longer therefore there is a plateau in depolarisation. Excitation-Contraction Coupling:  Excitation of membrane opening of voltage-sensitive plasma- membrane  Ca channels in the T tubules  Flow Ca into cytosol  Ca binds to Ryodin Receptor (RYR)  opening of Ca channels intrinsic to these receptors  flow of Ca into cytosol  Increased cystolic Ca concentration  Contraction  Calcium entry occurs at the T tubules L-Type channels  Entry of Ca
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