HK 3810 Package 1 notes.docx

When we fill the left ventricle and start to contract

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When we fill the left ventricle and start to contract down on that volume, pressure increases pressure will close the valve between the atria and ventricle, papillary muscles and chordae tendonae will hold on so it doesn’t evert back up the volume now has no where to go because it is closed we continue to contract down until pressure is reached that will open aortic valve the pressure generated needs to be > the pressure keeping the valve shut Preload: volume in ventricle just prior to contraction Afterload: volume in the aorta that the ventricle is working against Two types of cells in the heart Nodal cells – electrical system o Generate APs o Triggers for contraction, spontaneous depolarizer (does not need a stimulus to generate AP) o In the sinoatrial (SA) node and atrioventricular (AV) node o Nodal cell APs Nodal cells do not have a stable membrane potential, there is a point where it is at -70mV where it is leakier to Na+ than normal Na+ enters the cell to depolarize itself (If – funny current) cell continues to depolarize until threshold is reached for voltage gated Ca2+ channels to open Membrane is more permeable to Ca2+ and it rushes into the cell trying to reach its equilibrium potential of +120mV causing membrane potential to go up voltage gated Ca2+ channels become inactive (no flux) as membrane potential nears 0mV, threshold is reached for voltage gated K+ channels to open K+ has an equilibrium potential of -106mV so it will move out so membrane potential undergoes repolarization phase voltage gated K+ channels close then back down at minimum membrane potential Repolarization finishes at around 200 ms There are consequences to the inactive state of voltage gated Ca2+ channels, which is the effective refractory period (another AP cannot be generated in this time frame even threshold is reached) There is a relative refractory period where another AP can be generated if the stimulus > normal Muscle cells – contractile system o In a ventricular/atrial myocyte it is sitting at a resting membrane potential because it is not a spontaneous depolarizer, it is waiting for a change in membrane potential or stimulus coming through gap junctions from nodal cell (for atrial) or purkinje fibres (for ventricular) o Change in membrane potential occurs and is passed on to atrial/ventricular myocyte quickly changes membrane potential to open voltage gated Na+ channels threshold is quickly reached Na+ flux in and quickly go from open to inactive state K+ movement out due to chemical and electrical gradient (passive) threshold is reached to open voltage gated Ca2+ channels Ca2+ rushes in causing depolarization (trigger for contraction) Ca2+ causes shortening in the muscle cells Voltage gated Ca2+ channels inactive repolarization because K+ flux out > Ca2+ flux in voltage gate Na+ channels close
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HK 3810 Package 1 o K+ permeability decreases during the duration of the AP; if we allow K+ to
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  • Fall '16
  • Coral Murrant
  • AP

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