BIOL 460 1st Edition Lecture 19Outline of Last Lecture I. Valves a. AV valvesb. Semilunar valvesII. Path of Blood in HeartIII. Cardiac Cycle Outline of Current Lecture I. Cardiac Cycle ContinuedII. Valve sounds III. Electrical Activity of the Heart IV. Electrical Activity of cells of SA nodea. Pacemaker potential Current LectureCardiac Cycle Continued1. Phasesa. Before left ventricle can eject blood it has to open semi lunar valve in the aorta, this means the pressure in the left ventricle has to be higher than the aortai. Blood pressure (BP) in aorta before VS is 80 mmHGii. First shaded part is isovolumetric contractions 1. Period of time a beginning of VS when the ventricles are not ejecting any blood; the volume of ventricle isn’t changing at all2. Pressure in ventricle is enough to close bicuspid valve but not great enough to open aortic semi lunar valve; all valves into and out of left ventricle are closedThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.3. When pressure in left ventricles gets above 80, pressure in left ventricle is greater than pressure in aorta, which cause semi lunar valve to open allowing the ventricle to eject blood4. This ejection phase; left ventricle is greater than aorta, opening semi lunar valve; pressure begins to falliii. When pressure is less than 80- isovolumetric relaxation1. Ventricles still in systole but begging to relax2. Pressure in left ventricle is great enough to keep bicuspid valve closed, but not high enough to open semi lunar valve because it is less than 803. Both valves closed2. Valve soundsa. Lub and Dub or Lup and dupb. Lub is first valve sound, caused by closing of AV valvei. Creates noise ii. For AV valves to close, pressure in ventricle must be greater than pressurein atria iii. Pressure in atria is very low, so valves slam shut1. After AS and before VSiv. Only closing of valves makes noise, not opening c. Dub is the second valve sound, caused by closing of semi lunar valvei. close the second the pressure in the aorta is greater than the pressure in the ventriclesii. To open valve pressure in ventricle must be higher than aorta, but close isoppositeiii. Occurs moment aortic pressure is greater than ventriclesiv. At begging of isovolumetric relaxation. 3. Electrical activity of the Hearta. The sinoatrial node (SA), is the pacemaker of the heartb. Located very near the entrance of the superior vena cave in the right atriac. The SA node shows phenomenon of automaticity i. Means cells of SA node spontaneously generate action potentials ii. Automaticity rate of 100 ap per miniii. This rate is constantly modified by autonomic motor systemiv. Sympathetic innervation increases, parasympathetic decrease (most of the time). v. Other region can show automaticity 1. These include: AV node, bundle branches, perkinji fibers 2. Normally don’t, because SA node has faster inherent rate than other parts of the heart. SA node generates AP depolarizing cells of listed structures before they can generate their own depolarization.3. Damage to heart (scar tissue) may block movement of AP in heart,so other parts of heart can get AP from SA node so they generate their own AP. 4. Called ectopic focus (pacemaker)vi. Cells of SA node are modified cardiac myocytes (muscle cells)1. Not neurons, just muscle cells2. Do not have many myofibrils, so they contract very weakly with apd. Electrical Activity of cells of SA node. i. Graph in notes ii. Typical neuron has resting potential 1. Cells of SA node do not have resting potential (stable membrane potential) 2. Slowly depolarizes from -60 to -40, at -40 we reach threshold and we generate action potential. 3. Repeats it’s self , .8 s (one cardiac cycle) iii. Cells of SA node show slow depolarization, called pacemaker potential, also called diastolic depolarization. (depolarization that occurs in diastole). iv. Action potential 1. repolarization caused by the opening of K gated channels. Down slope. K out of cell2. Depolarization caused by calcium voltage gated channels, when pacemaker potential depolarizes to -40 at that point Ca voltage gated channels open. Ca rushes in causing depolarization.a. Ca that goes into cells binds to troponin C and causes cells to contract weakly. v. Pacemaker potential1. Caused by unique kind of channel called the HcN channel. Found in pacemaker cells in body (in brainstem also, generate spontaneous depolarization) a. HCN channels of SA node are called If channelsi. I=E/R ----- Ohms lawii. F stands for funny. Read out was oddb. Channels are similar to nicotinic channels, they are permeable to both Na and K ions. Like nicotininic channels this causes EPSP or depolarization.c. HCn stands for:…: these are the things that can open the HCN channels. i. H-hyper polarization- designated the very end of repolarization as a hyperpolarization (membrane potential becoming more and more negative) 1. When HCn channels open Na goes in and K goes out, but more Na in, causes slow depolarization.2. Once threshold is reached Ca channels openand we get depolarization. As pm gets moreand more positive HCn channels close and by -40 Ca vg channels open.ii. Cn- cyclic nucleotide 1. Open in response to a cyclic nucleotide2. Comes from sympathetic division of autonomic nervous system. Makes pacemaker potential more steep/faster. Sympathetic comes from adrenergic Beta 1. iii. Norepinepherine binds to G-protein linked recpetor(B1) activates adenylate cyclase results in production of cyclicAMP. That is cyclic AMP that opens HCn channels. Causes it to depolarize faster.d. Parasympathetic receptors use muscurinic receptors. Ach turns on g-protein which opens separate K channel, more K leaves cell than usual, effect of IPSPi. When IPSP and pacemaker potential, slope of pacemaker potential is decreased (more