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USC BISC 307L - Heart As A Pump
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Cardiovascular SystemSympathetic stimulation increases heart rateHow NTs modulate heart rateSympathetic (norepi) increases heart rate by affecting the nodal tissueIncreases the strength of cardiac contractionRate determined by the rate of the SA nodeEpinephrinebinds to beta adrenergic receptortwo effects: 1. Increases mean open time of the calcium channel which increases calcium current which lowers the threshold and 2. The HCN channel increases its mean open time which increases the inward funny current through the HCN channel which increases rate at which inward current coming in so this causes more depolarizationRed is normal without sympathetic stimulation and blue is with sympathetic stimulationParasympathetic Stimulation Slows Heart RateSlows down the heart by…Acetylcholine binds to muscarinic receptorvia g protein this activates a type of potassium channel called a GIRK channel (G protein activated inwardly rectifying potassium channel) causes an increase in opening of this channel since at hyperpolarized levels it is openthis reduces the slope of the pacemaker potential (less depolarization) less net inward current heart rate slowed downHeart PumpSlide 1- Electrical Conduction in the hearthave an action potential generated by SA node (connected to these are the contractile cells of the right atrium by gap junctions). inward current through one cell crosses outward current across another cell and this propagates the action potential. Behaves like one big cellB: relaxation phase: purple dot indicates that action potential generated by SA nodeC: Action potential spreads through the atria (first right then left)D: Atrial ventricular node receives action potential (like SA node tissue- has a action potential with a slow graded rise whereas the action potential in the contractile tissue spreads fast)  spreads slowly through the AV node which gives time for the contraction of the atria to empty whatever blood they have into the ventriclesE: Action potential goes through the purkinje fibers which conduct fast (bundles of hiss are the bundles of purkinje fibers)conducting action potentials to the apex at the bottom . This is fast (4m/s). Efficient because the openings are at the top of the ventricles which helps milk the blood out of the ventricles more efficientlyThe action potential does not spread directly into the ventricles because there is a layer of tissue in which there aren’t gap junctions so the action potential cannot spread directlybundle of hiss is very important to get the ventricles to contract (any blockage could be a serious problem)ECG and Electrical Events in the Heartpolarity has something to do with the spread of the action potential toward or away from the electrodesthe amplitude is how much current is flowing and the synchrony of the cellsNormal and Abnormal ECGsAbnormalities: in the middle (1. atrial fibrillation- missing p waves and the interval between the R peaks is irregular. Uncoordinated electrical contraction in heart and without coordination you cannot get the P wave and the atria aren’t pumping very well. This is a problem but not immediately life threatening). Correctable-implantation of pacemaker device2. Ventricular fibrillation: ventricles uncoordinated (damage – MI- or bundle dysfunction) This is life threatening because cannot generate blood pressure and then blood cant flow. The treatment is called defibrillation- done with paddles) This will pass the current throughMechanics of the cardiac cycleHeart contractions: systoleRelaxation phase: diastoleThe 2 atria do things at the same time and the ventricles do the same thing at the same time but the atria and ventricles are not doing the same thingIn order for blood to flow in the proper direction (right side to pulmonary arteries to pulmonary veins into left atrium to left ventricles to aorta to body)How the blood moves: pressure gradients at the appropriate times1. Late diastole: whole heart relaxed (pressure close to zero in atria and ventricles)- pressure in the heart has to be lower than the pressure in the central vein which is already very low so this works. Blood flows in from the vena cava into the right atrium and from the pulmonary veins into the left atrium. AV nodes open and the heart is filled. This is the filling phase. 80% of the ventricular volume is filled this waysemilunar valves between the ventricles and the arteries- these are closed because the arteries still have pressure in them and now the heart is relaxed so the elastic recoil in the arterial walls is delivering some of the stored energy back into the blood- so the artery pressure can never be too low. This keeps the semilunar valves closed2. The SA node fires and the AP spreads across atria and atrial systole occurs. Creates further pressure in the atria which pushes the final 20% of blood into the ventricles3. Ventricular contraction. The pressure inside the ventricles goes up which closes the AV valves (back pressure- THE LUB) but there is a little bit of time before the semilunar valves are opened- this is called isovolumic ventricular contraction- blood isn’t leaving but the ventricles are contracting. The atrial filling begins again4. The increase in ventricular pressure causes the semilunar valves to open allowing blood out the aorta and the pulmonary artery. Ventricular ejection phase at high pressure and there is a pulse of high pressure blood stretching the walls of the arteries5. The ventricles are now relaxed and the pressure begins to fall and the semilunar valves close (CAUSING THE DUB sound) but this pressure is still higher than the artrial pressure (0) so the AV valves stay closed. This is called isovolumic ventricular relaxation. When the ventricular pressure falls below the atrial pressure this causes the AV valves to open againPressure-Volume Changes in Left VentricleSummary of everythingFocuses on the left ventriclePlot of the pressure in the left ventricle and the volumeA: the left ventricle has completed its relaxation and has not yet begun to refill- pressure at a minimum. And volume at a minimum because after ejection phaseB: the ventricles start to fill – increase volume (flat part due to the fact that the blood is trickling) No change in pressure. At the end the pressure does go up a little due to the atrium contracting for the final bit of fillingBISC 307L 1st Edition Lecture 25 Current Lecture Cardiovascular System- Sympathetic


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