BISC 307L 1st Edition Lecture 25 Current Lecture Cardiovascular System Sympathetic stimulation increases heart rate o o o o o o How NTs modulate heart rate Sympathetic norepi increases heart rate by affecting the nodal tissue Increases the strength of cardiac contraction Rate determined by the rate of the SA node Epinephrine 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 depolarization o Red is normal without sympathetic stimulation and blue is with sympathetic stimulation Parasympathetic Stimulation Slows Heart Rate o o Slows down the heart by o 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 down Heart Pump Slide 1 Electrical Conduction in the heart o o have 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 cell o B relaxation phase purple dot indicates that action potential generated by SA node o C Action potential spreads through the atria first right then left o 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 ventricles o E 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 efficiently o The 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 Heart o o polarity has something to do with the spread of the action potential toward or away from the electrodes o the amplitude is how much current is flowing and the synchrony of the cells Normal and Abnormal ECGs o o Abnormalities 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 device o 2 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 through Mechanics of the cardiac cycle o o Heart contractions systole o Relaxation phase diastole o The 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 thing o In 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 o How the blood moves pressure gradients at the appropriate times o 1 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 way o semilunar 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 closed o 2 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 ventricles o 3 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 again o 4 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 arteries o 5 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 again Pressure Volume Changes in Left Ventricle o o o o o Summary of everything Focuses on the left ventricle Plot of the pressure in the left ventricle and the volume A 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 phase o B 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 filling