Professor: Merrill. each paragraph is one slide. Cardiac electrophysiology and the control of heart rate (HR) Know this!!! Heart picture. Conduction system. Green lines = specialized modified muscle cells. Conduction system is not a nerve system it is muscular. Sinoatrial node -> atrioventricular - > bundle of his -> -> perkinje … know the pathway!!!!! On left: three action potentials taken from cells in different parts of the av conduction system. Focus on ventricle and sa node. Identify electrophysiological differences. Each number = a different phase of an action potential in that cell. Theres more detail in the ventricular myocyte one than in the sa nodal myocyte. Ventricle is more complex … called a fast response cell, or fast myocyte. Second one is a slow response cell/slow myocyte. Fast can mean rate at which the ion channels open and allow current in, or it can mean the rate at which the action potential is conducted from one cell to the next. Conduction velocity is greater than in sa nodal cells. Shapes of action potentials are also different. Top has a spike and a plateau, the second does not. Sa nodal graph does not have a resting membrane potential! The book is wrong. There is continuous change; change during stage 4 allows them to act as pacemakers. Diastolic depolarization = stage 4. gives them automaticity; if you isolate that cell, it will generate the action potential continuously…it needs no innervation, the a.p. is intrinsic. pacemaker potential is similar to diastolic depolarization. The heart is in its diastole in stage 4. 0: depolarization. In 1, opening of na channels (rapid). In 2, opening of ca channels (but slowly) membrane excitable is the ease in which a resting potential can be converted to an action potential is an action potential conducted? 1. magnitude of resting potential. The more polarized it is, the more excitable it will be. 2. amplitude of the action potential. The greater the amplitude, the more excitable. 3. rate of change of phase 0 depolarization. How rapidly membrane depolarizes. dV/dt potassium equilibrium potentials are responsible for polarization of the membrane summary of above. Left picture could be ventricular myocyte or sa nodal. Right picture. Illustrates influence of potassium. In disease states, its possible to change the behavior of a fast response cell to a slow response cell using potassium. Decreasing potassium causes amplitude to decrease, resting potential becomes more positive, cell becomes more like slow cells. There are states that mess with potassium homeostasis; such as decreased blood flow … blood cells become ischemic, which elevates external potassium. End result = a few missed beats, or sudden cardiac death (arrest of heart in diastole). Summary. Functional significance: allows ventricles to fill with blood Regulation of heart rate. The conduction system is NOT not influenced by the nervous system (ans). Just not regulated directly by it. Thoracic and lumbar is sympathetic. Brain stem and peripheral tissues all have some influence through nerves on heart rate. Everyone is arrhythmic. Mechanism. On left: influcen of a single stimulus on vagus nerve going to an isolated sa node in lab experiment. On right: summary of the only ways it is possible to change heart rate. Left: numbers on top = length of cardiac cycle in msec. greater duration of cycle, slower the heart rate. After stimulus, action potential does not occur, then the cell hyperpolarizes; in next several cycles, cycle length has increase (hr has decreased). One impulse from vagus nerve can cause arrhythmias plus a slower heart rate. Pacemaker potentials are reduced after the stimulus: slopes are more shallow. Reduced slope of stage 4 diastolic depolarization slows the heart. Right: if blue curves represent control condutions, 1 = slope of action potentials. 2 = slope changes, duration increases, hr decreases. Shows one way to change heart rate: reduce slope of pacemaker potential in sa node. Second way: hyperpolarize as shown from 3 to 4. two ways the vagus nerve works. Can ultimately lead to cardiac arrest. Sympathetic nerves take 1 and shift it to left, increasing slope, increasing hr. sympathetic nerves do not influence level of polarization, however. Three panels. Influence of ans on hr. panel a: stimulate vagus nerve, hr drops immediately by 100% or more. Turn off stimulus, hr recovers. Use sympathetic stimulation, same thing takes twice as long; hr also recovers slowly. Atropine blocks hch receptors. Propranalol blocks beta adrenergic receptors. Is there an influence of sympathetic or tonic under basal conditions? Yes vagus nerve exerts commanding influence in determining basal hr under resting conditions. Vagus contributes more than sympathetic system. Both are tonically active, but vagus overrides sympathetic. Summary. Respiratory influences. Respiratory sinus arrhythmia: if you look at respiratory cycle, and compare it with cardiac cycle, there are some correspondents. Dips = inspiration; decreases length of cardiac cycle. During inspiration, hr accelerates. During expiration, hr decelerates. Why, during inspiration, would hr increase? if you isolate main inspiratory nerve, and also sympathetic and vagus nerves. As phrenic nerve activity increases, so does sympathetic nerve (inspiration). During expiration, vagus nerve activity increases opposite the sympathetic nerve activity. During inspiration, hr is increasing bc as a thoracic cavity, lungs fill, large veins get compressed, blood gets sent forward to heart. Increased volume of blood fililng right atrium. Atrium has stretch receptors in its wall; afferent nerves send messages to increase hr. <- Bainbridge reflex. Increased hr and increased blood flow out of ventricles = increase in cardiac output -> increase in blood pressure in aorta, main branches. Response to increase in pressure: send messages to control center, slow down hr, pressure drops back down. Interactions. What happens to influence of symp nerves on hr if you stimulate vagus simultaneously. Top line, no vagus stimulation. Add vagal discharge, hr decreases bc sympathetic system cannot override vagus. Valsalva-weber. Study influence of respiration. Subject breathes out of tube, so pressure can be measured. Physician can montiro heart rate, blood pressure also. Asked to perform valsalva maneuver: straining at stool … like when constipated. Hyperventilate, then strain. Air stays in lungs. The longer the strain, the harder you force, the changes are more pronounced. Can lead to nothing or cerebral hemorrhage … stroke, etc. all veins upstream are congested. Results of above. Eat more fiber!!! So you don’t stroke out. Wednesday: 10-11 am room 336 arc. Dr. page is a tutor!!!