Cardiac Pacemakers and an Introduction to the Autonomic Control of the Heart
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2 Cardiac Pacemakers, Introduction to Autonomic Control Sinoatrial Node and Atrioventricular Node--cells do not contract, but serve only to generate electrical activity. Functions as the pacemaker, determining rate. At rest, pacemaker cells look pretty much like other cells. Pacemaker Potential (Depolarization procedes at a slow steady pace until threshold is attained and AP is triggered) The action potential is much slower than that of other cells, because nodal cells lack fast sodium channels so AP is generated solely by iCa, the slow inward current of Calcium ions. The slow speed of this action potential allows cardiac cells to contract and at least partially relax, before they contract again, thereby making it impossible for the heart muscle to go into sustained contraction, in which it could not pump. Ionic Currents contributing to diastolic depolarization of pacemaker cells 1. if --an inward Na+ current caused by hyperpolarization (the more negative the membrane potential, the greater the activation of if)--flow of Na+ ions into cell responsible for spontaneous potential decay. The slope of this decay determines HR. 2. iCa --an inward Ca++ current (becomes active when membrane potential depolarizes to approx threshold potential; T-type Ca++ channels activate at this transmembrane potential; the Ca++ influx accelerates depolarization, which then leads to AP. Thus decreasing external Ca++ concentration or blocking Ca++ channels can diminish amplitude of AP and slow pacemaker rate. 3. iK --an outward K+ current is responsible for repolarizing the cell after the AP. It continues at a slower rate through early phase of depolarization for next cycle. The fastest pacemaker cell becomes the pacemaker for the heart, determining heart rate. Because the cells in the Sinus node reach threshold before the cells of the AV Node, a Sinus Node cell is always the pacemaker in healthy people. AV Node can take over if Sinus Node is damaged. Overdrive suppression--caused by overworking Sodium/Potassium Pump Sinus Node Recovery Time Sick Sinus Syndrome > syncope Intrinsic HR > 100 bpm (Pacemaker rate temperature-sensitive) Discharge frequency of pacemaker cells may be modified by a change in: 1. the rate of depolarization 2. the threshold potential 3. the resting potential Autonomic Control of Pacemaker Cells Increased symp activity to SA node speeds up heart--tachycardia Increased parasymp activity to SA node slows down heart--bradycardia Obviously PS dominates at rest Vagus Nerve Efferents from Dorsal Motor Nucleus and Nucleus Ambiguus Post-gangliotic Cells are on the heart itself (most near SA node and AV conduction tissue) Sympathetic Pathways Emerge from C6 to T5 of spinal cord Synapse in the Stellate Ganglia, then join with parasympathetic pathways to heart Sympathetic: Adrenergic neurotransmitters increase all three currents, but augment if and iCa more than iK, thus increasing the slope of the diastolic depolarization. In addition to those contributed by sympathetic nerves to the heart, circulating catecholamines have similar effects. Effects are slower than parasympathetic (cannot exert beat-to-beat control, like vagus). Sympathetic effects decay slowly as most NE is reuptaken into terminals (remainder carried into bloodstream) Parasympathetic: Acetylcholine hyperpolarizes the cells by opening choline-sensitive K+ channels, and also depresses if and iCa currents. It also slows the slope because of its effect on if. ACh effects very rapid effect, and lots of cholinesterase in SA (and AV) node means effects are very short-lasting. Sympathetic and Parasympathetic systems --Push/Pull (reciprocal) relationship Changes in HR usually due to changes in both symp and parasymp activation: In exercise--increased symp and reduced PS
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