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WEEK 19:
Electrical event in the cardiac cycle:
| Question | Answer |
|---|---|
| SA node bpm (intrinsic spontaneous beating rate) | 105 - meaning its activity drives that of all the other parts of the heart |
| ions causing 105bpm in SA | Na+ and Ca+ through slow channels |
| ventricular myocytes bpm | 25-40 |
| ions causing 25-40bpm in ventricular myocytes | Na+ fast then Ca+ slow |
| patient suffering atrial block would have a vbpm of | 30 |
| describe the normal path for conduction of electrical activity through the heart | SAN spontaneous discharge -> electrical activity across atria insulating tissue between A + V forcing signal down AVN -> slight pause in discharge of AVN (allow filling) -> AVN discharges + activates BOH + PFs for simultaneous depolarisation in Ventricles |
| parasympathetic activation on SAN | hyperpolarises SAN cells and decreases slop of pacemaker potential (mediated by increased opening of K+ ion channels and ensure SAN action potentials arise less frequency for a lower HR) |
| sympathetic activation on SAN | increases the slope of the pacemaker potential mediated by increased opening of funny channels and means that the SAN action potential arise more frequently (faster HR) |
| funny channels refer to (2) | Na+ and K+ channels |
| vagal tone damps down resting heart rate by | hyperpolarising SAN cells and decreasing slope of pacemaker potentials |
| membrane potential in ventricular myocytes | more negative and more stable |
| predominant source of Ca2+ ions | sarcoplasmic reticulum |
| vagal tone damps down | resting heart rate |
| what happens when both balance of vagal tone and sympathetic tone are blocked (ANS)** | intrinsic heart rate is till around 105bpm |
| high plasma K+ levels (hyperkalaemia) | affects cardiac excitability where resting potential becomes less negative so threshold reached more easily |
| SAN cells resting membrane potential | as a pacemaker area- SAN cells have a much less stable resting membrane than other parts of the heart |
| what would happen if the SAN is damaged | intrinsic resting heart rate decreases |
| what does the vagal tone do | damps down resting HR |
| sympathetic tone keeps heart rate up by | increasing slop of pacemaker potentials |
| sympathetic tone does what | keeps heart rate up |
| stages of the ionic bases for ventricular myocyte action potentials basic description (3) | up -> plateau -> down |
| why does depolarisation occur (up on ionic bases for ventricular myocyte action potentials) | rapid depolarisation due to Na+ inflow when voltage gated Na+ channels open |
| why does the graph plateau in ionic basis for ventricular myocyte AP | maintained depolarisation due to Ca2+ inflow when voltage gated slow Ca2+ channels open and some K+ channels close) |
| why does the graph drop in ionic basis for ventricular myocyte AP | repolarisation as K+ outflow when voltage gated K+ channels open |
| parts of the graph of ionic bases for SAN AP | threshold, AP, pacemaker potential, channels (L-type Ca2+ channels, K+ channels) |
| at what point do L-type Ca2+ channels open on the graph | once threshold is reached |
| when do K+ channels open on the graph | at peak |
| when do K+ channels close on the graph | at trough |
| why are K+ levels important (especially high levels) | if plasma K+ levels increase (hyperkalaemia) this can have catastrophic effects on cardiac excitability (makes resting membrane potential more negative and harder to reach threshold). |
Created by:
kablooey
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