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WEEK 19:

Electrical event in the cardiac cycle:

QuestionAnswer
SA node bpm 105
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
membrane potential in SA node cells less stable than other parts of the heart
what would happen in SA node is damaged intrinsic resting heart rate decreases
funny channels set of ion channels permeable to many ions (not just a specific one)
phat happens when pacemaker potential reaches resting potential** funny channels open
L-type Ca2+ channels
ionic basis for ventricular myocyte AP
membrane potential in ventricular myocytes more negative and more stable
predominant source of Ca2+ ions sarcoplasmic reticulum
nervous system influence on cardiac activity
autonomic effects of SA node AP
noradrenalin** B-adrenoceptors
Ach** muscarinic receptors (M2)
parasympathetic activation** mode of action both hyperpolarises SA node cells + decreases slop of pacemaker potential mediated by increases opening of K+ channels and ensure SA node has less frequent AP (slower heart rate)
sympathetic activation** mode of action increases slope of pacemaker potential (prepotential) mediated by increased openings of funny channels (means SA node AP = more frequent = faster heart rate)
vagal tone damps down resting heart rate
how does vagal tone damp down resting heart rate (2) by hyperpolarising SA node cells and by decreasing the slope of pacemaker potentials
sympathetic tone keeps heart rate up how by increasing slope of pacemaker potentials
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
Created by: kablooey
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