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21 Cards in this Set

  • Front
  • Back
what is a functional syncytium? whats its advantage?
2 atria, 2 ventricles contracting as seperate units but synchronised in order to increase force of contraction
what are the 3 features of a cardiomyocyte that enable functional syncytium?
1. source of rhythmic excitation (autorhythmic cells)
2. spread of electrical excitation is controlled (allowing adequate time for filling etc)
3. excitation of contractile cardiac cells (do mechanical work, dont initiate own AP)
What node of the heart is the 'pacemaker', what pace does it set?
The sinoatrial (SA node), 70-80 BPM
what are the other nodes of the heart and their targets?
Atrioventricular (AV node) has a left and right branch of bundle of His
Purkinje fibres innervate the myocardium of heart
how is it that autorhymic cells create rhythmic contraction?
dont have a resting membrane potential, drifts between AP with slow depolarisation, makes AP cyclic
explain the ionic basis behind autorhythmic cells
funny voltage gated Na open: Na floods in
K+ channels close
-membrane moves toward threshold
2nd half, funnys close and transient voltage gates Ca2+ open = influx of Ca2+
-threshold reached
transient Ca2+ channels close, long lasting open = large influx of Ca2+
depolarisation betwen AP begins with K+ channels opened and long lasting Ca2+ closed



why are funny channels called this?
voltage gated channels typically open when membrane becomes less negative (depolarises) but these open when the membrane becomes more negative at end of repolarisation from AP
what are the 4 layers of the heart?
endocardium (inner)
myocardium (middle)
epicardium (outer)
pericardial sac
explain the 3 conduction pathways of the heart
interatrial- AP from SA node spreads throughout atria both become depol, contract together

internodal- AP then spreads to AV node, slower conduction allowing ventricles to fill

ventricular- gap juctions allows rapid transmit down branches of His and into purkinje, ventricels contract at same time

explain the ionic basis behind contractile cells?
RMP= -90mV (until excited by pacemaker), K+ leaky open
voltage Na+ open, rapid influx = reach peak
then close and K+ transient open (brief repol)
plateau; long lasting Ca2+ open = slow influx of Ca2+
K+ channels slowely close
Ca2+ inactivated
delayed activation of K+ (rapid efflux)
close once RMP reached


How does an action potential bring about contraction?
AP travels down t-tubule
long lasting voltage Ca2+ channels open, small amount enters from ECF
this triggers a large amount to leave sarcoplasmic reticulum
increase in cytosolic calcium for cross bridging
why is the calcium removal process slow? and what is required for this to happen?
allows for a long period of contraction
requires energy
what is a refractory period? why does the heart require one?
second AP cant be triggered until membrane has recovered from previous AP (plateau period)
allows relaxation, and heart to fill
what ionic events do diastole and systole apply to?
diastole (relaxation) = repolarization

systole (contraction) = depol
what are the
isovolumetric ventricular contraction
isovolumetric ventricular relaxation
contraction = when ventricle is completely closed, AV valve closes and aortic valve not yet open

relaxation = after contr when ventricle pressure falls below aortic, aortic valve closes, pressure still higher than atria so AV valve still closed
what do 'lub' and 'dub' correlate to?
'lub'- closure of AV valve
'dub'- closure of semmilunar valve
explain the 2 types of valve malfunction
stenotic- stiff, doesnt open properly
insufficient- can close completely
what are the average CO, SV, HR?
CO = 4900ml/ min
SV= 70 ml/beat
HR= 70 BPM
what is the cardiac reserve?
diff between CO at rest and max volume of blood the heart can pump per minute
explain the parasympathetic control of HR
vagus nerve innervates atrium (SA & AV nodes)

acetylcholine
-hyperpolarises cell and slows depol; reaches threhold less freq = slow HR
- reduces AV node excitability (making transmission to ventricles even longer)
-shortens plataeu phase (weaker atrial contraction)

explain the sympathetic control of HR
nerves innervate atrium and ventricles

noradrenaline
- speeds up depolarisation
- decreases AV nodal delay
- speeds up spread of AP
increases contractile strength
-speeds up relaxation (enhancing slow Ca2+ pump in sarcoplasmic reticulum)