Electrical events in the cardiac cycle
Describe resting membrane potential, depolarisation & action potentials - ANS-The
membrane force at which the chemical & electrical forces are balanced & there is no net
movement of ions = equilibrium potential -->
K=-90mV
Na=70mV
Ca=100mV
Resting membrane potential = tends towards -90mV as most cells are far more
permeable to K than Na or Ca + pumps actively remove Na & Ca outside the cell
For depolarisation to occur the membrane potential becomes less negative so that a
threshold is reached & voltage-sensitive, ion-selective channels open = triggering an AP
--> membrane permeability to Na & Ca is rapidly increased, permeability to K is
decreased
At rest = K channels open, Na & Ca channels closed = membrane potential -90mV -->
when a stimulus enters & depolarises the membrane potential (AP from neighbouring
cell, chemical transmitter) = voltage threshold reached = K channels closed, Na
channels open first, then Ca channels
Depolarisation occurs = constant influx of positive ions increases membrane voltage to
+30mV
Describe the 3 intervals on ECG & implications if they are altered
1. PR interval
2. ST segment
3. QT interval - ANS-1. Atrial depolarisation to ventricular depolarisation = start of
P-wave to start of QRS complex (as Q often not visible) --> time for conduction of AP
from SA node to ventricular muscles
- normally 0.12-0.2 seconds (0.16 at normal HR)
- prolonged PR interval (0.2-0.35) = first degree heart block = electrical signal travels
through AV node slower than normal = impaired conduction at AV node
2. no change in electrical activity (phase 2 plateau) = flat segment between s-wave &
t-wave
- period when ventricles are fully depolarised = isoelectric = no current (plateau)
, - position relative to rest of ECG can indicate ischaemia (depressed) or infarction
(elevated)
3. ventricular systole = QRS complex to end of t-wave --> total time for which ventricles
depolarise to repolarise - varies with HR, age, gender
- should be 0.4sec at 70bpm
- if >50% = prolonged Q-T syndrome = predispose to ventricular arrhythmia, fibrillation
Describe the 5 phases of an AP in a ventricular myocyte - ANS-Phase 4 = resting phase
= myocyte at rest - membrane voltage -90mV --> K channels open (steady K efflux),
other channels closed
Phase 0 = depolarisation --> stimulus raises the membrane potential to -75mV (flow of
ions from gap junctions) = triggering fast voltage-gated Na channels to open & K
channels co close = rapid Na influx, K efflux ceases = rapid depolarisation to peak of
+20/30mV (all or nothing - if threshold isn't reached AP doesn't occur)
Phase 1 = initial repolarisation = fast voltage-gated Na channels close = depolarisation
finishes --> then voltage-fated K channels open = small K efflux (transient increase in
permeability to K) = small drop in membrane potential
Phase 2 = plateau phase (0.2sec) = slow voltage-gated Ca channels open = Ca influx
(counter-balances positive K efflux) = prolonged depolarisation (unique to cardiac
ventricular muscle) --> Ca influx initiates ventricular contraction
Phase 3 = repolarisation = slow voltage-gated Ca channels close (& any remaining
open Na channels close), K channels remain open = K efflux = net outward positive
current = decreasing membrane potential back to resting (-90mV)
some K channels close & the resting phase begins again
Describe the absolute & relative refractory period - ANS-Absolute refractory period
(200-250ms) = voltage-gated Na channels are inactivated & unavailable for another
depolarisation --> contraction cannot be stimulated regardless of stimulus strength
Relative refractory period (50ms) = some voltage-gated fast Na channels are activated,
some remain inactivated (proportion of ready channels increases overtime) -->
contraction can be stimulated by a higher-than-usual strength stimulus = as not the full
population of Na channels are available so a strong stimulus is required for
depolarisation
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